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Sample records for acute pulmonary inflammation

  1. Rosiglitazone dampens pulmonary inflammation in a porcine model of acute lung injury.

    Science.gov (United States)

    Mirakaj, Valbona; Mutz, Christian; Vagts, Dierk; Henes, Janek; Haeberle, Helene A; Husung, Susanne; König, Tony; Nöldge-Schomburg, Gabriele; Rosenberger, Peter

    2014-08-01

    The hallmarks of acute lung injury (ALI) are the compromised alveolar-capillary barrier and the extravasation of leukocytes into the alveolar space. Given the fact that the peroxisome proliferator-activated receptor-γ agonist rosiglitazone holds significant anti-inflammatory properties, we aimed to evaluate whether rosiglitazone could dampen these hallmarks of local pulmonary inflammation in a porcine model of lung injury. For this purpose, we used a model of lipopolysaccharide (LPS, 50 μg/kg)-induced ALI. One hundred twenty minutes following the infusion of LPS, we started the exposure to rosiglitazone through inhalation or infusion. We found that intravenous rosiglitazone significantly controlled local pulmonary inflammation as determined through the expression of cytokines within the alveolar compartment. Furthermore, we found a significant reduction of the protein concentration and neutrophil activity within the alveolar space. In summary, we therefore conclude that the treatment with rosiglitazone might dampen local pulmonary inflammation during the initial stages of ALI.

  2. Differences in inflammation and acute phase response but similar genotoxicity in mice following pulmonary exposure to graphene oxide and reduced graphene oxide

    DEFF Research Database (Denmark)

    Bengtson, Stefan; Knudsen, KB; Kyjovska, ZO

    2017-01-01

    the lowest dose was evaluated. GO induced a strong acute inflammatory response together with a pulmonary (Serum-Amyloid A, Saa3) and hepatic (Saa1) acute phase response. rGO induced less acute, but a constant and prolonged inflammation up to day 90. Lung histopathology showed particle agglomerates at day 90...... without signs of fibrosis. In addition, DNA damage in BAL cells was observed across time points and doses for both GO and rGO. In conclusion, pulmonary exposure to GO and rGO induced inflammation, acute phase response and genotoxicity but no fibrosis.......We investigated toxicity of 2-3 layered >1 μm sized graphene oxide (GO) and reduced graphene oxide (rGO) in mice following single intratracheal exposure with respect to pulmonary inflammation, acute phase response (biomarker for risk of cardiovascular disease) and genotoxicity. In addition, we...

  3. Acute effect of glucan-spiked office dust on nasal and pulmonary inflammation in guinea pigs

    DEFF Research Database (Denmark)

    Straszek, Sune; Adamcakova-Dodd, Andrea; Nervana, Metwali

    2007-01-01

     office dust and glucan on nasal and pulmonary inflammation. This is relevant for humans with occupational exposure in waste handling and farming and buildings with mold problems.  Office dust collected from Danish offices was spiked with 1% (1-3)-β-glucan (curdlan). Guinea pig nasal cavity volume was measured...... by acoustic rhinometry (AR) and animals were exposed by inhalation for 4 hr to curdlan spiked dust, unspiked dust, purified air (negative controls) or LPS (positive controls). After exposure (+5 hr) or the following day (+18 hr) measurements were repeated by AR and followed by bronchoalveolar lavage (BAL...... cells or IL-8 except in LPS-exposed controls. The delayed decrease of nasal cavity volume after exposure to glucan spiked dust suggests a slow effect on the upper airways for curdlan and office dust together, though no pulmonary response or direct signs of inflammation were observed. Glucan spiked...

  4. Regional pulmonary inflammation in an endotoxemic ovine acute lung injury model.

    Science.gov (United States)

    Fernandez-Bustamante, A; Easley, R B; Fuld, M; Mulreany, D; Chon, D; Lewis, J F; Simon, B A

    2012-08-15

    The regional distribution of inflammation during acute lung injury (ALI) is not well known. In an ovine ALI model we studied regional alveolar inflammation, surfactant composition, and CT-derived regional specific volume change (sVol) and specific compliance (sC). 18 ventilated adult sheep received IV lipopolysaccharide (LPS) until severe ALI was achieved. Blood and bronchoalveolar lavage (BAL) samples from apical and basal lung regions were obtained at baseline and injury time points, for analysis of cytokines (IL-6, IL-1β), BAL protein and surfactant composition. Whole lung CT images were obtained in 4 additional sheep. BAL protein and IL-1β were significantly higher in injured apical vs. basal regions. No significant regional surfactant composition changes were observed. Baseline sVol and sC were lower in apex vs. base; ALI enhanced this cranio-caudal difference, reaching statistical significance only for sC. This study suggests that apical lung regions show greater inflammation than basal ones during IV LPS-induced ALI which may relate to differences in regional mechanical events.

  5. Inflammation and pulmonary hypertension.

    Science.gov (United States)

    Mathew, Rajamma

    2010-01-01

    Pulmonary hypertension (PH) is a serious disorder with high morbidity and mortality rate. Evidence is accumulating to suggest that inflammation plays a significant role in the pathogenesis of PH. Endothelial cells play an important role in inflammation and immune reactions, and inflammatory cytokines cause endothelial dysfunction. Endothelial dysfunction is a hallmark of PH, consisting of reduced availability of vasodilators and antiproliferative factors and increased production of vasoconstrictors and vascular proliferative factors. Up-regulation of inflammatory cytokines and perivascular inflammatory cell infiltration have been detected in the lungs of patients with idiopathic PH. Prevalence of PH in patients with systemic inflammatory diseases is well documented. Interestingly, a significant loss of endothelial caveolin-1, a potent immunomodulator and an inhibitor of cell proliferation, has been reported in human and experimental forms of PH. Reduction in the expression of caveolin-1 is known to result in the removal of antiproliferative activities, thus, leading to deregulated vascular cell proliferation. This article summarizes the roles of inflammation and endothelial caveolin-1 and their possible interrelationship in PH.

  6. Effect and its clinical significance of different dose of glucocorticoids on inflammation mediators in patients with acute exacerbation of chronic obstructive pulmonary diseases

    Institute of Scientific and Technical Information of China (English)

    钟佰强

    2014-01-01

    Objective To explore the effect and its clinical significance of different dose of glucocorticoids on inflammation mediators in patients with acute exacerbation of chronic obstructive pulmonary diseases.Methods 45 patients admitted to our hospitals from March 2007 to March 2011were randomly divided into 3 groups:methylprednisolone40 mg group(methylprednisolone 40mg,iv,qd),meth-

  7. Histoplasmosis - acute (primary) pulmonary

    Science.gov (United States)

    ... this page: //medlineplus.gov/ency/article/000098.htm Histoplasmosis - acute (primary) pulmonary To use the sharing features on this page, please enable JavaScript. Acute pulmonary histoplasmosis is a respiratory infection that is caused by ...

  8. Regulation of pulmonary inflammation by mesenchymal cells

    NARCIS (Netherlands)

    Alkhouri, Hatem; Poppinga, Wilfred Jelco; Tania, Navessa Padma; Ammit, Alaina; Schuliga, Michael

    2014-01-01

    Pulmonary inflammation and tissue remodelling are common elements of chronic respiratory diseases such as asthma, chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), and pulmonary hypertension (PH). In disease, pulmonary mesenchymal cells not only contribute to tissue

  9. Alveolar recruitment of ficolin-3 in response to acute pulmonary inflammation in humans

    DEFF Research Database (Denmark)

    Plovsing, Ronni R; Berg, Ronan M G; Munthe-Fog, Lea;

    2016-01-01

    BACKGROUND: Ficolins serve as soluble recognition molecules in the lectin pathway of complement. They are known to participate in the systemic host-response to infection but their role in local pulmonary defence is still incompletely understood. The purpose of this study was to clarify whether...

  10. Acute Meteorite Dust Exposure and Pulmonary Inflammation - Implications for Human Space Exploration

    Science.gov (United States)

    Harrington, A. D.; McCubbin, F. M.; Kaur, J.; Smirnov, A.; Galdanes, K.; Schoonen, M. A. A.; Chen, L. C.; Tsirka, S. E.; Gordon, T.

    2017-01-01

    The previous manned missions to the Moon represent milestones of human ingenuity, perseverance, and intellectual curiosity. However, one of the major ongoing concerns is the array of hazards associated with lunar surface dust. Not only did the dust cause mechanical and structural integrity issues with the suits, the dust 'storm' generated upon reentrance into the crew cabin caused "lunar hay fever" and "almost blindness [1-3]" (Figure 1). It was further reported that the allergic response to the dust worsened with each exposure [4]. The lack of gravity exacerbated the exposure, requiring the astronauts to wear their helmet within the module in order to avoid breathing the irritating particles [1]. Due to the prevalence of these high exposures, the Human Research Roadmap developed by NASA identifies the Risk of Adverse Health and Performance Effects of Celestial Dust Exposure as an area of concern [5]. Extended human exploration will further increase the probability of inadvertent and repeated exposures to celestial dusts. Going forward, hazard assessments of celestial dusts will be determined through sample return efforts prior to astronaut deployment. Studies on the lunar highland regolith indicate that the dust is not only respirable but also reactive [2, 6-9], and previous studies concluded that it is moderately toxic; generating a greater response than titanium oxide but a lower response than quartz [6]. The presence of reactive oxygen species (ROS) on the surface of the dust has been implicated. However, there is actually little data related to physicochemical characteristics of particulates and pulmonary toxicity, especially as it relates to celestial dust exposure. As a direct response to this deficit, the present study evaluates the role of a particulate's innate geochemical features (e.g., bulk chemistry, internal composition, morphology, size, and reactivity) in generating adverse toxicological responses in vitro and in vivo. This highly interdisciplinary

  11. Sequential Treatments with Tongsai and Bufei Yishen Granules Reduce Inflammation and Improve Pulmonary Function in Acute Exacerbation-Risk Window of Chronic Obstructive Pulmonary Disease in Rats

    Directory of Open Access Journals (Sweden)

    Xiaofan Lu

    2016-01-01

    Full Text Available Background. Sequential treatments of Chinese medicines for acute exacerbation of chronic obstructive pulmonary disease (AECOPD risk window (RW have benefits for preventing reoccurrences of AEs; however, the effects on pulmonary function, pulmonary, and systemic inflammatory biomarkers remain unclear. Methods. Cigarette-smoke/bacterial infections induced rats were randomized into Control, COPD, AECOPD, Tongsai Granule/normal saline (TSG/NS, moxifloxacin + salbutamol/NS (MXF+STL/NS, TSG/Bufei Yishen Granule (BYG, MXF+STL/STL, and TSG+MXF+STL/BYG+STL groups and given corresponding medicine(s in AE- and/or RW phase. Body temperature, pulmonary function, blood cytology, serum amyloid A (SAA and C-reactive protein (CRP, pulmonary histomorphology and myeloperoxidase (MPO, polymorphonuclear (PMN elastase, interleukins IL-1β, IL-6, and IL-10, and tumor necrosis factor- (TNF- α expressions were determined. Results. Body temperature, inflammatory cells and cytokines, SAA, CRP, and pulmonary impairment were higher in AECOPD rats than stable COPD, while pulmonary function declined and recovered to COPD level in 14–18 days. All biomarkers were improved in treated groups with shorter recovery times of 4–10 days, especially in TSG+MXF+STL/BYG+STL group. Conclusion. Sequential treatments with Tongsai and Bufei Yishen Granules, during AECOPD-RW periods, can reduce inflammatory response and improve pulmonary function and shorten the recovery courses of AEs, especially the integrated Chinese and Western medicines.

  12. Sequential Treatments with Tongsai and Bufei Yishen Granules Reduce Inflammation and Improve Pulmonary Function in Acute Exacerbation-Risk Window of Chronic Obstructive Pulmonary Disease in Rats

    Science.gov (United States)

    Lu, Xiaofan; Li, Ya; Wang, Haifeng; Wu, Zhaohuan; Li, Hangjie; Wang, Yang

    2016-01-01

    Background. Sequential treatments of Chinese medicines for acute exacerbation of chronic obstructive pulmonary disease (AECOPD) risk window (RW) have benefits for preventing reoccurrences of AEs; however, the effects on pulmonary function, pulmonary, and systemic inflammatory biomarkers remain unclear. Methods. Cigarette-smoke/bacterial infections induced rats were randomized into Control, COPD, AECOPD, Tongsai Granule/normal saline (TSG/NS), moxifloxacin + salbutamol/NS (MXF+STL/NS), TSG/Bufei Yishen Granule (BYG), MXF+STL/STL, and TSG+MXF+STL/BYG+STL groups and given corresponding medicine(s) in AE- and/or RW phase. Body temperature, pulmonary function, blood cytology, serum amyloid A (SAA) and C-reactive protein (CRP), pulmonary histomorphology and myeloperoxidase (MPO), polymorphonuclear (PMN) elastase, interleukins IL-1β, IL-6, and IL-10, and tumor necrosis factor- (TNF-) α expressions were determined. Results. Body temperature, inflammatory cells and cytokines, SAA, CRP, and pulmonary impairment were higher in AECOPD rats than stable COPD, while pulmonary function declined and recovered to COPD level in 14–18 days. All biomarkers were improved in treated groups with shorter recovery times of 4–10 days, especially in TSG+MXF+STL/BYG+STL group. Conclusion. Sequential treatments with Tongsai and Bufei Yishen Granules, during AECOPD-RW periods, can reduce inflammatory response and improve pulmonary function and shorten the recovery courses of AEs, especially the integrated Chinese and Western medicines. PMID:27563333

  13. Tight junctions in pulmonary epithelia during lung inflammation

    OpenAIRE

    Wittekindt, Oliver H.

    2016-01-01

    Inflammatory lung diseases like asthma bronchiale, chronic obstructive pulmonary disease and allergic airway inflammation are widespread public diseases that constitute an enormous burden to the health systems. Mainly classified as inflammatory diseases, the treatment focuses on strategies interfering with local inflammatory responses by the immune system. Inflammatory lung diseases predispose patients to severe lung failures like alveolar oedema, respiratory distress syndrome and acute lung ...

  14. Effects of Mikania glomerata Spreng. and Mikania laevigata Schultz Bip. ex Baker (Asteraceae) extracts on pulmonary inflammation and oxidative stress caused by acute coal dust exposure

    Energy Technology Data Exchange (ETDEWEB)

    Freitas, T.P.; Silveira, P.C.; Rocha, L.G.; Rezin, G.T.; Rocha, J.; Citadini-Zanette, V.; Romao, P.T.; Dal-Pizzol, F.; Pinho, R.A.; Andrade, V.M.; Streck, E.L. [University Extremo Catarinense, Criciuma (Brazil)

    2008-12-15

    Several studies have reported biological effects of Mikania glomerata and Mikania laevigata, used in Brazilian folk medicine for respiratory diseases. Pneumoconiosis is characterized by pulmonary inflammation caused by coal dust exposure. In this work, we evaluated the effect of pretreatment with M. glomerata and M. laevigata extracts (MGE and MLE, respectively) (100 mg/kg, s.c.) on inflammatory and oxidative stress parameters in lung of rats subjected to a single coal dust intratracheal instillation. Rats were pretreated for 2 weeks with saline solution, MGE, or MLE. On day 15, the animals were anesthetized, and gross mineral coal dust or saline solutions were administered directly in the lung by intratracheal instillation. Fifteen days after coal dust instillation, the animals were killed. Bronchoalveolar lavage (BAL) was obtained; total cell count and lactate dehydrogenase (LDH) activity were determined. In the lung, myeloperoxidase activity, thiobarbituric acid-reactive substances (TBARS) level, and protein carbonyl and sulfhydryl contents were evaluated. In BAL of treated animals, we verified an increased total cell count and LDH activity. MGE and MLE prevented the increase in cell count, but only MLE prevented the increase in LDH. Myeloperoxidase and TBARS levels were not affected, protein carbonylation was increased, and the protein thiol levels were decreased by acute coal dust intratracheal administration. The findings also suggest that both extracts present an important protective effect on the oxidation of thiol groups. Moreover, pretreatment with MGE and MLE also diminished lung inflammatory infiltration induced by coal dust, as assessed by histopathologic analyses.

  15. Ozone-Induced Pulmonary Injury and Inflammation are Modulated by Adrenal-Derived Stress Hormones

    Science.gov (United States)

    Ozone exposure promotes pulmonary injury and inflammation. Previously we have characterized systemic changes that occur immediately after acute ozone exposure and are mediated by neuro-hormonal stress response pathway. Both HPA axis and sympathetic tone alterations induce the rel...

  16. DNA strand breaks, acute phase response and inflammation following pulmonary exposure by instillation to the diesel exhaust particle NIST1650b in mice

    DEFF Research Database (Denmark)

    Kyjovska, Zdenka O.; Jacobsen, Nicklas R.; Saber, Anne T.

    2015-01-01

    by the alkaline comet assay as DNA strand breaks in BAL cells, lung and liver tissue. The pulmonary acute phase response was analysed by Saa3 mRNA levels by real-time quantitative polymerase chain reaction. Instillation of DEP induced a strong neutrophil influx 1 and 3 days, but not 28 days post-exposure. Saa3 m...

  17. Characteristics of pulmonary inflammation in combined pulmonary fibrosis and emphysema

    Institute of Scientific and Technical Information of China (English)

    ZHAO Ying; CUI Ai; WANG Feng; WANG Xiao-juan; CHEN Xing; JIN Mu-lan; HUANG Ke-wu

    2012-01-01

    Background The condition of concomitant upper lobe emphysema and lower lobe fibrosis as identified by computer tomography is known as combined pulmonary fibrosis and emphysema (CPFE).CPFE has distinct clinical characteristics compared with emphysema alone (EA) and idiopathic pulmonary fibrosis (IPF) without emphysema.However,the pulmonary inflammation characteristics of CPFE are not well known,and the differences between CPFE and the other two diseases with regards to pulmonary inflammation need to be explored.The pulmonary inflammatory characteristics were investigated in CPFE patients and compared with EA and IPF.Methods Fraction exhaled nitric oxide (Fe,NO) and differential cell counts,the concentrations of monokine induced by interferon gamma (MIG/CXCL9),interferon-inducible protein 10 (IP-10/CXCL10),and interferon-inducible T cell alpha chemoattractant (I-TAC/CXCL11) were measured in induced sputum obtained from subjects with CPFE (n=22),EA (n=22),IPF (n=14),and healthy volunteers (HV,n=12).In addition,immunohistochemistry was used to quantify the expression of nitric oxide synthases in alveolar macrophages in 23 lung tissues from patients and control subjects.Results The CPFE group had higher alveolar NO than subjects in the EA and HV groups (P=0.009,P=0.001,respectively) but not than the IPF group (P >0.05).Numbers of sputum eosinophils were significantly elevated in CPFE and IPF groups compared with the HV group (P=0.001,P=-0.008).In contrast,eosinophil counts in EA group did not differ from those in the HV group.Compared with the EA and HV groups,the CPFE group had a lower concentration of Ⅰ-TAC/CXCL11 in sputum supernatants (P=-0.003,P=0.004).Immunoreactivity for inducible nitric oxide synthase (iNOS)was higher in the CPFE group than in the EA group (P=-0.018,P=0.006,respectively).Conclusions The pulmonary inflammation of CPFE group is more similar to IPF group,while the distal airway inflammation is more significant in CPFE and IPF groups than in EA

  18. Sympathetic crashing acute pulmonary edema.

    Science.gov (United States)

    Agrawal, Naman; Kumar, Akshay; Aggarwal, Praveen; Jamshed, Nayer

    2016-12-01

    Sympathetic crashing acute pulmonary edema (SCAPE) is the extreme end of the spectrum of acute pulmonary edema. It is important to understand this disease as it is relatively common in the emergency department (ED) and has better outcomes when managed appropriately. The patients have an abrupt redistribution of fluid in the lungs, and when treated promptly and effectively, these patients will rapidly recover. Noninvasive ventilation and intravenous nitrates are the mainstay of treatment which should be started within minutes of the patient's arrival to the ED. Use of morphine and intravenous loop diuretics, although popular, has poor scientific evidence.

  19. Fever in acute pulmonary embolism.

    Science.gov (United States)

    Stein, P D; Afzal, A; Henry, J W; Villareal, C G

    2000-01-01

    Although fever has been reported in several case series of acute pulmonary embolism (PE), the extent to which fever may be caused by PE, and not associated disease, has not been adequately sorted out. Clarification of the frequency and severity of fever in acute PE may assist in achieving an accurate clinical impression, and perhaps avoid an inadvertent exclusion of the diagnosis. The purpose of this investigation is to evaluate the extent to which fever is caused by acute PE. Patients participated in the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED). Temperature was evaluated among patients with angiographically proven PE. A determination of whether other causes of fever were present was based on a retrospective analysis of discharge summaries, PIOPED summaries, and a computerized list of all discharge diagnoses. Among patients with PE and no other source of fever, fever was present in 43 of 311 patients (14%). Fever in patients with pulmonary hemorrhage or infarction was not more frequent than among those with no pulmonary hemorrhage or infarction, 39 of 267 patients (15%) vs 4 of 44 patients (9%; not significant). Clinical evidence of deep venous thrombosis was often present in patients with PE and otherwise unexplained fever. Low-grade fever is not uncommon in PE, and high fever, although rare, may occur. Fever need not be accompanied by pulmonary hemorrhage or infarction.

  20. Acute pulmonary embolism.

    Science.gov (United States)

    Kuriakose, Jean; Patel, Smita

    2010-02-01

    CT pulmonary angiography has become a first-line imaging test for evaluation of PE because of its high accuracy, ease of use, and ready availability. PIOPED II supports the use of multidetector CT as a first-line test especially in outpatients. Technological advances continue to evolve, and with refinements in technology, we will continue to optimize imaging for PE detection. lonizing radiation remains a concern particularly in the young and in pregnant patients, and methods to decrease these are being advocated. SPECT V/Q may play a bigger role in PE diagnosis in the future and the role of MR is yet to be determined in the PIOPED ll study, with the potential of solving some of the issues regarding radiation in a select group of patients.

  1. Chlamydial heat shock protein 60 induces acute pulmonary inflammation in mice via the Toll-like receptor 4- and MyD88-dependent pathway.

    Science.gov (United States)

    Bulut, Yonca; Shimada, Kenichi; Wong, Michelle H; Chen, Shuang; Gray, Pearl; Alsabeh, Randa; Doherty, Terence M; Crother, Timothy R; Arditi, Moshe

    2009-07-01

    Heat shock protein 60 derived from Chlamydia pneumoniae (cHSP60) activates Toll-like receptor 4 (TLR4) signaling through the MyD88 pathway in vitro, but it is not known how cHSP60 contributes to C. pneumoniae-induced lung inflammation. We treated wild-type (WT), TLR2(-/-), TLR4(-/-), or MyD88(-/-) mice intratracheally (i.t.) with recombinant cHSP60 (50 microg), UV-killed C. pneumoniae (UVCP; 5 x 10(6) inclusion-forming units/mouse), lipopolysaccharide (2 microg), or phosphate-buffered saline (PBS) and sacrificed mice 24 h later. Bronchoalveolar lavage (BAL) was obtained to measure cell counts and cytokine levels, lungs were analyzed for histopathology, and lung homogenate chemokine concentrations were determined. Bone marrow-derived dendritic cells (BMDDCs) were generated and stimulated with live C. pneumoniae (multiplicity of infection [MOI], 5), UVCP (MOI, 5), or cHSP60 for 24 h, and the expression of costimulatory molecules (CD80 and CD86) was measured by fluorescence-activated cell sorting. cHSP60 induced acute lung inflammation with the same intensity as that of UVCP-induced inflammation in WT mice but not in TLR4(-/-) or MyD88(-/-) mice. cHSP60- and UVCP-induced lung inflammation was associated with increased numbers of cells in BAL, increased neutrophil recruitment, and elevated BAL interleukin-6 (IL-6) levels. Both cHSP60 and UVCP induced IL-6 release and CD80 and CD86 expression in WT cells but not in MyD88(-/-) BMDDCs. cHSP60 stimulated DC activation in a TLR4- and MyD88-dependent manner with an intensity similar to that induced by UVCP. These data suggest that cHSP60 promotes lung inflammation and DC activation via TLR4 and MyD88 and therefore may play a significant role in the pathogenesis of C. pneumoniae-induced chronic inflammatory lung diseases.

  2. Pulmonary edema in acute carbon monoxide poisoning

    Energy Technology Data Exchange (ETDEWEB)

    Kim, Kun Sang; Chang, Kee Hyun; Lee, Myung Uk [Seoul National University College of Medicine, Seoul (Korea, Republic of)

    1974-10-15

    Acute carbon monoxide poisoning has frequently occurred in Korean, because of the coal briquette being widely used as fuel in Korean residences. Carbon monoxide poisoning has been extensively studied, but it has been sparsely reported that pulmonary edema may develop in acute CO poisoning. We have noticed nine cases of pulmonary edema in acute CO poisoning last year. Other possible causes of pulmonary edema could be exclude in all cases but one. The purpose of this paper is to describe nine cases of pulmonary edema complicated in acute CO poisoning and discuss the pathogenesis and the prognosis.

  3. Hfe deficiency impairs pulmonary neutrophil recruitment in response to inflammation.

    Directory of Open Access Journals (Sweden)

    Karolina Benesova

    Full Text Available Regulation of iron homeostasis and the inflammatory response are tightly linked to protect the host from infection. Here we investigate how imbalanced systemic iron homeostasis in a murine disease model of hereditary hemochromatosis (Hfe(-/- mice affects the inflammatory responses of the lung. We induced acute pulmonary inflammation in Hfe(-/- and wild-type mice by intratracheal instillation of 20 µg of lipopolysaccharide (LPS and analyzed local and systemic inflammatory responses and iron-related parameters. We show that in Hfe(-/- mice neutrophil recruitment to the bronchoalveolar space is attenuated compared to wild-type mice although circulating neutrophil numbers in the bloodstream were elevated to similar levels in Hfe(-/- and wild-type mice. The underlying molecular mechanisms are likely multifactorial and include elevated systemic iron levels, alveolar macrophage iron deficiency and/or hitherto unexplored functions of Hfe in resident pulmonary cell types. As a consequence, pulmonary cytokine expression is out of balance and neutrophils fail to be recruited efficiently to the bronchoalveolar compartment, a process required to protect the host from infections. In conclusion, our findings suggest a novel role for Hfe and/or imbalanced iron homeostasis in the regulation of the inflammatory response in the lung and hereditary hemochromatosis.

  4. Aged red garlic extract reduces lipopolysaccharide-induced nitric oxide production in RAW 264.7 macrophages and acute pulmonary inflammation through haeme oxygenase-1 induction.

    Science.gov (United States)

    Park, H-J; Jeon, B T; Kim, H C; Roh, G S; Shin, J-H; Sung, N-J; Han, J; Kang, D

    2012-05-01

    It is known that garlic has antioxidative and anti-inflammatory properties. Aged red garlic (ARG), a novel aged garlic formulation, has higher antioxidant effects than fresh raw garlic. This study was performed to examine the anti-inflammatory effects of ARG extract (ARGE). The anti-inflammatory effects of ARGE were evaluated in the lipopolysaccharide (LPS)-treated Raw 264.7 macrophages and acute lung inflammatory mice. NO production was determined by the Griess method, and iNOS, HO-1 and COX-2 expressions were measured using Western blot analysis. Histology and inflammation extent of lung were analysed using haematoxylin-eosin staining and immunohistochemistry. ARGE treatment markedly reduced LPS-induced nitrite production in RAW 264.7 macrophages and reduced inducible nitric oxide synthase (iNOS) expression. Treatment of cells with ARGE led to a significant increase in haeme oxygenase-1 (HO-1) protein expression, which was mediated by stimulating the expression of nuclear factor erythroid 2-related factor 2 (Nrf2). Treatment with zinc protoporphyrin, a selective inhibitor of HO-1, significantly reversed the ARGE-mediated inhibition of nitrite production (P < 0.05). In LPS-induced inflammatory mice, ARGE treatment down-regulated iNOS and COX-2 expressions, while it up-regulated HO-1 expression. These results show that ARGE reduces LPS-induced nitric oxide production in RAW 264.7 macrophages through HO-1 induction and suggest that ARGE may have potential effects on prevention and treatment of acute inflammatory lung injury. © 2012 The Authors Acta Physiologica © 2012 Scandinavian Physiological Society.

  5. Acute exacerbations and pulmonary hypertension in advanced idiopathic pulmonary fibrosis.

    LENUS (Irish Health Repository)

    Judge, Eoin P

    2012-07-01

    The aim of this study was to evaluate the risk factors for and outcomes of acute exacerbations in patients with advanced idiopathic pulmonary fibrosis (IPF), and to examine the relationship between disease severity and neovascularisation in explanted IPF lung tissue. 55 IPF patients assessed for lung transplantation were divided into acute (n=27) and non-acute exacerbation (n=28) groups. Haemodynamic data was collected at baseline, at the time of acute exacerbation and at lung transplantation. Histological analysis and CD31 immunostaining to quantify microvessel density (MVD) was performed on the explanted lung tissue of 13 transplanted patients. Acute exacerbations were associated with increased mortality (p=0.0015). Pulmonary hypertension (PH) at baseline and acute exacerbations were associated with poor survival (p<0.01). PH at baseline was associated with a significant risk of acute exacerbations (HR 2.217, p=0.041). Neovascularisation (MVD) was significantly increased in areas of cellular fibrosis and significantly decreased in areas of honeycombing. There was a significant inverse correlation between mean pulmonary artery pressure and MVD in areas of honeycombing. Acute exacerbations were associated with significantly increased mortality in patients with advanced IPF. PH was associated with the subsequent development of an acute exacerbation and with poor survival. Neovascularisation was significantly decreased in areas of honeycombing, and was significantly inversely correlated with mean pulmonary arterial pressure in areas of honeycombing.

  6. Immune Inflammation and Disease Progression in Idiopathic Pulmonary Fibrosis.

    Directory of Open Access Journals (Sweden)

    Elisabetta Balestro

    Full Text Available The clinical course in idiopathic pulmonary fibrosis (IPF is highly heterogeneous, with some patients having a slow progression and others an accelerated clinical and functional decline. This study aims to clinically characterize the type of progression in IPF and to investigate the pathological basis that might account for the observed differences in disease behavior. Clinical and functional data were analyzed in 73 IPF patients, followed long-time as candidates for lung transplantation. The forced vital capacity (FVC change/year (< or ≥10% predicted was used to define "slow" or "rapid" disease progression. Pathological abnormalities were quantified in the explanted lung of 41 out of 73 patients undergoing lung transplantation. At diagnosis, slow progressors (n = 48 showed longer duration of symptoms and lower FVC than rapid progressors (n = 25. Eleven slow and 3 rapid progressors developed an acute exacerbation (AE during follow-up. Quantitative lung pathology showed a severe innate and adaptive inflammatory infiltrate in rapid progressors, markedly increased compared to slow progressors and similar to that observed in patients experiencing AE. The extent of inflammation was correlated with the yearly FVC decline (r = 0.52, p = 0.005. In conclusion an innate and adaptive inflammation appears to be a prominent feature in the lung of patients with IPF and could contribute to determining of the rate of disease progression.

  7. Immune Inflammation and Disease Progression in Idiopathic Pulmonary Fibrosis.

    Science.gov (United States)

    Balestro, Elisabetta; Calabrese, Fiorella; Turato, Graziella; Lunardi, Francesca; Bazzan, Erica; Marulli, Giuseppe; Biondini, Davide; Rossi, Emanuela; Sanduzzi, Alessandro; Rea, Federico; Rigobello, Chiara; Gregori, Dario; Baraldo, Simonetta; Spagnolo, Paolo; Cosio, Manuel G; Saetta, Marina

    2016-01-01

    The clinical course in idiopathic pulmonary fibrosis (IPF) is highly heterogeneous, with some patients having a slow progression and others an accelerated clinical and functional decline. This study aims to clinically characterize the type of progression in IPF and to investigate the pathological basis that might account for the observed differences in disease behavior. Clinical and functional data were analyzed in 73 IPF patients, followed long-time as candidates for lung transplantation. The forced vital capacity (FVC) change/year (slow" or "rapid" disease progression. Pathological abnormalities were quantified in the explanted lung of 41 out of 73 patients undergoing lung transplantation. At diagnosis, slow progressors (n = 48) showed longer duration of symptoms and lower FVC than rapid progressors (n = 25). Eleven slow and 3 rapid progressors developed an acute exacerbation (AE) during follow-up. Quantitative lung pathology showed a severe innate and adaptive inflammatory infiltrate in rapid progressors, markedly increased compared to slow progressors and similar to that observed in patients experiencing AE. The extent of inflammation was correlated with the yearly FVC decline (r = 0.52, p = 0.005). In conclusion an innate and adaptive inflammation appears to be a prominent feature in the lung of patients with IPF and could contribute to determining of the rate of disease progression.

  8. [Acute pulmonary edema secondary to acute upper airway obstruction].

    Science.gov (United States)

    Sánchez-Ortega, J L; Carpintero-Moreno, F; Olivares-López, A; Borrás-Rubio, E; Alvarez-López, M J; García-Izquierdo, A

    1992-01-01

    We report a 72 years old woman with mild arterial hypertension and no other pathological history who presented an acute pulmonary edema due to acute obstruction of the upper airway secondary to vocal chord paralysis developing during the immediate postoperative phase of thyroidectomy. The acute pulmonary edema resolved after application of tracheal reintubation, mechanical ventilation controlled with end expiratory positive pressure, diuretics, morphine, and liquid restriction. We discuss the possible etiopathogenic possibilities of this infrequent clinical picture and we suggest that all patients who suffered and acute obstruction of the upper airways require a careful clinical surveillance in order to prevent the development of the pulmonary syndrome.

  9. Anatomic distribution of embolus at CT pulmonary angiography in patients suspected acute pulmonary embolism

    Institute of Scientific and Technical Information of China (English)

    朱力

    2013-01-01

    Objective To summarize and analyze the morphology and distribution of embolus in patients suspected acute pulmonary embolism. Methods The CT pulmonary angiography(CTPA) imagings of 279 patients suspected acute pulmonary embolism were analyzed retrospectively in

  10. Balance impairment and systemic inflammation in chronic obstructive pulmonary disease

    Directory of Open Access Journals (Sweden)

    Tudorache E

    2015-09-01

    Full Text Available Emanuela Tudorache,1 Cristian Oancea,1 Claudiu Avram,2 Ovidiu Fira-Mladinescu,1 Lucian Petrescu,3 Bogdan Timar4 1Department of Pulmonology, University of Medicine and Pharmacy “Victor Babes”, 2Physical Education and Sport Faculty, West University of Timisoara, 3Department of Cardiology, University of Medicine and Pharmacy “Victor Babes”, 4Department of Biostatistics and Medical Informatics, University of Medicine and Pharmacy “Victor Babes”, Timisoara, Romania Background/purpose: Chronic obstructive pulmonary disease (COPD, especially in severe forms, is commonly associated with systemic inflammation and balance impairment. The aim of our study was to evaluate the impact on equilibrium of stable and exacerbation (acute exacerbation of COPD [AECOPD] phases of COPD and to investigate if there is a connection between lower extremity muscle weakness and systemic inflammation.Methods: We enrolled 41 patients with COPD (22 stable and 19 in AECOPD and 20 healthy subjects (control group, having no significant differences regarding the anthropometric data. We analyzed the differences in balance tests scores: Falls Efficacy Scale-International (FES-I questionnaire, Berg Balance Scale (BBS, Timed Up and Go (TUG test, Single Leg Stance (SLS, 6-minute walking distance (6MWD, isometric knee extension (IKE between these groups, and also the correlation between these scores and inflammatory biomarkers.Results: The presence and severity of COPD was associated with significantly decreased score in IKE (P<0.001, 6MWD (P<0.001, SLS (P<0.001, and BBS (P<0.001, at the same time noting a significant increase in median TUG score across the studied groups (P<0.001. The AECOPD group vs stable group presented a significant increase in high-sensitive C-reactive protein (hs-CRP levels (10.60 vs 4.01; P=0.003 and decrease in PaO2 (70.1 vs 59.1; P<0.001. We observed that both IKE scores were significantly and positive correlated with all the respiratory volumes

  11. Clinical Practice Guidelines for Acute Pulmonary Edema.

    Directory of Open Access Journals (Sweden)

    Pablo Rodríguez Díaz

    2009-03-01

    Full Text Available Clinical Practice Guidelines for Acute Pulmonary Edema. It has been defined as an abrupt and severe failure of the left ventricular function which causes pulmonary edema or cardiac origin interfering with the normal oxygen exchange at pulmonary level. This document includes a review and update of the main clinical aspects allowing the early diagnosis and immediate therapeutic treatment. It includes assessment guidelines focused on the most important aspects to be accomplished.

  12. Postischemic Inflammation in Acute Stroke

    Science.gov (United States)

    Consoli, Arturo; Arnaboldi, Marco; Consoli, Domenico

    2017-01-01

    Cerebral ischemia is caused by arterial occlusion due to a thrombus or an embolus. Such occlusion induces multiple and concomitant pathophysiological processes that involve bioenergetic failure, acidosis, loss of cell homeostasis, excitotoxicity, and disruption of the blood-brain barrier. All of these mechanisms contribute to neuronal death, mainly via apoptosis or necrosis. The immune system is involved in this process in the early phases after brain injury, which contributes to potential enlargement of the infarct size and involves the penumbra area. Whereas inflammation and the immune system both exert deleterious effects, they also contribute to brain protection by stimulating a preconditioning status and to the concomitant repair of the injured parenchyma. This review describes the main phases of the inflammatory process occurring after arterial cerebral occlusion, with an emphasis on the role of single mediators. PMID:28079313

  13. [Measurement of pulmonary inflammation in cystic fibrosis].

    Science.gov (United States)

    Fayon, M; Chiron, R; Abely, M

    2008-06-01

    Lung inflammation is a pivotal phenomenon in the pathogenesis of cystic fibrosis. Inflammation can be measured and quantified within a research perspective, as well as in daily clinical practice. In this review paper, the "Inflammation Task Force" of the "Société Française de Mucoviscidose" has reviewed the literature regarding the various techniques currently available (bronchoalveolar lavage, sputum analysis, nasal wash and brushing, exhaled breath condensates, carbon monoxide and nitric oxide, and systemic measurements (plasma and urine)). The interpretation of all these determinations in children and adults is also discussed.

  14. Balance impairment and systemic inflammation in chronic obstructive pulmonary disease

    Science.gov (United States)

    Tudorache, Emanuela; Oancea, Cristian; Avram, Claudiu; Fira-Mladinescu, Ovidiu; Petrescu, Lucian; Timar, Bogdan

    2015-01-01

    Background/purpose Chronic obstructive pulmonary disease (COPD), especially in severe forms, is commonly associated with systemic inflammation and balance impairment. The aim of our study was to evaluate the impact on equilibrium of stable and exacerbation (acute exacerbation of COPD [AECOPD]) phases of COPD and to investigate if there is a connection between lower extremity muscle weakness and systemic inflammation. Methods We enrolled 41 patients with COPD (22 stable and 19 in AECOPD) and 20 healthy subjects (control group), having no significant differences regarding the anthropometric data. We analyzed the differences in balance tests scores: Falls Efficacy Scale-International (FES-I) questionnaire, Berg Balance Scale (BBS), Timed Up and Go (TUG) test, Single Leg Stance (SLS), 6-minute walking distance (6MWD), isometric knee extension (IKE) between these groups, and also the correlation between these scores and inflammatory biomarkers. Results The presence and severity of COPD was associated with significantly decreased score in IKE (P<0.001), 6MWD (P<0.001), SLS (P<0.001), and BBS (P<0.001), at the same time noting a significant increase in median TUG score across the studied groups (P<0.001). The AECOPD group vs stable group presented a significant increase in high-sensitive C-reactive protein (hs-CRP) levels (10.60 vs 4.01; P=0.003) and decrease in PaO2 (70.1 vs 59.1; P<0.001). We observed that both IKE scores were significantly and positive correlated with all the respiratory volumes. In both COPD groups, we observed that fibrinogen reversely and significantly correlated with the 6MWD, and FES-I questionnaire is correlated positively with TUG test. Hs-CRP correlated reversely with the walking test and SLS test, while correlating positively with TUG test and FES-I questionnaire. Conclusion According to this study, COPD in advanced and acute stages is associated with an increased history of falls, systemic inflammation, balance impairment, and lower extremity

  15. Acute Exacerbations of Idiopathic Pulmonary Fibrosis

    OpenAIRE

    Collard, Harold R.; Moore, Bethany B.; Flaherty, Kevin R.; Brown, Kevin K.; Kaner, Robert J.; King, Talmadge E.; Lasky, Joseph A.; Loyd, James E.; Noth, Imre; Olman, Mitchell A.; Raghu, Ganesh; Roman, Jesse; Ryu, Jay H.; Zisman, David A.; Hunninghake, Gary W.

    2007-01-01

    The natural history of idiopathic pulmonary fibrosis (IPF) has been characterized as a steady, predictable decline in lung function over time. Recent evidence suggests that some patients may experience a more precipitous course, with periods of relative stability followed by acute deteriorations in respiratory status. Many of these acute deteriorations are of unknown etiology and have been termed acute exacerbations of IPF. This perspective is the result of an international effort to summariz...

  16. Grouping nanomaterials to predict their potential to induce pulmonary inflammation

    NARCIS (Netherlands)

    Braakhuis, Hedwig M; Oomen, Agnes G; Cassee, Flemming R

    2016-01-01

    The rapidly expanding manufacturing, production and use of nanomaterials have raised concerns for both worker and consumer safety. Various studies have been published in which induction of pulmonary inflammation after inhalation exposure to nanomaterials has been described. Nanomaterials can vary in

  17. Airborne fine particulate matter induced pulmonary inflammation as well as oxidative stress in neonate rats

    Institute of Scientific and Technical Information of China (English)

    DING Li-ren; WANG Kai; Baher Fahmy; SHEN Hua-hao; Cormier Stephania

    2010-01-01

    Background Airborne fine particulate matter (PM) can induce pulmonary inflammation which may adversely affect human health, but very few reports about its effect on the neonate rats are available. This study aimed to observe the potential impact and toxicity of fine PMs on the airway in neonate rats.Methods Pulmonary inflammation, cytotoxicity, histopathology, and antioxidants as well as oxidant products were assessed 24 hours after intratracheal instillation of fine PM consecutively for 3 days. Cytotoxicity of fine PM was measured in Hep-2 cells.Results Rats treated with high dose fine PM developed significant pulmonary inflammation characterized by neutrophiland macrophage infiltration. The inflammatory process was related to elevated level of TNF-α and prooxidant/antioxidant imbalance in the lung. Cytotoxicity studies performed in human epithelial cells indicated that high dose fine PM significantly reduced cell viability.Conclusion The study demonstrated acute exposure to fine PM induced airway inflammation as well as increased oxidative stress in addition to its direct toxic effect on airway epithelium cells.

  18. [Acute heart failure: acute cardiogenic pulmonary edema and cardiogenic shock].

    Science.gov (United States)

    Sánchez Marteles, Marta; Urrutia, Agustín

    2014-03-01

    Acute cardiogenic pulmonary edema and cardiogenic shock are two of the main forms of presentation of acute heart failure. Both entities are serious, with high mortality, and require early diagnosis and prompt and aggressive management. Acute pulmonary edema is due to the passage of fluid through the alveolarcapillary membrane and is usually the result of an acute cardiac episode. Correct evaluation and clinical identification of the process is essential in the management of acute pulmonary edema. The initial aim of treatment is to ensure hemodynamic stability and to correct hypoxemia. Other measures that can be used are vasodilators such as nitroglycerin, loop diuretics and, in specific instances, opioids. Cardiogenic shock is characterized by sustained hypoperfusion, pulmonary wedge pressure > 18 mmHg and a cardiac index 30 mmHg) and absent or reduced diuresis (< 0.5 ml/kg/h). The most common cause is left ventricular failure due to acute myocardial infarction. Treatment consists of general measures to reverse acidosis and hypoxemia, as well as the use of vasopressors and inotropic drugs. Early coronary revascularization has been demonstrated to improve survival in shock associated with ischaemic heart disease.

  19. Acute pulmonary edema after near strangulation

    Energy Technology Data Exchange (ETDEWEB)

    Shumaker, D.; Kottamasu, S.; Preston, G.; Treloar, D.

    1988-11-01

    We report a case of acute, noncardiogenic pulmonary edema in an 11 year old boy who suffered strangulation during an altercation. The clinical presentation was characterized by moderate respiratory distress and hemoptysis. Both the radiographic and clinical findings resolved during the three day admission which followed. A review of the literature is presented, and possible pathogenesis is discussed.

  20. An uncommon cause of acute pulmonary edema.

    Science.gov (United States)

    Nepal, Santosh; Giri, Smith; Bhusal, Mohan; Siwakoti, Krishmita; Pathak, Ranjan

    2016-09-01

    Acute cardiogenic pulmonary edema secondary to catecholamine-induced cardiomyopathy is a very uncommon and fatal initial presentation of pheochromocytoma. However, with early clinical suspicion and aggressive management, the condition is reversible. This case report describes a patient who presented with hypertension, dyspnea, and cough with bloody streaks, and who recovered within 48 hours after appropriate treatment.

  1. Acute Exacerbations of Idiopathic Pulmonary Fibrosis

    Science.gov (United States)

    Collard, Harold R.; Moore, Bethany B.; Flaherty, Kevin R.; Brown, Kevin K.; Kaner, Robert J.; King, Talmadge E.; Lasky, Joseph A.; Loyd, James E.; Noth, Imre; Olman, Mitchell A.; Raghu, Ganesh; Roman, Jesse; Ryu, Jay H.; Zisman, David A.; Hunninghake, Gary W.; Colby, Thomas V.; Egan, Jim J.; Hansell, David M.; Johkoh, Takeshi; Kaminski, Naftali; Kim, Dong Soon; Kondoh, Yasuhiro; Lynch, David A.; Müller-Quernheim, Joachim; Myers, Jeffrey L.; Nicholson, Andrew G.; Selman, Moisés; Toews, Galen B.; Wells, Athol U.; Martinez, Fernando J.

    2007-01-01

    The natural history of idiopathic pulmonary fibrosis (IPF) has been characterized as a steady, predictable decline in lung function over time. Recent evidence suggests that some patients may experience a more precipitous course, with periods of relative stability followed by acute deteriorations in respiratory status. Many of these acute deteriorations are of unknown etiology and have been termed acute exacerbations of IPF. This perspective is the result of an international effort to summarize the current state of knowledge regarding acute exacerbations of IPF. Acute exacerbations of IPF are defined as acute, clinically significant deteriorations of unidentifiable cause in patients with underlying IPF. Proposed diagnostic criteria include subjective worsening over 30 days or less, new bilateral radiographic opacities, and the absence of infection or another identifiable etiology. The potential pathobiological roles of infection, disordered cell biology, coagulation, and genetics are discussed, and future research directions are proposed. PMID:17585107

  2. Acute inflammation decreases the expression of connexin 40 in mouse lung.

    Science.gov (United States)

    Rignault, Stéphanie; Haefliger, Jacques-Antoine; Waeber, Bernard; Liaudet, Lucas; Feihl, François

    2007-07-01

    Transmigration of neutrophil polymorphonuclear leukocytes through the microvascular endothelium is a cardinal event of acute inflammation. In vitro, this process can be restricted by gap junctional intercellular communication, but whether it also occurs in vivo is unknown. Connexin 40 (Cx40) is a gap junctional protein abundantly present in the lung, notably in vascular endothelium. We hypothesized that acute lung inflammation would be aggravated in knockout mice genetically deficient in Cx40. This hypothesis was tested in two different models: 1) intranasal instillation of LPS at either supramaximal (50 microg/mouse) or inframaximal dose (0.01 microg/mouse) and 2) pulmonary inflammation as a distant consequence of an abdominal infection caused by cecal ligation and perforation. Pulmonary transmigration of neutrophils was assessed by counting these cells in bronchoalveolar lavage fluid (LPS model) or with the myeloperoxidase assay in homogenates of blood-free tissue (cecal ligation and perforation model). Pulmonary content in Cx40 and Cx43 was evaluated with immunoblots. In wild-type mice, there was a time-dependent decrease of Cx40 expression in both models. The time points for studies with the knockout mice were chosen in such a manner that inflammation was clearly present and Cx40 still largely expressed in wild-type animals. In either model, the development of lung inflammation did not differ between wild-type and Cx40-deficient mice. In conclusion, the pulmonary expression of the Cx40 protein is progressively and markedly decreased in two different murine models of acute lung inflammation, but there is no causal relationship between this process and the pulmonary transmigration of neutrophils.

  3. Unilateral pulmonary edema following acute subglottic edema.

    Science.gov (United States)

    Morisaki, H; Ochiai, R; Takeda, J; Nagano, M

    1990-01-01

    Presented here is a case of unilateral pulmonary edema following acute subglottic edema after removal of an endotracheal tube. A 3-year-old boy, diagnosed as having nondiphtheric croup and pectus excavatum deformity, was scheduled for repair of a cleft lip. No complication occurred during the operation. After removal of the endotracheal tube, he showed dyspnea and cyanosis and was later found to have acute subglottic edema. After reintubation of the trachea, frothy pink fluid was discharged from the tube, and chest roentgenogram showed a right-sided alveolar infiltrate. Many factors may cause unilateral pulmonary edema, but it is suggested that acute subglottic edema and unilateral bronchial fragility strongly affected this episode.

  4. Modeling and Hemofiltration Treatment of Acute Inflammation

    Directory of Open Access Journals (Sweden)

    Robert S. Parker

    2016-10-01

    Full Text Available The body responds to endotoxins by triggering the acute inflammatory response system to eliminate the threat posed by gram-negative bacteria (endotoxin and restore health. However, an uncontrolled inflammatory response can lead to tissue damage, organ failure, and ultimately death; this is clinically known as sepsis. Mathematical models of acute inflammatory disease have the potential to guide treatment decisions in critically ill patients. In this work, an 8-state (8-D differential equation model of the acute inflammatory response system to endotoxin challenge was developed. Endotoxin challenges at 3 and 12 mg/kg were administered to rats, and dynamic cytokine data for interleukin (IL-6, tumor necrosis factor (TNF, and IL-10 were obtained and used to calibrate the model. Evaluation of competing model structures was performed by analyzing model predictions at 3, 6, and 12 mg/kg endotoxin challenges with respect to experimental data from rats. Subsequently, a model predictive control (MPC algorithm was synthesized to control a hemoadsorption (HA device, a blood purification treatment for acute inflammation. A particle filter (PF algorithm was implemented to estimate the full state vector of the endotoxemic rat based on time series cytokine measurements. Treatment simulations show that: (i the apparent primary mechanism of HA efficacy is white blood cell (WBC capture, with cytokine capture a secondary benefit; and (ii differential filtering of cytokines and WBC does not provide substantial improvement in treatment outcomes vs. existing HA devices.

  5. Sequential exposure to carbon nanotubes and bacteria enhances pulmonary inflammation and infectivity.

    Science.gov (United States)

    Shvedova, Anna A; Fabisiak, James P; Kisin, Elena R; Murray, Ashley R; Roberts, Jenny R; Tyurina, Yulia Y; Antonini, James M; Feng, Wei Hong; Kommineni, Choudari; Reynolds, Jeffrey; Barchowsky, Aaron; Castranova, Vince; Kagan, Valerian E

    2008-05-01

    Carbon nanotubes (CNT), with their applications in industry and medicine, may lead to new risks to human health. CNT induce a robust pulmonary inflammation and oxidative stress in rodents. Realistic exposures to CNT may occur in conjunction with other pathogenic impacts (microbial infections) and trigger enhanced responses. We evaluated interactions between pharyngeal aspiration of single-walled CNT (SWCNT) and bacterial pulmonary infection of C57BL/6 mice with Listeria monocytogenes (LM). Mice were given SWCNT (0, 10, and 40 mug/mouse) and 3 days later were exposed to LM (10(3) bacteria/mouse). Sequential exposure to SWCNT/LM amplified lung inflammation and collagen formation. Despite this robust inflammatory response, SWCNT pre-exposure significantly decreased the pulmonary clearance of LM-exposed mice measured 3 to 7 days after microbial infection versus PBS/LM-treated mice. Decreased bacterial clearance in SWCNT-pre-exposed mice was associated with decreased phagocytosis of bacteria by macrophages and a decrease in nitric oxide production by these phagocytes. Pre-incubation of naïve alveolar macrophages with SWCNT in vitro also resulted in decreased nitric oxide generation and suppressed phagocytizing activity toward LM. Failure of SWCNT-exposed mice to clear LM led to a continued elevation in nearly all major chemokines and acute phase cytokines into the later course of infection. In SWCNT/LM-exposed mice, bronchoalveolar lavage neutrophils, alveolar macrophages, and lymphocytes, as well as lactate dehydrogenase level, were increased compared with mice exposed to SWCNT or LM alone. In conclusion, enhanced acute inflammation and pulmonary injury with delayed bacterial clearance after SWCNT exposure may lead to increased susceptibility to lung infection in exposed populations.

  6. PULMONARY AND CARDIAC GENE EXPRESSION FOLLOWING ACUTE ULTRAFINE CARBON PARTICLE INHALATION IN HYPERTENSIVE RATS

    Science.gov (United States)

    Inhalation of ultrafine carbon particles (ufCP) causes cardiac physiological changes without marked pulmonary injury or inflammation. We hypothesized that acute ufCP exposure of 13 months old Spontaneously Hypertensive (SH) rats will cause differential effects on the lung and hea...

  7. Impact of interleukin-6 on hypoxia-induced pulmonary hypertension and lung inflammation in mice

    Directory of Open Access Journals (Sweden)

    Izziki Mohamed

    2009-01-01

    Full Text Available Abstract Background Inflammation may contribute to the pathogenesis of various forms of pulmonary hypertension (PH. Recent studies in patients with idiopathic PH or PH associated with underlying diseases suggest a role for interleukin-6 (IL-6. Methods To determine whether endogenous IL-6 contributes to mediate hypoxic PH and lung inflammation, we studied IL-6-deficient (IL-6-/- and wild-type (IL-6+/+ mice exposed to hypoxia for 2 weeks. Results Right ventricular systolic pressure, right ventricle hypertrophy, and the number and media thickness of muscular pulmonary vessels were decreased in IL-6-/- mice compared to wild-type controls after 2 weeks' hypoxia, although the pressure response to acute hypoxia was similar in IL-6+/+ and IL-6-/- mice. Hypoxia exposure of IL-6+/+ mice led to marked increases in IL-6 mRNA and protein levels within the first week, with positive IL-6 immunostaining in the pulmonary vessel walls. Lung IL-6 receptor and gp 130 (the IL-6 signal transducer mRNA levels increased after 1 and 2 weeks' hypoxia. In vitro studies of cultured human pulmonary-artery smooth-muscle-cells (PA-SMCs and microvascular endothelial cells revealed prominent synthesis of IL-6 by PA-SMCs, with further stimulation by hypoxia. IL-6 also markedly stimulated PA-SMC migration without affecting proliferation. Hypoxic IL-6-/- mice showed less inflammatory cell recruitment in the lungs, compared to hypoxic wild-type mice, as assessed by lung protein levels and immunostaining for the specific macrophage marker F4/80, with no difference in lung expression of adhesion molecules or cytokines. Conclusion These data suggest that IL-6 may be actively involved in hypoxia-induced lung inflammation and pulmonary vascular remodeling in mice.

  8. Inhibition of chlorine-induced pulmonary inflammation and edema by mometasone and budesonide

    Energy Technology Data Exchange (ETDEWEB)

    Chen, Jing; Mo, Yiqun; Schlueter, Connie F.; Hoyle, Gary W., E-mail: Gary.Hoyle@louisville.edu

    2013-10-15

    Chlorine gas is a widely used industrial compound that is highly toxic by inhalation and is considered a chemical threat agent. Inhalation of high levels of chlorine results in acute lung injury characterized by pneumonitis, pulmonary edema, and decrements in lung function. Because inflammatory processes can promote damage in the injured lung, anti-inflammatory therapy may be of potential benefit for treating chemical-induced acute lung injury. We previously developed a chlorine inhalation model in which mice develop epithelial injury, neutrophilic inflammation, pulmonary edema, and impaired pulmonary function. This model was used to evaluate nine corticosteroids for the ability to inhibit chlorine-induced neutrophilic inflammation. Two of the most potent corticosteroids in this assay, mometasone and budesonide, were investigated further. Mometasone or budesonide administered intraperitoneally 1 h after chlorine inhalation caused a dose-dependent inhibition of neutrophil influx in lung tissue sections and in the number of neutrophils in lung lavage fluid. Budesonide, but not mometasone, reduced the levels of the neutrophil attractant CXCL1 in lavage fluid 6 h after exposure. Mometasone or budesonide also significantly inhibited pulmonary edema assessed 1 day after chlorine exposure. Chlorine inhalation resulted in airway hyperreactivity to inhaled methacholine, but neither mometasone nor budesonide significantly affected this parameter. The results suggest that mometasone and budesonide may represent potential treatments for chemical-induced lung injury. - Highlights: • Chlorine causes lung injury when inhaled and is considered a chemical threat agent. • Corticosteroids may inhibit lung injury through their anti-inflammatory actions. • Corticosteroids inhibited chlorine-induced pneumonitis and pulmonary edema. • Mometasone and budesonide are potential rescue treatments for chlorine lung injury.

  9. Postpartum Acute Pulmonary Oedema with Sub clinical Rheumatic Heart Disease

    OpenAIRE

    2015-01-01

    Acute dyspnea with pulmonary oedema in postpartum is uncommon but life-threatening event. Contributing factors for pulmonary oedema include, administration of tocolytics, underlying cardiac disease, iatrogenic fluid overload and preeclampsia acounting 0.08% of pregnancies. Pulmonary embolism, amniotic fluid embolism, pneumonia, aspiration and pulmonary oedema are some of the potentially devastating conditions that should be considered by the attending physician.

  10. Pathophysiology of pulmonary complications of acute pancreatitis

    Institute of Scientific and Technical Information of China (English)

    George W Browne; CS Pitchurnoni

    2006-01-01

    Acute pancreatitis in its severe form is complicated by multiple organ system dysfunction, most importantly by pulmonary complications which include hypoxia,acute respiratory distress syndrome, atelectasis, and pleural effusion. The pathogenesis of some of the above complications is attributed to the production of noxious cytokines. Clinically significant is the early onset of pleural effusion, which heralds a poor outcome of acute pancreatitis. The role of circulating trypsin, phospholipase A2, platelet activating factor, release of free fatty acids,chemoattractants such as tumor necrsosis factor (TNF)-alpha, interleukin (IL)-1, IL-6, IL-8, fMet-leu-phe (a bacterial wall product), nitric oxide, substance P, and macrophage inhibitor factor is currently studied. The hope is that future management of acute pancreatitis with a better understanding of the pathogenesis of lung injury will be directed against the production of noxious cytokines.

  11. Acute pulmonary edema after intramyometrial prostodin

    Directory of Open Access Journals (Sweden)

    Neha Baduni

    2011-01-01

    Full Text Available A 25 year old, 68 kg, primigravida, was taken up for emergency caesarean section for meconium stained liquor and fetal distress. She was a known case of pre eclampsia and her blood pressure was controlled on tab methyl dopa. she was administered general anaesthesia. after delivery of baby she went into postpartum hemorrhage which was controlled with intramyometrial prostodin. but immediately after its administration she went into acute pulmonary edema.

  12. Rosette nanotubes show low acute pulmonary toxicity in vivo

    Directory of Open Access Journals (Sweden)

    W Shane Journeay

    2008-10-01

    Full Text Available W Shane Journeay1, Sarabjeet S Suri1, Jesus G Moralez2, Hicham Fenniri2, Baljit Singh11Immunology Research Group, Toxicology Graduate Program and Department of Veterinary Biomedical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, 52 Campus Drive, Saskatoon, SK, S7N 5B4, Canada; 2National Institute of Nanotechnology, National Research Council (NINT-NRC and Department of Chemistry, University of Alberta, 11421 Saskatchewan Drive, Edmonton, AB, T6G 2M9, CanadaAbstract: Nanotubes are being developed for a large variety of applications ranging from electronics to drug delivery. Common carbon nanotubes such as single-walled and multi-walled carbon nanotubes have been studied in the greatest detail but require solubilization and removal of catalytic contaminants such as metals prior to being introduced to biological systems for medical application. The present in vivo study characterizes the degree and nature of inflammation caused by a novel class of self-assembling rosette nanotubes, which are biologically inspired, naturally water-soluble and free of metal content upon synthesis. Upon pulmonary administration of this material we examined responses at 24 h and 7d post-exposure. An acute inflammatory response is triggered at 50 and 25 μg doses by 24 h post-exposure but an inflammatory response is not triggered by a 5 μg dose. Lung inflammation observed at a 50 μg dose at 24 h was resolving by 7d. This work suggests that novel nanostructures with biological design may negate toxicity concerns for biomedical applications of nanotubes. This study also demonstrates that water-soluble rosette nanotube structures represent low pulmonary toxicity, likely due to their biologically inspired design, and their self-assembled architecture.Keywords: nanotoxicology, biocompatibility, nanomedicine, pulmonary drug delivery, lung inflammation

  13. Impact of agglomeration state of nano- and submicron sized gold particles on pulmonary inflammation

    Directory of Open Access Journals (Sweden)

    Cassee Flemming R

    2010-12-01

    Full Text Available Abstract Background Nanoparticle (NP toxicity testing comes with many challenges. Characterization of the test substance is of crucial importance and in the case of NPs, agglomeration/aggregation state in physiological media needs to be considered. In this study, we have addressed the effect of agglomerated versus single particle suspensions of nano- and submicron sized gold on the inflammatory response in the lung. Rats were exposed to a single dose of 1.6 mg/kg body weight (bw of spherical gold particles with geometric diameters of 50 nm or 250 nm diluted either by ultrapure water or by adding phosphate buffered saline (PBS. A single dose of 1.6 mg/kg bw DQ12 quartz was used as a positive control for pulmonary inflammation. Extensive characterization of the particle suspensions has been performed by determining the zetapotential, pH, gold concentration and particle size distribution. Primary particle size and particle purity has been verified using transmission electron microscopy (TEM techniques. Pulmonary inflammation (total cell number, differential cell count and pro-inflammatory cytokines, cell damage (total protein and albumin and cytotoxicity (alkaline phosphatase and lactate dehydrogenase were determined in bronchoalveolar lavage fluid (BALF and acute systemic effects in blood (total cell number, differential cell counts, fibrinogen and C-reactive protein 3 and 24 hours post exposure. Uptake of gold particles in alveolar macrophages has been determined by TEM. Results Particles diluted in ultrapure water are well dispersed, while agglomerates are formed when diluting in PBS. The particle size of the 50 nm particles was confirmed, while the 250 nm particles appear to be 200 nm using tracking analysis and 210 nm using TEM. No major differences in pulmonary and systemic toxicity markers were observed after instillation of agglomerated versus single gold particles of different sizes. Both agglomerated as well as single nanoparticles were

  14. Particle-induced pulmonary acute phase response may be the causal link between particle inhalation and cardiovascular disease

    DEFF Research Database (Denmark)

    Saber, Anne T.; Jacobsen, Nicklas R.; Jackson, Petra

    2014-01-01

    Inhalation of ambient and workplace particulate air pollution is associated with increased risk of cardiovascular disease. One proposed mechanism for this association is that pulmonary inflammation induces a hepatic acute phase response, which increases risk of cardiovascular disease. Induction...... epidemiological studies. In this review, we present and review emerging evidence that inhalation of particles (e.g., air diesel exhaust particles and nanoparticles) induces a pulmonary acute phase response, and propose that this induction constitutes the causal link between particle inhalation and risk...

  15. Negative spiral CT in acute pulmonary embolism

    Energy Technology Data Exchange (ETDEWEB)

    Nilsson, T.; Olausson, A. [Karolinska Hospital, Stockholm (Sweden). Dept. of Thoracic Radiology; Johnsson, H. [Karolinska Hospital, Stockholm (Sweden). Dept. of Internal Medicine; Nyman, U. [County Hospital, Trelleborg (Sweden). Dept. of Radiology; Aspelin, P. [Huddinge Univ. Hospital (Sweden). Dept. of Radiology

    2002-09-01

    Purpose: To retrospectively evaluate the clinical outcome of non-anticoagulated patients with clinically suspected acute pulmonary embolism (PE) and no symptoms or signs of deep venous thrombosis (DVT) following a negative contrast medium-enhanced spiral CT of the pulmonary arteries (s-CTPA). Material and Methods: During a 24-month period, 739 of 751 patients underwent s-CTPA with acceptable diagnostic quality for clinically suspected acute PE. All patients who had a CT study not positive for PE were followed up with a questionnaire, a telephone interview and review of all medical reports, including autopsies and death certificates for any episodes of venous thromboembolism (VTE) during a 3-month period. Results: PE was diagnosed in 158 patients. Of the remaining 581 patients with a negative s-CTPA, 45 patients were lost to follow-up. 88 patients were excluded because of anticoagulation treatment (cardiac disorder n=32, chronic VTE or acute symptomatic DVT n=31, PE diagnosed at pulmonary angiography n=1, thrombus prophylaxis during diagnostic work-up or other reasons than VTE n=24) and 7 patients undergoing lower extremity venous studies because of symptoms of DVT (all negative). Thus, 441 patients with a negative s-CTPA and no DVT symptoms, venous studies or anticoagulant treatment constituted the follow-up cohort. Four of these patients had proven VTE (all PE) during the 3-month follow-up period. Two of the PE episodes contributed to the patient's death. Conclusion: Patients with clinically suspected acute PE, no symptoms or signs of DVT and a negative single slice s-CTPA using 3-5 mm collimation, may safely be left without anticoagulation treatment unless they are critically ill, have a limited cardiopulmonary reserve and/or if a high clinical suspicion remains.

  16. Grouping nanomaterials to predict their potential to induce pulmonary inflammation.

    Science.gov (United States)

    Braakhuis, Hedwig M; Oomen, Agnes G; Cassee, Flemming R

    2016-05-15

    The rapidly expanding manufacturing, production and use of nanomaterials have raised concerns for both worker and consumer safety. Various studies have been published in which induction of pulmonary inflammation after inhalation exposure to nanomaterials has been described. Nanomaterials can vary in aspects such as size, shape, charge, crystallinity, chemical composition, and dissolution rate. Currently, efforts are made to increase the knowledge on the characteristics of nanomaterials that can be used to categorise them into hazard groups according to these characteristics. Grouping helps to gather information on nanomaterials in an efficient way with the aim to aid risk assessment. Here, we discuss different ways of grouping nanomaterials for their risk assessment after inhalation. Since the relation between single intrinsic particle characteristics and the severity of pulmonary inflammation is unknown, grouping of nanomaterials by their intrinsic characteristics alone is not sufficient to predict their risk after inhalation. The biokinetics of nanomaterials should be taken into account as that affects the dose present at a target site over time. The parameters determining the kinetic behaviour are not the same as the hazard-determining parameters. Furthermore, characteristics of nanomaterials change in the life-cycle, resulting in human exposure to different forms and doses of these nanomaterials. As information on the biokinetics and in situ characteristics of nanomaterials is essential but often lacking, efforts should be made to include these in testing strategies. Grouping nanomaterials will probably be of the most value to risk assessors when information on intrinsic characteristics, life-cycle, biokinetics and effects are all combined.

  17. Multidetector computed tomography pulmonary angiography in childhood acute pulmonary embolism

    Energy Technology Data Exchange (ETDEWEB)

    Tang, Chun Xiang; Zhang, Long Jiang; Lu, Guang Ming [Medical School of Nanjing University, Department of Medical Imaging, Jinling Hospital, Nanjing, Jiangsu (China); Schoepf, U.J. [Medical School of Nanjing University, Department of Medical Imaging, Jinling Hospital, Nanjing, Jiangsu (China); Medical University of South Carolina, Department of Radiology and Radiological Science, Charleston, SC (United States); Medical University of South Carolina, Department of Pediatrics, Charleston, SC (United States); Chowdhury, Shahryar M. [Medical University of South Carolina, Department of Pediatrics, Charleston, SC (United States); Fox, Mary A. [Medical University of South Carolina, Department of Radiology and Radiological Science, Charleston, SC (United States)

    2015-09-15

    Pulmonary embolism is a life-threatening condition affecting people of all ages. Multidetector row CT pulmonary angiography has improved the imaging of pulmonary embolism in both adults and children and is now regarded as the routine modality for detection of pulmonary embolism. Advanced CT pulmonary angiography techniques developed in recent years, such as dual-energy CT, have been applied as a one-stop modality for pulmonary embolism diagnosis in children, as they can simultaneously provide anatomical and functional information. We discuss CT pulmonary angiography techniques, common and uncommon findings of pulmonary embolism in both conventional and dual-energy CT pulmonary angiography, and radiation dose considerations. (orig.)

  18. Inflammation and airway microbiota during cystic fibrosis pulmonary exacerbations.

    Directory of Open Access Journals (Sweden)

    Edith T Zemanick

    Full Text Available BACKGROUND: Pulmonary exacerbations (PEx, frequently associated with airway infection and inflammation, are the leading cause of morbidity in cystic fibrosis (CF. Molecular microbiologic approaches detect complex microbiota from CF airway samples taken during PEx. The relationship between airway microbiota, inflammation, and lung function during CF PEx is not well understood. OBJECTIVE: To determine the relationships between airway microbiota, inflammation, and lung function in CF subjects treated for PEx. METHODS: Expectorated sputum and blood were collected and lung function testing performed in CF subjects during early (0-3d. and late treatment (>7d. for PEx. Sputum was analyzed by culture, pyrosequencing of 16S rRNA amplicons, and quantitative PCR for total and specific bacteria. Sputum IL-8 and neutrophil elastase (NE; and circulating C-reactive protein (CRP were measured. RESULTS: Thirty-seven sputum samples were collected from 21 CF subjects. At early treatment, lower diversity was associated with high relative abundance (RA of Pseudomonas (r = -0.67, p<0.001, decreased FEV(1% predicted (r = 0.49, p = 0.03 and increased CRP (r = -0.58, p = 0.01. In contrast to Pseudomonas, obligate and facultative anaerobic genera were associated with less inflammation and higher FEV₁. With treatment, Pseudomonas RA and P. aeruginosa by qPCR decreased while anaerobic genera showed marked variability in response. Change in RA of Prevotella was associated with more variability in FEV₁ response to treatment than Pseudomonas or Staphylococcus. CONCLUSIONS: Anaerobes identified from sputum by sequencing are associated with less inflammation and higher lung function compared to Pseudomonas at early exacerbation. CF PEx treatment results in variable changes of anaerobic genera suggesting the need for larger studies particularly of patients without traditional CF pathogens.

  19. Diagnostic imaging of acute pulmonary embolism.

    Science.gov (United States)

    Christiansen, F

    1997-01-01

    The common strategy of combining clinical information, lung scintigraphy and pulmonary angiography in the diagnosis of acute pulmonary embolism (PE), has many limitations in clinical use. The major causes are that pulmonary angiography and lung scintigraphy are not universally available, and that pulmonary angiography is very expensive. The purpose of this thesis was to analyse different aspects of validity in regard to lung scintigraphy, pulmonary angiography, spiral CT, and ultrasound of the legs, with the subsequent intention of discussing new diagnostic strategies. Observer variations in lung scintigraphy interpretation when applying the PIOPED criteria were tested in 2 studies with 2 and 3 observers respectively and expressed as kappa values. The ability to improve agreement in lung scintigraphy interpretation was tested by training 2 observers from different hospitals. The impact of 3 observers' variations in lung scintigraphy interpretation when compared to pulmonary angiography, was tested by comparing the ROC areas of the observers. The value of combining subjectively derived numerical probabilities and the PIOPED categorical probabilities in lung scintigraphy reporting was compared to using the PIOPED categorization only, and this was tested by comparing ROC areas. The sensitivity and specificity of detecting an embolic source in the deep veins of the legs by ultrasound as a sign of PE when lung scintigraphy is inconclusive, was tested by comparison with pulmonary angiography. The sensitivity and specificity of spiral CT, compared to pulmonary angiography, was tested by comparison to pulmonary angiography. The inter- and intra-observer kappa values were in the range of moderate and fair. It was not possible to achieve better kappa values after training. Although observer variations were substantial, the accuracy did not differ significantly between the 3 observers. Incoorporating subjectively derived probabilities into lung scan reporting could not reduce

  20. Association of current smoking with airway inflammation in chronic obstructive pulmonary disease and asymptomatic smokers

    NARCIS (Netherlands)

    Willemse, BWM; ten Hacken, NHT; Rutgers, B; Postma, DS; Timens, W

    2005-01-01

    Background: Inflammation in the airways and lung parenchyma underlies fixed airway obstruction in chronic obstructive pulmonary disease. The exact role of smoking as promoting factor of inflammation in chronic obstructive pulmonary disease is not clear, partly because studies often do not distinguis

  1. Thioredoxin-1 protects against neutrophilic inflammation and emphysema progression in a mouse model of chronic obstructive pulmonary disease exacerbation.

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    Naoya Tanabe

    Full Text Available BACKGROUND: Exacerbations of chronic obstructive pulmonary disease (COPD are characterized by acute enhancement of airway neutrophilic inflammation under oxidative stress and can be involved in emphysema progression. However, pharmacotherapy against the neutrophilic inflammation and emphysema progression associated with exacerbation has not been established. Thioredoxin-1 has anti-oxidative and anti-inflammatory properties and it can ameliorate neutrophilic inflammation through anti-chemotactic effects and prevent cigarette smoke (CS-induced emphysema. We aimed to determine whether thioredoxin-1 can suppress neutrophilic inflammation and emphysema progression in a mouse model of COPD exacerbation and if so, to reveal the underlying mechanisms. RESULTS: Mice were exposed to CS and then challenged with polyinosine-polycytidylic acid [poly(I:C], an agonist for virus-induced innate immunity. Airway neutrophilic inflammation, oxidative stress and lung apoptosis were enhanced in smoke-sensitive C57Bl/6, but not in smoke-resistant NZW mice. Exposure to CS and poly(I:C challenge accelerated emphysema progression in C57Bl/6 mice. Thioredoxin-1 suppressed neutrophilic inflammation and emphysema progression. Poly(I:C caused early neutrophilic inflammation through keratinocyte-derived chemokine and granulocyte-macrophage colony-stimulating factor (GM-CSF release in the lung exposed to CS. Late neutrophilic inflammation was caused by persistent GM-CSF release, which thioredoxin-1 ameliorated. Thioredoxin-1 enhanced pulmonary mRNA expression of MAP kinase phosphatase 1 (MKP-1, and the suppressive effects of thioredoxin-1 on prolonged GM-CSF release and late neutrophilic inflammation disappeared by inhibiting MKP-1. CONCLUSION: Using a mouse model of COPD exacerbation, we demonstrated that thioredoxin-1 ameliorated neutrophilic inflammation by suppressing GM-CSF release, which prevented emphysema progression. Our findings deepen understanding of the mechanisms

  2. Glyphosate Poisoning with Acute Pulmonary Edema

    Science.gov (United States)

    Thakur, Darshana Sudip; Khot, Rajashree; Joshi, P. P.; Pandharipande, Madhuri; Nagpure, Keshav

    2014-01-01

    GlySH-surfactant herbicide (GlySH), one of the most commonly used herbicides worldwide, has been considered as minimally toxic to humans. However, clinical toxicologists occasionally encounter cases of severe systemic toxicity. The US Environmental Protection Agency (EPA) states that ‘GlySH’ is of relatively low oral and acute dermal toxicity. It does not have anticholinesterase effect and no organophosphate-like central nervous system (CNS) effects. The clinical features range from skin and throat irritation to hypotension and death. Severe GlySH-surfactant poisoning is manifested by gastroenteritis, respiratory disturbances, altered mental status, hypotension refractory to the treatment, renal failure, and shock.[1] GlySH intoxication has a case fatality rate 3.2–29.3%. Pulmonary toxicity and renal toxicity seem to be responsible for mortality. Metabolic acidosis, abnormal chest X-ray, arrhythmias, and elevated serum creatinine levels are useful prognostic factors for predicting GlySH mortality.[2] There is no antidote and the mainstay of treatment for systemic toxicity is decontamination and aggressive supportive therapy. We report a case of acute pulmonary edema, which is a rare but severe manifestation of oral GlySH poisoning, where patient survived with aggressive supportive therapy. PMID:25948977

  3. Present state of radiological diagnostics in acute pulmonary failure

    Energy Technology Data Exchange (ETDEWEB)

    Jaspers, C.; Hoetzinger, H.; Toedt, H.C.; Beyer, H.K.

    1989-03-01

    Acute pulmonary failure is a very serious cause of respiratory failure. Radiological diagnosis occupies a central position in intensive-care monitoring. X-ray film of the thorax is performed not only for detecting any complications, but mainly for noninvasive and semiquantitative determination of the extravascular pulmonary fluid and hence of the fluid balance. Other methods such as MR or methods of nuclear medicine have not acquired substantial importance in respect of diagnosis and monitoring acute pulmonary failure. (orig./GDG).

  4. Decreased pulmonary inflammation after ethanol exposure and burn injury in intercellular adhesion molecule-1 knockout mice.

    Science.gov (United States)

    Bird, Melanie D; Morgan, Michelle O; Ramirez, Luis; Yong, Sherri; Kovacs, Elizabeth J

    2010-01-01

    Clinical and laboratory evidence suggests that alcohol consumption dysregulates immune function. Burn patients who consume alcohol before their injuries demonstrate higher rates of morbidity and mortality, including acute respiratory distress syndrome, than patients without alcohol at the time of injury. Our laboratory observed higher levels of proinflammatory cytokines and leukocyte infiltration in the lungs of mice after ethanol exposure and burn injury than with either insult alone. To understand the mechanism of the increased pulmonary inflammatory response in mice treated with ethanol and burn injury, we investigated the role of intercellular adhesion molecule (ICAM)-1. Wild-type and ICAM-1 knockout (KO) mice were treated with vehicle or ethanol and subsequently given a sham or burn injury. Twenty-four hours postinjury, lungs were harvested and analyzed for indices of inflammation. Higher numbers of neutrophils were observed in the lungs of wild-type mice after burn and burn with ethanol treatment. This increase in pulmonary inflammatory cell accumulation was significantly lower in the KO mice. In addition, levels of KC, interleukin-1beta, and interleukin-6 in the lung were decreased in the ICAM-1 KO mice after ethanol exposure and burn injury. Interestingly, no differences were observed in serum or lung tissue content of soluble ICAM-1 24 hours postinjury. These data suggest that upregulation of adhesion molecules such as ICAM-1 on the vascular endothelium may play a critical role in the excessive inflammation seen after ethanol exposure and burn injury.

  5. Cannabidiol improves lung function and inflammation in mice submitted to LPS-induced acute lung injury.

    Science.gov (United States)

    Ribeiro, A; Almeida, V I; Costola-de-Souza, C; Ferraz-de-Paula, V; Pinheiro, M L; Vitoretti, L B; Gimenes-Junior, J A; Akamine, A T; Crippa, J A; Tavares-de-Lima, W; Palermo-Neto, J

    2015-02-01

    We have previously shown that the prophylactic treatment with cannabidiol (CBD) reduces inflammation in a model of acute lung injury (ALI). In this work we analyzed the effects of the therapeutic treatment with CBD in mice subjected to the model of lipopolysaccharide (LPS)-induced ALI on pulmonary mechanics and inflammation. CBD (20 and 80 mg/kg) was administered (i.p.) to mice 6 h after LPS-induced lung inflammation. One day (24 h) after the induction of inflammation the assessment of pulmonary mechanics and inflammation were analyzed. The results show that CBD decreased total lung resistance and elastance, leukocyte migration into the lungs, myeloperoxidase activity in the lung tissue, protein concentration and production of pro-inflammatory cytokines (TNF and IL-6) and chemokines (MCP-1 and MIP-2) in the bronchoalveolar lavage supernatant. Thus, we conclude that CBD administered therapeutically, i.e. during an ongoing inflammatory process, has a potent anti-inflammatory effect and also improves the lung function in mice submitted to LPS-induced ALI. Therefore the present and previous data suggest that in the future cannabidiol might become a useful therapeutic tool for the attenuation and treatment of inflammatory lung diseases.

  6. Chemical and physical characteristics of cellulose insulation particulates, and evaluation of potential acute pulmonary toxicity.

    Science.gov (United States)

    Morgan, Daniel L; Su, Yin-Fong; Dill, Jeffrey A; Turnier, John C; Westerberg, R Bruce; Smith, Cynthia S

    2004-12-01

    During installation of cellulose insulation (CI) in new and older houses, significant quantities of airborne material are generated. This study characterized the chemical and physical properties, and potential acute pulmonary toxicity of CI. CI from four manufacturers was analyzed for inorganic additives and trace element impurities. Aerosols were generated and size fractionated. The number and size of fibrous and nonfibrous particles in the respirable fractions were determined. Respirable CI particulates were intratracheally instilled in rats (5 mg/kg) to evaluate potential pulmonary toxicity. CI samples were similar in composition with small differences due primarily to fire retardants. Less than 0.1% of CI was respirable and contained few fibers. Acute exposure to CI caused transient inflammation in the lungs and increased 4-hydroxyproline. Microscopic evaluation revealed a minimal to mild, non-progressing granulomatous pneumonitis. Low concentrations of respirable particles were found in CI aerosols. Particles consisted primarily of fire retardants with few fibers, and caused mild pulmonary toxicity in rats.

  7. Pulmonary Inflammatory Responses to Acute Meteorite Dust Exposures - to Acute Meteorite Dust Exposures - Exploration

    Science.gov (United States)

    Harrington, A. D.; McCubbin, F. M.; Kaur, J.; Smirnov, A.; Galdanes, K.; Schoonen, M. A. A.; Chen, L. C.; Tsirka, S. E.; Gordon, T.

    2017-01-01

    New initiatives to begin lunar and martian colonization within the next few decades are illustrative of the resurgence of interest in space travel. One of NASA's major concerns with extended human space exploration is the inadvertent and repeated exposure to unknown dust. This highly interdisciplinary study evaluates both the geochemical reactivity (e.g. iron solubility and acellular reactive oxygen species (ROS) generation) and the relative toxicity (e.g. in vitro and in vivo pulmonary inflammation) of six meteorite samples representing either basalt or regolith breccia on the surface of the Moon, Mars, and Asteroid 4Vesta. Terrestrial mid-ocean ridge basalt (MORB) is also used for comparison. The MORB demonstrated higher geochemical reactivity than most of the meteorite samples but caused the lowest acute pulmonary inflammation (API). Notably, the two martian meteorites generated some of the highest API but only the basaltic sample is significantly reactive geochemically. Furthermore, while there is a correlation between a meteorite's soluble iron content and its ability to generate acellular ROS, there is no direct correlation between a particle's ability to generate ROS acellularly and its ability to generate API. However, assorted in vivo API markers did demonstrate strong positive correlations with increasing bulk Fenton metal content. In summary, this comprehensive dataset allows for not only the toxicological evaluation of astromaterials but also clarifies important correlations between geochemistry and health.

  8. Coincident helminth infection modulates systemic inflammation and immune activation in active pulmonary tuberculosis.

    Directory of Open Access Journals (Sweden)

    Parakkal Jovvian George

    Full Text Available Helminth infections are known to modulate innate and adaptive immune responses in active and latent tuberculosis (TB. However, the role of helminth infections in modulating responses associated with inflammation and immune activation (reflecting disease activity and/or severity in TB is not known.We measured markers of inflammation and immune activation in active pulmonary TB individuals (ATB with co-incidental Strongyloides stercoralis (Ss infection. These included systemic levels of acute phase proteins, matrix metalloproteinases and their endogenous inhibitors and immune activation markers. As a control, we measured the systemic levels of the same molecules in TB-uninfected individuals (NTB with or without Ss infection.Our data confirm that ATB is associated with elevated levels of the various measured molecules when compared to those seen in NTB. Our data also reveal that co-incident Ss infection in ATB individuals is associated with significantly decreased circulating levels of acute phase proteins, matrix metalloproteinases, tissue inhibitors of matrix metalloproteinases as well as the systemic immune activation markers, sCD14 and sCD163. These changes are specific to ATB since they are absent in NTB individuals with Ss infection.Our data therefore reveal a profound effect of Ss infection on the markers associated with TB disease activity and severity and indicate that co-incidental helminth infections might dampen the severity of TB disease.

  9. Clarithromycin ameliorates pulmonary inflammation induced by short term cigarette smoke exposure in mice.

    Science.gov (United States)

    Nakamura, Masuo; Wada, Hiroo; Honda, Kojiro; Nakamoto, Keitaro; Inui, Toshiya; Sada, Mitsuru; Watanabe, Masato; Takata, Saori; Yokoyama, Takuma; Saraya, Takeshi; Kurai, Daisuke; Ishii, Haruyuki; Goto, Hajime; Kamma, Hiroshi; Takizawa, Hajime

    2015-12-01

    Cigarette smoking is considered to be one of major causes of acute worsening of asthma as well as chronic obstructive pulmonary disease (COPD). Macrolide antibiotics have been reported to reduce the risk of exacerbations of COPD, and possibly neutrophilic asthma. However, the effect of clarithromycin (CAM) on pulmonary inflammation caused by short term exposure to cigarette smoke still remains to be investigated. C57BL/6J female mice were daily exposed to tobacco smoke using a tobacco smoke exposure system, or clean air for 8 days, while simultaneously treated with either oral CAM or vehicles. Twenty four hours after the last exposure, mice were anaesthetized and sacrificed, and bronchoalveolar lavage (BAL) fluids were collected. Cellular responses in BAL fluids were evaluated. Levels of cytokine mRNA in the lung tissues were measured by quantitative RT-PCR. Paraffin-embedded lung tissues were evaluated to quantitate degree of neutrophil infiltration. The numbers of total cells, macrophages and neutrophils in the BAL fluid of smoke-exposed mice were significantly increased as compared to clean air group. These changes were significantly ameliorated in CAM-treated mice. The lung morphological analysis confirmed decrease of neutrophils by CAM treatment. Studies by quantitative PCR demonstrated CAM treatment significantly reduced lung expression levels of IL-17A, keratinocyte-derived chemokine (KC), granulocyte-macrophage colony stimulating factor (GM-CSF) and MMP-9 induced by cigarette smoke. We demonstrate that CAM administration resolves enhanced pulmonary inflammation induced by short term cigarette smoke exposure in mice. Copyright © 2015 Elsevier Ltd. All rights reserved.

  10. Clinical Characteristics of Patients with Acute Pulmonary Embolism

    Science.gov (United States)

    Stein, Paul D.; Beemath, Afzal; Matta, Fadi; Weg, John G.; Yusen, Roger D.; Hales, Charles A.; Hull, Russell D.; Leeper, Kenneth V.; Sostman, H Dirk; Tapson, Victor F.; Buckley, John D.; Gottschalk, Alexander; Goodman, Lawrence R.; Wakefied, Thomas W.; Woodard, Pamela K.

    2007-01-01

    BACKGROUND Selection of patients for diagnostic tests for acute pulmonary embolism requires recognition of the possibility of pulmonary embolism based on the clinical characteristics. Patients in the Prospective Investigation of Pulmonary Embolism Diagnosis II (PIOPED II) had a broad spectrum of severity, which permits an evaluation of the subtle characteristics of mild pulmonary embolism as well as the characteristics of severe pulmonary embolism. METHODS Data are from the national collaborative study, PIOPED II. RESULTS There may be dyspnea only on exertion. The onset of dyspnea is usually, but not always, rapid. Orthopnea may occur. In patients with pulmonary embolism in main or lobar pulmonary arteries, dyspnea or tachypnea occurred in 92%, but in only 65% in whom the largest pulmonary embolism was in segmental pulmonary arteries. In general, signs and symptoms were similar in elderly and younger patients, but dyspnea or tachypnea were less frequent in elderly patients with no prior cardiopulmonary disease. Dyspnea may be absent even in patients with circulatory collapse. Patients with a low probability objective clinical assessment sometimes had pulmonary embolism, even in proximal vessels. CONCLUSION Symptoms may be mild and generally recognized symptoms may be absent, particularly in patients with pulmonary embolism only in segmental pulmonary branches, but they may be absent even with severe pulmonary embolism. A high or intermediate probability objective clinical assessment may suggest the need for diagnostic studies, but a low probability objective clinical assessment does not exclude the diagnosis. Maintenance of a high level of suspicion is critical. PMID:17904458

  11. Protective role of interleukin-10 in Ozone-induced pulmonary inflammation**

    Science.gov (United States)

    Background: The mechanisms underlying ozone (03)-induced pulmonary inflammation remain unclear. Interleukin-10 (IL-10) is an anti-inflammatory cytokine that is known to inhibit inflammatory mediators. Objectives: We investigated the molecular mechanisms underlying interleuken-10...

  12. Pulmonary oxidative stress, inflammation and dysregulated iron homeostatis in rat models of cardiovascular disease

    Science.gov (United States)

    Underlying cardiovascular disease (CVD) is considered a risk factor for the exacerbation of air pollution health effects. Therefore, rodent models of CVD are increasingly used to examine mechanisms ofvariation in susceptibility. Pulmonary oxidative stress, inflammation and altere...

  13. Dynamic hyperinflation and pulmonary inflammation: a potentially relevant relationship?

    Directory of Open Access Journals (Sweden)

    A. Agusti

    2006-12-01

    Full Text Available In patients with moderate-to-severe chronic obstructive pulmonary disease (COPD, end-expiratory lung volume increases under conditions of greater minute ventilation (e.g. exercise. This abnormal response is termed dynamic hyperinflation (DH and has now been recognised as a key determinant of symptomatology and exercise intolerance in COPD. Reduced elastic recoil, loss of alveolar attachments and increased airway resistance are the mechanical factors traditionally invoked to explain the occurrence of DH in COPD. An abnormal inflammatory response to, most frequently, tobacco smoking is a key pathophysiological component of COPD, but its potential relationship with DH has not been directly investigated and is poorly understood. The present article discusses, first, the mechanisms by which DH can enhance inflammation in COPD (including cellular stretching, tissue damage and danger signals, hyperventilation and hypoxia. It then reviews how the abnormal inflammatory response that characterises the disease can augment DH (oedema and increased airway resistance, increased mucus production and alveolar destruction. Finally, it speculates that if these relationships eventually prove to be real, then the use of long-acting bronchodilators may help reduce the inflammatory load of these patients and, conversely, the use of anti-inflammatory therapy can contribute to the reduction of DH.

  14. Acute coronary disease Athero-Inflammation: Therapeutic approach

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    Altman Raul

    2003-06-01

    Full Text Available Abstract Antithrombotic therapy is the cornerstone of the treatment of acute coronary syndromes, but there is now evidence which indicates that by blocking inflammation, thrombosis and thus, acute coronary events, could be lowered. The concept of athero-inflammation emerges as the meeting point of different morbidities; dyslipemia, diabetes, hypertension, obesity, immunity, infection, hyperhomocyteinemia, smoking, etc. usual named as risk factors. Thus, beside specific drugs, earliest treatment, in the stage of inflammation, using anti-inflammatory drugs, should be considered since in patients with increased risk of acute coronary process are likely to have many point of origen throughout the coronary arteries. There are a body of evidences for supporting the potential of anti-inflammatory therapy to the prevention of inflammation and atherosclerosis. COX-2 inhibition may decrease endothelial inflammation reducing monocytes infiltration improving vascular cells function, plaque stability and probably resulting in a decrease of coronary atherothrombotic events. Trials including large numbers of patients in prospective double-blind randomized studies worthwhile to confirm the efficacy of NSAID, mainly, COX-2 inhibitors, together with aspirin in the prevention of coronary events in patients with acute coronary disease.

  15. Anti-inflammation of MgSO4 on acute pulmonary hypertension%硫酸镁抗急性肺动脉高压的炎症机制

    Institute of Scientific and Technical Information of China (English)

    卢宏志; 高国芹; 李昨飞; 单冰竹

    2013-01-01

    Objective To investigate the effect and the anti-inflammatory mechanism of magnesium sulfate (MgSO4) on acute pulmonary hypertension.Methods 30 mongrel dogs were randomly divided into five groups:control group,surgical group,MgSO4 7.0 group,MgSO4 8.0 group,and MgSO4 9.0 group.The control group was not given any treatment,and the surgical group was operated to induce acute pulmonary hypertension,and the three MgSO4 groups were given MgSO4 to maintain intravenous concentration with 7.0 mmol/L,8.0 mmol/L,and 9.0 mmol/L respectively after acute pulmonary hypertension.The mean pulmonary artery pressure (MPAP) and circulation mean arterial pressure (MAP) were detected.Interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in serum were measured by enzyme-linked immunosorbent assay and radioimmunoassay,monocyte chemoattractant protein-1 (MCP-1) expression in the lung tissue was determined by western blot.Results ①MPAP,TNF-α,IL-6,and MCP 1 protein expression were significantly higher in surgical group than those in control group,and were decreased significantly in MgSO4 7.0 group,MgSO4 8.0 group,and MgSO4 9.0 group with dose dependence.②MAP was significantly lower in surgical group than that in control group.MAP in MgSO4 7.0 group,MgSO4 8.0 group,and MgSO4 9.0 group was significantly increased compared with surgical group and MAP in MgSO4 9.0 group was the highest.Conclusions MgSO4 significantly reduces pulmonary hypertension,which is probably associated with reduction of the inflammatory response by inhibition of MCP-1 expression in lung tissue and decrease of TNF-α and IL-6 in serum.%目的 探讨硫酸镁(MgSO4)对急性肺栓塞肺动脉高压的影响及其抗炎机制.方法 30只雄性杂种犬,体质量(15±2.1) kg,随机分为5组:空白组、对照组以及MgSO47.0组、MgSO48.0组、MgSO4 9.0组,每组6只,其中空白组不给予任何处理;对照组造成急性肺动脉高压;其余三组造成急性肺动脉高压后给予MgSO4静滴,稳定30

  16. Effects of asphalt fume condensate exposure on acute pulmonary responses

    Energy Technology Data Exchange (ETDEWEB)

    Ma, J.Y.C.; Barger, M.W.; Castranova, V. [Health Effects Lab. Div., National Inst. for Occupational Safety and Health, Morgantown, WV (United States); Kriech, A.J. [Heritage Research Group, Indianapolis, IN (United States)

    2000-10-01

    The present study was carried out to characterize the effects of in vitro exposure to paving asphalt fume condensate (AFC) on alveolar macrophage (AM) functions and to monitor acute pulmonary responses to in vivo AFC exposure in rats. Methods: For in vitro studies, rat primary AM cultures were incubated with various concentrations of AFC for 24 h at 37 C. AM-conditioned medium was collected and assayed for lactate dehydrogenase (LDH) as a marker of cytotoxicity. Tumor necrosis factor-{alpha} (TNF-{alpha}) and interleukin-1 (IL-1) production were assayed in AM-conditioned medium to monitor AM function. The effect of AFC on chemiluminescence (CL) generated by resting AM or AM in response to zymosan or PMA stimulation was also determined as a marker of AM activity. For in vivo studies, rats received either (1) a single intratracheal (IT) instillation of saline, or 0.1 mg or 0.5 mg AFC and were killed 1 or 3 days later; or (2) IT instillation of saline, or 0.1, 0.5, or 2 mg AFC for three consecutive days and were killed the following day. Differential counts of cells harvested by bronchoalveolar lavage were measured to monitor inflammation. Acellular LDH and protein content in the first lavage fluid were measured to monitor damage. CL generation, TNF-{alpha} and IL-1 production by AM were assayed to monitor AM function. Results: In vitro AFC exposure at <200 {mu}g/ml did not induce cytotoxicity, oxidant generation, or IL-1 production by AM, but it did cause a small but significant increase in TNF-{alpha} release from AM. In vitro exposure of AM to AFC resulted in a significant decline of CL in response to zymosan or PMA stimulation. The in vivo studies showed that AFC exposure did not induce significant neutrophil infiltration or alter LDH or protein content in acellular lavage samples. Macrophages obtained from AFC-exposed rats did not show significant differences in oxidant production or cytokine secretion at rest or in response to LPS in comparison with control

  17. H2S inhibits pulmonary arterial endothelial cell inflammation in rats with monocrotaline-induced pulmonary hypertension.

    Science.gov (United States)

    Feng, Shasha; Chen, Siyao; Yu, Wen; Zhang, Da; Zhang, Chunyu; Tang, Chaoshu; Du, Junbao; Jin, Hongfang

    2017-03-01

    This study aimed to determine whether hydrogen sulfide (H2S) inhibits pulmonary arterial endothelial inflammation in rats with monocrotaline (MCT)-induced pulmonary hypertension and its possible mechanisms. Twenty-four male Wistar rats were divided randomly into control, MCT, and MCT+H2S treatment groups. Human pulmonary arterial endothelial cells (HPAEC) were cultured and divided into four groups: control, MCT, MCT+H2S, and H2S. Pulmonary artery pressure was determined using a right cardiac catheterization procedure 3 weeks after MCT administration. Pulmonary vascular morphological changes and inflammatory infiltration were measured. Endogenous H2S levels, cystathionine-γ-lyase (CSE) expression, and inflammatory cytokines were determined both in vivo and in vitro. In addition, phosphorylation of NF-κB p65 and IκBα was detected by western blotting, and NF-κB p65 nuclear translocation, as well as its DNA-binding activity, was determined. Pulmonary hypertension and vascular remolding developed 3 wks after MCT administration, with elevated lung tissue inflammatory infiltration and cytokine level associated with activation of the NF-κB pathway, both in vivo and in vitro. However, the endogenous H2S/CSE pathway was downregulated in MCT rats. By contrast, an H2S donor markedly reduced pulmonary artery pressure, pulmonary vascular structural remolding, and increased lung inflammatory infiltration and cytokine levels of MCT-treated rats. Meanwhile, H2S reversed the activation of the NF-κB pathway successfully. The downregulated pulmonary arterial endothelial H2S/CSE pathway is involved in the pulmonary inflammatory response in MCT-treated pulmonary hypertensive rats. H2S attenuated endothelial inflammation by inhibiting the NF-κB pathway.

  18. Rescue surgical pulmonary embolectomy for acute massive pulmonary embolism

    Directory of Open Access Journals (Sweden)

    Ahmed Abdulrahman Elassal

    2016-08-01

    Conclusion: Surgical pulmonary embolectomy is a rescue operation in high-risk PE. It could save patients with preoperative cardiac arrest. Early diagnosis, interdisciplinary team action, appropriate and emergent treatment strategy are necessary for favorable outcome.

  19. Postpartum Acute Pulmonary Oedema with Sub clinical Rheumatic Heart Disease.

    Science.gov (United States)

    R, Padmaja; Gande, Sri Krishna Padma Challa Rao

    2015-02-01

    Acute dyspnea with pulmonary oedema in postpartum is uncommon but life-threatening event. Contributing factors for pulmonary oedema include, administration of tocolytics, underlying cardiac disease, iatrogenic fluid overload and preeclampsia acounting 0.08% of pregnancies. Pulmonary embolism, amniotic fluid embolism, pneumonia, aspiration and pulmonary oedema are some of the potentially devastating conditions that should be considered by the attending physician. Here, we report a case of postpartum acute pulmonary oedema referred to causality after an emergency caesarean section in a private hospital. No matter what the underlying pathology, prompt administration and appropriate resuscitation is always the first priority. Only after the patient has been stabilized attention must be turned to diagnosis and specific treatment. A diagnosis of severe Mitral Stenosis, probably of rheumatic origin was made after stabilizing the patient.

  20. Macrophage CD74 contributes to MIF-induced pulmonary inflammation

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    Al-Abed Yousef

    2009-05-01

    Full Text Available Abstract Background MIF is a critical mediator of the host defense, and is involved in both acute and chronic responses in the lung. Neutralization of MIF reduces neutrophil accumulation into the lung in animal models. We hypothesized that MIF, in the alveolar space, promotes neutrophil accumulation via activation of the CD74 receptor on macrophages. Methods To determine whether macrophage CD74 surface expression contributes MIF-induced neutrophil accumulation, we instilled recombinant MIF (r-MIF into the trachea of mice in the presence or absence of anti-CD74 antibody or the MIF specific inhibitor, ISO-1. Using macrophage culture, we examined the downstream pathways of MIF-induced activation that lead to neutrophil accumulation. Results Intratracheal instillation of r-MIF increased the number of neutrophils as well as the concentration of macrophage inflammatory protein 2 (MIP-2 and keratinocyte-derived chemokine (KC in BAL fluids. CD74 was found to be expressed on the surface of alveolar macrophages, and MIF-induced MIP-2 accumulation was dependent on p44/p42 MAPK in macrophages. Anti-CD74 antibody inhibited MIF-induced p44/p42 MAPK phosphorylation and MIP-2 release by macrophages. Furthermore, we show that anti-CD74 antibody inhibits MIF-induced alveolar accumulation of MIP-2 (control IgG vs. CD74 Ab; 477.1 ± 136.7 vs. 242.2 ± 102.2 pg/ml, p 4 vs. 1.90 ± 0.61 × 104, p Conclusion MIF-induced neutrophil accumulation in the alveolar space results from interaction with CD74 expressed on the surface of alveolar macrophage cells. This interaction induces p44/p42 MAPK activation and chemokine release. The data suggest that MIF and its receptor, CD74, may be useful targets to reduce neutrophilic lung inflammation, and acute lung injury.

  1. Systemic inflammation as a therapeutic target in acute ischemic stroke.

    Science.gov (United States)

    Dziedzic, Tomasz

    2015-05-01

    Acute systemic inflammatory reaction superimposed on chronic low-grade inflammation accompanies acute ischemic stroke. Elevated blood levels of systemic inflammatory markers such as IL-6 or C-reactive protein are associated with an unfavorable functional outcome and increased mortality after stroke. Animal studies have demonstrated a causal relationship between systemic inflammation and ischemic brain damage. The mechanisms linking systemic inflammation with poor outcome include increased neutrophil infiltration of cerebral cortex, disruption of the blood-brain barrier, impaired tissue reperfusion, increased platelet activation and microvascular coagulation and complement-dependent brain injury. Non-selective (e.g., by statins) or selective (e.g., by inhibition of IL-6) attenuation of systemic inflammation, enhancement of systemic anti-inflammatory response (e.g., by infusion of IL-1 receptor antagonist), prevention of infections that exacerbate systemic inflammation or inhibition of neuronal pathways triggering inflammatory reaction are potential therapeutic targets in stroke patients. This review discusses the relationship between systemic inflammation, cerebral ischemia and prognosis in the context of therapeutic strategies.

  2. CT pulmonary angiography findings that predict 30-day mortality in patients with acute pulmonary embolism

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    Bach, Andreas Gunter, E-mail: mail@andreas-bach.de [Department of Radiology, Martin-Luther-University Halle-Wittenberg, Ernst-Grube-Str. 40, 06120 Halle (Germany); Nansalmaa, Baasai; Kranz, Johanna [Department of Radiology, Martin-Luther-University Halle-Wittenberg, Ernst-Grube-Str. 40, 06120 Halle (Germany); Taute, Bettina-Maria [Department of Internal Medicine, Martin-Luther-University Halle-Wittenberg, Ernst-Grube-Str. 40, 06120 Halle (Germany); Wienke, Andreas [Institute of Medical Epidemiology, Biostatistics and Informatics, Martin-Luther-University Halle-Wittenberg, Magdeburger-Str. 8, 06112 Halle (Germany); Schramm, Dominik; Surov, Alexey [Department of Radiology, Martin-Luther-University Halle-Wittenberg, Ernst-Grube-Str. 40, 06120 Halle (Germany)

    2015-02-15

    Highlights: • In patients with acute pulmonary embolism contrast reflux in inferior vena cava is significantly stronger in non-survivors (odds ratio 3.29; p < 0.001). • This finding is independent from the following comorbidities: heart insufficiency and pulmonary hypertension. • Measurement of contrast reflux is a new and robust radiologic method for predicting 30-day mortality in patients with acute pulmonary embolism. • Measurement of contrast reflux is a better predictor of 30-day mortality after acute pulmonary embolism than any other existing radiologic predictor. This includes thrombus distribution, and morphometric measurements of right ventricular dysfunction. - Abstract: Purpose: Standard computed tomography pulmonary angiography (CTPA) can be used to diagnose acute pulmonary embolism. In addition, multiple findings at CTPA have been proposed as potential tools for risk stratification. Therefore, the aim of the present study is to examine the prognostic value of (I) thrombus distribution, (II) morphometric parameters of right ventricular dysfunction, and (III) contrast reflux in inferior vena cava on 30-day mortality. Material and methods: In a retrospective, single-center study from 06/2005 to 01/2010 365 consecutive patients were included. Inclusion criteria were: presence of acute pulmonary embolism, and availability of 30-day follow-up. A review of patient charts and images was performed. Results: There were no significant differences between the group of 326 survivors and 39 non-survivors in (I) thrombus distribution, and (II) morphometric measurements of right ventricular dysfunction. However, (III) contrast reflux in inferior vena cava was significantly stronger in non-survivors (odds ratio 3.29; p < 0.001). Results were independent from comorbidities like heart insufficiency and pulmonary hypertension. Conclusion: Measurement of contrast reflux is a new and robust method for predicting 30-day mortality in patients with acute pulmonary

  3. Pulmonary and extrapulmonary acute respiratory distress syndrome: myth or reality?

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    Rocco, Patricia R M; Pelosi, Paolo

    2008-02-01

    The pathogenesis of acute respiratory distress syndrome has been explained by the presence of a direct (pulmonary) or indirect (extrapulmonary) insult to the lung parenchyma. Evidence indicates that the pathophysiology of acute respiratory distress syndrome may differ according to the type of the insult. This article presents a brief overview of the differences between pulmonary and extrapulmonary acute respiratory distress syndrome, and discusses the interactions between lung functional, morphological aspects, and response to different therapies, both in experimental models and in patients with acute respiratory distress syndrome. Many researchers recognize that experimental pulmonary and extrapulmonary acute respiratory distress syndrome are not identical when considering morpho-functional aspects, the response to positive end-expiratory pressure and recruitment manoeuvre, prone position and other adjunctive therapies. Contradictory results have been reported in different clinical studies, however, which may be attributed to the difficulty of classifying acute respiratory distress syndrome in one or the other category, and being confident of the onset, the phase and the severity of acute respiratory distress syndrome in all patients. Heterogeneous acute respiratory distress syndrome patients are still considered to suffer from one syndrome, and are treated in the same way. Understanding the range of different pathways that lead to pulmonary dysfunction makes it possible to better target clinical treatment.

  4. CT Pulmonary Angiography and Suspected Acute Pulmonary Embolism

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    Enden, T.; Kloew, N.E. [Ullevaal Univ. Hospital, Oslo (Norway). Dept. of Cardiovascular Radiology

    2003-05-01

    Purpose: To evaluate the use and quality of CT pulmonary angiography in our department, and to relate the findings to clinical parameters and diagnoses. Material and Methods: A retrospective study of 324 consecutive patients referred to CT pulmonary angiography with clinically suspected pulmonary embolism (PE). From the medical records we registered clinical parameters, blood gases, D-dimer, risk factors and the results of other relevant imaging studies. Results: 55 patients (17%) had PE detected on CT. 39 had bilateral PE, and 8 patients had isolated peripheral PE. 87% of the examinations showing PE had satisfactory filling of contrast material including the segmental pulmonary arteries, and 60% of the subsegmental arteries. D-dimer test was performed in 209 patients, 85% were positive. A negative D-dimer ruled out PE detected at CT. Dyspnea and concurrent symptoms or detection of deep vein thrombosis (DVT), contraceptive pills and former venous thromboembolism (VTE) were associated with PE. The presence of only one clinical parameter indicated a negative PE diagnosis (p < 0.017), whereas two or more suggested a positive PE diagnosis (p < 0.002). CT also detected various ancillary findings such as consolidation, pleural effusion, nodule or tumor in nearly half of the patients; however, there was no association with the PE diagnosis. Conclusion: The quality of CT pulmonary angiography was satisfactory as a first-line imaging of PE. CT also showed additional pathology of importance in the chest. Our study confirmed that a negative D-dimer ruled out clinically suspected VTE.

  5. Role of pulmonary artery reactivity and nitric oxide in injury and inflammation following lung contusion.

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    Lakshminrusimha, Satyan; Suresh, Madathilparambil V; Knight, Paul R; Gugino, Sylvia F; Davidson, Bruce A; Helinski, Jadwiga D; Nielsen, Lori C; Russell, James A; Yu, Bi; Zeng, Lixia; Pennathur, Subramaniam; Raghavendran, Krishnan

    2013-03-01

    The mechanisms contributing to hypoxia in lung contusion (LC) remain unclear and not temporally associated with the peak onset of acute inflammation. We investigated the role of oxidative stress in alteration of pulmonary arterial (PA) reactivity following LC. In addition, the role of antioxidants in reversing this process was examined. PaO2 and PA reactivity were measured in rats subjected to bilateral LC. Rings were pretreated with a nitric oxide synthase (NOS) inhibitor, L-nitro arginine (10(-3) M), or PEG-superoxide dismutase (SOD) and PEG-catalase (CAT), or both (L-nitro arginine + SOD/CAT). Rings were constricted with norepinephrine and relaxed with an NOS agonist (A23187) or NO donor (SNAP [S-nitrosyl amino penicillamine]). Immunochemical and mass spectrometric quantification for nitrotyrosine was performed. Rats were hypoxemic at 4 h after contusion compared with controls, but recovered by 24 h (PaO(2)/FIO(2) ratio: baseline, 443 ± 28; 4 h, 288 ± 46; and 24 h, 417 ± 23). Pulmonary arterial constriction to NOS inhibition and relaxation to A23187 were impaired 4 h after LC. Pulmonary arterial relaxation to SNAP was decreased at 4 and 24 h after LC. These alterations in PA reactivity were reversed by SOD/CAT pretreatment. SOD1 and 2 mRNA were upregulated, and soluble guanylyl cyclase mRNA was downregulated 24 h after LC. Immunohistochemistry and mass spectrometry revealed that levels of 3-nitrotyrosine were increased markedly at 4 h following LC consistent with superoxide generation and formation of peroxynitrite. Collectively, these data suggest that consumption of NO due to excess superoxide resulting in peroxynitrite formation leads to diminished vascular reactivity following LC.

  6. Pulmonary hypertension due to acute respiratory distress syndrome

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    S.A. Ñamendys-Silva

    2014-10-01

    Full Text Available Our aims were to describe the prevalence of pulmonary hypertension in patients with acute respiratory distress syndrome (ARDS, to characterize their hemodynamic cardiopulmonary profiles, and to correlate these parameters with outcome. All consecutive patients over 16 years of age who were in the intensive care unit with a diagnosis of ARDS and an in situ pulmonary artery catheter for hemodynamic monitoring were studied. Pulmonary hypertension was diagnosed when the mean pulmonary artery pressure was >25 mmHg at rest with a pulmonary artery occlusion pressure or left atrial pressure <15 mmHg. During the study period, 30 of 402 critically ill patients (7.46% who were admitted to the ICU fulfilled the criteria for ARDS. Of the 30 patients with ARDS, 14 met the criteria for pulmonary hypertension, a prevalence of 46.6% (95% CI; 28-66%. The most common cause of ARDS was pneumonia (56.3%. The overall mortality was 36.6% and was similar in patients with and without pulmonary hypertension. Differences in patients' hemodynamic profiles were influenced by the presence of pulmonary hypertension. The levels of positive end-expiratory pressure and peak pressure were higher in patients with pulmonary hypertension, and the PaCO2 was higher in those who died. The level of airway pressure seemed to influence the onset of pulmonary hypertension. Survival was determined by the severity of organ failure at admission to the intensive care unit.

  7. [TLR-4 involvement in pyroptosis of mice with pulmonary inflammation infected by Actinobacillus pleuropneumoniae].

    Science.gov (United States)

    Hu, Peipei; Huang, Fushen; Niu, Junchao; Tang, Zhaoshan

    2015-05-04

    Pyroptosis is a caspase-1 dependent programmed cell death and involves pathogenesis of infectious diseases by releasing many pro-inflammatory cytokines to induced inflammation. TLR-4 plays an important role in mediating pathogenesis of some infectious diseases. In this study, we detected the expression of TLR-4 and some molecules (e. g caspase-1, TNF-α, IL-1β, IL-6, IL-18 ) related with pyroptosis to determine its involvement and mechanisms of pulmonary inflammation in mice infected by A. pleuropneumoniae. Mice were intranasally infected by A. pleuropneumoniae and killed 48 hours post infection. Pulmonary gross lesion and histological pathology by H-E were observed. Expression levels of caspase-1 , caspase-3, TNF-α, IL-1β, IL-6, IL-18, and TLR-4 in lung of mice were detected by RT-PCR and qPCR. Serious pulmonary hemorrhage and inflammation in infected mice were observed. Expression levels of caspase-1, caspase-3, TNF-α, IL-1β, IL-6, IL-18 and TLR-4 increased, and expression levels of caspase-3 were not changed in lung of infected mice. TLR-4 might be involved in pulmonary inflammation of mice infected by A. pleuropneumoniae. After induced by activated TLR-4 some cells in this lesion expressed pro-inflammatory cytokines. These cytokines would induce pulmonary inflammation. This lesion might involve pyroptosis with caspase-1 expression.

  8. Pancreatic and pulmonary mast cells activation during experimental acute pancreatitis

    Institute of Scientific and Technical Information of China (English)

    Inmaculada; Lopez-Font; Sabrina; Gea-Sorlí; Enrique; de-Madaria; Luis; M; Gutiérrez; Miguel; Pérez-Mateo; Daniel; Closa

    2010-01-01

    AIM:To study the activation of pancreatic and pulmonary mast cells and the effect of mast cell inhibition on the activation of peritoneal and alveolar macrophages during acute pancreatitis.METHODS:Pancreatitis was induced by intraductal infusion of 5% sodium taurodeoxycholate in rats.The mast cell inhibitor cromolyn was administered intraperitoneally(i.p.) 30 min before pancreatitis induction.The pancreatic and pulmonary tissue damage was evaluated histologically and mast cells and their state of activation...

  9. Endothelial RAGE exacerbates acute postischaemic cardiac inflammation.

    Science.gov (United States)

    Ziegler, Tilman; Horstkotte, Melanie; Lange, Philipp; Ng, Judy; Bongiovanni, Dario; Hinkel, Rabea; Laugwitz, Karl-Ludwig; Sperandio, Markus; Horstkotte, Jan; Kupatt, Christian

    2016-08-01

    Advanced glycation end-products (AGEs) interact with their receptor RAGE, leading to an inflammatory state. We investigated the role of RAGE in postischaemic leukocyte adhesion after myocardial infarction and its effect on postischaemic myocardial function. Wildtype (WT), ICAM-1-/-, RAGE-/- or ICAM-1/RAGE-/- mice underwent 20 minutes (min) of LAD-occlusion followed by 15 min of reperfusion. We applied in vivo fluorescence microscopy visualising Rhodamine-6G labelled leukocytes. To differentiate between endothelial and leukocyte RAGE, we generated bone marrow chimeric mice. Invasive hemodynamic measurements were performed in mice undergoing 45 min of myocardial ischaemia (via LAD-occlusion) followed by 24 hours of reperfusion. Left-ventricular developed pressure (LVDP) was assessed by insertion of a millar-tip catheter into the left ventricle. In the acute model of myocardial ischaemia, leukocyte retention (WT 68 ± 4 cells/hpf) was significantly reduced in ICAM-1-/- (40 ± 3 cells/hpf) and RAGE-/- mice (38 ± 4 cells/hpf). ICAM-1/RAGE-/- mice displayed an additive reduction of leukocyte retention (ICAM-1/RAGE-/- 15 ± 3 cells/hpf). Ly-6G+ neutrophil were predominantly reduced in ICAM-1/RAGE-/- hearts (28 %), whereas Ly-6C+ proinflammatory monocytes decreased to a lesser extent (55 %). Interestingly, PMN recruitment was not affected in chimeric mice with RAGE deficiency in BM cells (WT mice reconstituted with ICAM-1/RAGE-/- BM: 55 ± 4 cells/hpf) while in mice with global RAGE deficiency (ICAM-1/RAGE-/- mice reconstituted with ICAM-1/RAGE-/- BM) leucocyte retention was significantly reduced (13 ± 1 cells/hpf), similar to non-transplanted ICAM/RAGE-/- mice. Furthermore, postischaemic LVDP increased in ICAM-1/RAGE-/- animals (98 ± 4 mmHg vs 86 ± 4 mmHg in WT mice). In conclusion, combined deficiency of ICAM-1 and RAGE reduces leukocyte influx into infarcted myocardium and improves LV function during the acute phase after myocardial ischaemia and reperfusion

  10. Spiral CT of acute pulmonary thromboembolism: evaluation of pleuroparenchymal abnormalities.

    Science.gov (United States)

    Johnson, P T; Wechsler, R J; Salazar, A M; Fisher, A M; Nazarian, L N; Steiner, R M

    1999-01-01

    The goal of this work was to identify and categorize the spectrum of pulmonary parenchymal and pleural abnormalities identified by CT in patients with acute pulmonary thromboembolism (PE). A review of interpretations from 4,715 consecutive contrast-enhanced thoracic CT studies identified 41 examinations in which the diagnosis of PE was reported. Thirty-four studies were available for review, and two radiologists confirmed intraluminal defects in 31 patients. The number of emboli were counted and localized using bronchopulmonary nomenclature. Associated parenchymal and pleural abnormalities were tabulated. Of the 31 patients, 13 underwent confirmatory or correlative studies including angiography, radionuclide study, or autopsy. In addition, deep venous thrombosis was confirmed by ultrasound or MRI in 13 patients. An average of 7.5 emboli per patient was detected. Pleuroparenchymal findings were as follows: Nine patients (29%) had no acute pulmonary parenchymal or pleural abnormality. In the remaining 22 patients, pleural effusion was the most common abnormality, found in 14 of 31 (45%). Ten patients (32%) had peripheral wedge-shaped parenchymal opacities suggestive of pulmonary infarction. Normally enhancing lobar atelectasis was seen in nine patients (29%). Six patients (19%) demonstrated heterogeneous parenchymal enhancement within nonaerated lung, two of whom had pathologically proven pulmonary infarct. Thirteen of 31 patients underwent high resolution CT; a typical mosaic perfusion pattern was seen in only 1 patient. Twenty-nine percent of patients with acute PE had no acute lung parenchymal abnormality on CT; thus, the absence of parenchymal abnormality on CT does not exclude PE. High resolution CT mosaic perfusion was not a common feature of acute pulmonary embolism. Regions of decreased enhancement within nonaerated lung, seen in 19%, may prove to be an indicator of pulmonary infarction; however, this is a nonspecific finding.

  11. Incidence of pulmonary embolism in patients with acute exacerbations of chronic obstructive pulmonary disease:a meta-analysis

    Institute of Scientific and Technical Information of China (English)

    王芳

    2013-01-01

    Objective To evaluate the incidence of pulmonary embolism in patients with acute exacerbations of chronic obstructive pulmonary disease (COPD) .Methods Comprehensive searches as of June 2012 were performed in PubMed (1966—) ,Embase (1974—) ,Chinese

  12. The role of inflammation and autoimmunity in the pathophysiology of pulmonary arterial hypertension.

    Science.gov (United States)

    Kherbeck, Nada; Tamby, Mathieu C; Bussone, Guillaume; Dib, Hanadi; Perros, Frederic; Humbert, Marc; Mouthon, Luc

    2013-02-01

    Pulmonary arterial hypertension is characterized by a remodeling of pulmonary arteries with endothelial cell, fibroblast, and vascular smooth muscle cell activation and proliferation. Since pulmonary arterial hypertension occurs frequently in autoimmune conditions such as systemic sclerosis, inflammation and autoimmunity have been suspected to play a critical role in both idiopathic pulmonary arterial hypertension and systemic sclerosis-associated pulmonary arterial hypertension. High levels of pro-inflammatory cytokines such as interleukin-1 and interleukin-6, platelet-derived growth factor, or macrophage inflammatory protein 1 have been found in lung samples of patients with pulmonary arterial hypertension, along with inflammatory cell infiltrates mainly composed of macrophages and dendritic cells, T and B lymphocytes. In addition, circulating autoantibodies are found in the peripheral blood of patients. Thus, autoimmunity and inflammation probably play a role in the development of pulmonary arterial hypertension. In this setting, it would be important to set-up new experimental models of pulmonary arterial hypertension, in order to define novel therapeutics that specifically target immune disturbances in this devastating condition.

  13. Role of inflammation and its mediators in acute ischemic stroke

    Science.gov (United States)

    Jin, Rong; Liu, Lin; Zhang, Shihao; Nanda, Anil; Li, Guohong

    2013-01-01

    Inflammation plays an important role in the pathogenesis of ischemic stroke and other forms of ischemic brain injury. Increasing evidence suggests that inflammatory response is a double-edged sword, as it not only exacerbates secondary brain injury in the acute stage of stroke but also beneficially contributes to brain recovery after stroke. In this article, we provide an overview on the role of inflammation and its mediators in acute ischemic stroke. We discuss various pro-inflammatory and anti-inflammatory responses in different phases after ischemic stroke and the possible reasons for their failures in clinical trials. Undoubtedly, there is still much to be done in order to translate promising pre-clinical findings into clinical practice. A better understanding of the dynamic balance between pro- and anti-inflammatory responses and identifying the discrepancies between pre-clinical studies and clinical trials may serve as a basis for designing effective therapies. PMID:24006091

  14. Creatine kinase activity in dogs with experimentally induced acute inflammation

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    Dimitrinka Zapryanova

    2013-01-01

    Full Text Available The main purpose of this study was to investigate the effect of acute inflammation on total creatine kinase (CK activity in dogs. In these animals, CK is an enzyme found predominantly in skeletal muscle and significantly elevated serum activity is largely associated with muscle damage. Plasma increases in dogs are associated with cell membrane leakage and will therefore be seen in any condition associated with muscular inflammation. The study was induced in 15 mongrel male dogs (n=9 in experimental group and n=6 in control group at the age of two years and body weight 12-15 kg. The inflammation was reproduced by inoculation of 2 ml turpentine oil subcutaneously in lumbar region. The plasma activity of creatine kinase was evaluated at 0, 6, 24, 48, 72 hours after inoculation and on days 7, 14 and 21 by a kit from Hospitex Diagnostics. In the experimental group, the plasma concentrations of the CK-activity were increased at the 48th hour (97.48±6.92 U/L and remained significantly higher (p<0.05 at the 72 hour (97.43±2.93 U/L compared to the control group (77.08±5.27 U/L. The results of this study suggest that the evaluation of creatine kinase in dogs with experimentally induced acute inflammation has a limited diagnostic value. It was observed that the creatine kinase activity is slightly affected by the experimentally induced acute inflammation in dogs.

  15. IRF5 controls both acute and chronic inflammation.

    Science.gov (United States)

    Weiss, Miriam; Byrne, Adam J; Blazek, Katrina; Saliba, David G; Pease, James E; Perocheau, Dany; Feldmann, Marc; Udalova, Irina A

    2015-09-01

    Whereas the importance of macrophages in chronic inflammatory diseases is well recognized, there is an increasing awareness that neutrophils may also play an important role. In addition to the well-documented heterogeneity of macrophage phenotypes and functions, neutrophils also show remarkable phenotypic diversity among tissues. Understanding the molecular pathways that control this heterogeneity should provide abundant scope for the generation of more specific and effective therapeutics. We have shown that the transcription factor IFN regulatory factor 5 (IRF5) polarizes macrophages toward an inflammatory phenotype. IRF5 is also expressed in other myeloid cells, including neutrophils, where it was linked to neutrophil function. In this study we explored the role of IRF5 in models of acute inflammation, including antigen-induced inflammatory arthritis and lung injury, both involving an extensive influx of neutrophils. Mice lacking IRF5 accumulate far fewer neutrophils at the site of inflammation due to the reduced levels of chemokines important for neutrophil recruitment, such as the chemokine (C-X-C motif) ligand 1. Furthermore we found that neutrophils express little IRF5 in the joints and that their migratory properties are not affected by the IRF5 deficiency. These studies extend prior ones suggesting that inhibiting IRF5 might be useful for chronic macrophage-induced inflammation and suggest that IRF5 blockade would ameliorate more acute forms of inflammation, including lung injury.

  16. Home-based pulmonary rehabilitation improves clinical features and systemic inflammation in chronic obstructive pulmonary disease patients.

    Science.gov (United States)

    do Nascimento, Eloisa Sanches Pereira; Sampaio, Luciana Maria Malosá; Peixoto-Souza, Fabiana Sobral; Dias, Fernanda Dultra; Gomes, Evelim Leal Freitas Dantas; Greiffo, Flavia Regina; Ligeiro de Oliveira, Ana Paula; Stirbulov, Roberto; Vieira, Rodolfo Paula; Costa, Dirceu

    2015-01-01

    Chronic obstructive pulmonary disease (COPD) is a respiratory disease characterized by chronic airflow limitation that leads beyond the pulmonary changes to important systemic effects. COPD is characterized by pulmonary and systemic inflammation. However, increases in the levels of inflammatory cytokines in plasma are found even when the disease is stable. Pulmonary rehabilitation improves physical exercise capacity and quality of life and decreases dyspnea. The aim of this study was to evaluate whether a home-based pulmonary rehabilitation (HBPR) program improves exercise tolerance in COPD patients, as well as health-related quality of life and systemic inflammation. This prospective study was conducted at the Laboratory of Functional Respiratory Evaluation, Nove de Julho University, São Paulo, Brazil. After anamnesis, patients were subjected to evaluations of health-related quality of life and dyspnea, spirometry, respiratory muscle strength, upper limbs incremental test, incremental shuttle walk test, and blood test for quantification of systemic inflammatory markers (interleukin [IL]-6 and IL-8). At the end of the evaluations, patients received a booklet containing the physical exercises to be performed at home, three times per week for 8 consecutive weeks. Around 25 patients were enrolled, and 14 completed the pre- and post-HBPR ratings. There was a significant increase in the walked distance and the maximal inspiratory pressure, improvements on two components from the health-related quality-of-life questionnaire, and a decrease in plasma IL-8 levels after the intervention. The HBPR is an important and viable alternative to pulmonary rehabilitation for the treatment of patients with COPD; it improves exercise tolerance, inspiratory muscle strength, quality of life, and systemic inflammation in COPD patients.

  17. Variability in ozone-induced pulmonary injury and inflammation in healthy and cardiovascular-compromised rat models.

    Science.gov (United States)

    Kodavanti, Urmila P; Ledbetter, Allen D; Thomas, Ronald F; Richards, Judy E; Ward, William O; Schladweiler, Mette C; Costa, Daniel L

    2015-01-01

    The molecular bases for variability in air pollutant-induced pulmonary injury due to underlying cardiovascular (CVD) and/or metabolic diseases are unknown. We hypothesized that healthy and genetic CVD-prone rat models will exhibit exacerbated response to acute ozone exposure dependent on the type and severity of disease. Healthy male 12-14-week-old Wistar Kyoto (WKY), Wistar (WS) and Sprague Dawley (SD); and CVD-compromised spontaneously hypertensive (SH), Fawn-Hooded hypertensive (FHH), stroke-prone spontaneously hypertensive (SHSP), obese spontaneously hypertensive heart failure (SHHF) and obese JCR (JCR) rats were exposed to 0.0, 0.25, 0.5, or 1.0 ppm ozone for 4 h; pulmonary injury and inflammation were analyzed immediately following (0-h) or 20-h later. Baseline bronchoalveolar lavage fluid (BALF) protein was higher in CVD strains except for FHH when compared to healthy. Ozone-induced increases in protein and inflammation were concentration-dependent within each strain but the degree of response varied from strain to strain and with time. Among healthy rats, SD were least affected. Among CVD strains, lean rats were more susceptible to protein leakage from ozone than obese rats. Ozone caused least neutrophilic inflammation in SH and SHHF while SHSP and FHH were most affected. BALF neutrophils and protein were poorly correlated when considering the entire dataset (r = 0.55). The baseline and ozone-induced increases in cytokine mRNA varied markedly between strains and did not correlate with inflammation. These data illustrate that the degree of ozone-induced lung injury/inflammation response is likely influenced by both genetic and physiological factors that govern the nature of cardiovascular compromise in CVD models.

  18. Systemic and pulmonary inflammation is independent of skeletal muscle changes in patients with chronic obstructive pulmonary disease.

    Science.gov (United States)

    Barker, Bethan L; McKenna, Susan; Mistry, Vijay; Pancholi, Mitesh; Patel, Hemu; Haldar, Koirobi; Barer, Michael R; Pavord, Ian D; Steiner, Michael C; Brightling, Christopher E; Bafadhel, Mona

    2014-01-01

    Nutritional depletion is an important manifestation of chronic obstructive pulmonary disease (COPD), which has been related to systemic inflammation. It remains unclear to what degree airway inflammation contributes to the presence or progression of nutritional depletion. To determine whether airway inflammation and lung bacterial colonization are related to nutritional status or predict progressive weight loss and muscle atrophy in patients with COPD. Body composition using dual energy X-ray absorptiometry, indices of airway inflammation, and bacterial colonization were measured in 234 COPD patients. Systemic inflammation was assessed from serum C reactive protein (CRP) and circulating total and differential leukocyte counts. Nutritional depletion was defined as a body mass index (BMI) less than 21 kg/m(2) and/or fat-free mass index (FFMI) less than 15 or 17 kg/m(2) in women and men, respectively. FFMI was calculated as the fat-free mass (FFM) corrected for body surface area. Measurements were repeated in 94 patients after a median 16-month follow-up. Regression analysis was used to assess the relationships of weight change and FFM change with indices of bacterial colonization and airway and systemic inflammation. Nutritional depletion occurred in 37% of patients. Lung function was worsened in patients with nutritional depletion compared to those without (forced expiratory volume in 1 second 1.17 L versus 1.41 L, mean difference 0.24, 95% confidence interval 0.10 to 0.38, Pnutritional depletion. At baseline, BMI correlated positively with serum CRP (rs=0.14, P=0.04). Change in weight and change in FFM over time could not be predicted from baseline patient characteristics. Nutritional depletion and progressive muscle atrophy are not related to airway inflammation or bacterial colonization. Overspill of pulmonary inflammation is not a key driver of muscle atrophy in COPD.

  19. Antibody/doxycycline combined therapy for pulmonary ricinosis: Attenuation of inflammation improves survival of ricin-intoxicated mice

    Directory of Open Access Journals (Sweden)

    Yoav Gal

    2014-01-01

    Full Text Available Ricin, a highly toxic plant-derived toxin, is considered a potential weapon in biological warfare due to its high availability and ease of preparation. Pulmonary exposure to ricin results in the generation of an acute edematous inflammation followed by respiratory insufficiency and death. Passive immunization with polyclonal anti-ricin antibodies conferred protection against pulmonary ricinosis, however, at clinically-relevant time points for treatment, survival rates were limited. In this study, intranasal instillation of a lethal dose of ricin to mice, served as a lung challenge model for the evaluation and comparison of different therapeutic modalities against pulmonary ricinosis. We show that treatment with doxycycline resulted in a significant reduction of pro-inflammatory cytokines, markers of oxidative stress and capillary permeability in the lungs of the mice. Moreover, survival rates of mice intoxicated with ricin and treated 24 h later with anti-ricin antibody were significantly improved by co-administration of doxycycline. In contrast, co-administration of the steroid drug dexamethasone with anti-ricin antibodies did not increase survival rates when administered at late hours after intoxication, however dexamethasone did exert a positive effect on survival when applied in conjunction with the doxycycline treatment. These studies strongly suggest that combined therapy, comprised of neutralizing anti-ricin antibodies and an appropriate anti-inflammatory agent, can promote high-level protection against pulmonary ricinosis at clinically-relevant time points post-exposure.

  20. MDCT of acute thrombotic and nonthrombotic pulmonary emboli.

    Science.gov (United States)

    Bhalla, Sanjeev; Lopez-Costa, Ignacio

    2007-10-01

    Acute pulmonary embolism (PE) remains a common clinical challenge. MDCT pulmonary angiography has become the first line imaging study in the diagnosis of PE because of its speed, accuracy, low-interobserver variability, and ability to provide alternative diagnoses. This review article highlights the role of MDCT in the evaluation of acute thrombotic PE in the era of PIOPED 2. MDCT findings of acute PE and some potential pitfalls are covered as well as some of the controversies in imaging young and pregnant patients. MDCT findings of acute non-thrombotic PE are also covered. This latter group may be occult on the angiographic portion of the study but may declare themselves through secondary findings. Their findings and potential mimics are included so that the interpreting radiologist can make the most of a CT to rule out PE.

  1. MDCT of acute thrombotic and nonthrombotic pulmonary emboli

    Energy Technology Data Exchange (ETDEWEB)

    Bhalla, Sanjeev [Division of Cardiothoracic Imaging, Mallinckrodt Institute of Radiology, 510 South Kingshighway Blvd., St. Louis, MO 63110 (United States)], E-mail: bhallas@mir.wustl.edu; Lopez-Costa, Ignacio [Division of Cardiothoracic Imaging, Mallinckrodt Institute of Radiology, 510 South Kingshighway Blvd., St. Louis, MO 63110 (United States)], E-mail: ignacio.lc@mac.com

    2007-10-15

    Acute pulmonary embolism (PE) remains a common clinical challenge. MDCT pulmonary angiography has become the first line imaging study in the diagnosis of PE because of its speed, accuracy, low-interobserver variability, and ability to provide alternative diagnoses. This review article highlights the role of MDCT in the evaluation of acute thrombotic PE in the era of PIOPED 2. MDCT findings of acute PE and some potential pitfalls are covered as well as some of the controversies in imaging young and pregnant patients. MDCT findings of acute non-thrombotic PE are also covered. This latter group may be occult on the angiographic portion of the study but may declare themselves through secondary findings. Their findings and potential mimics are included so that the interpreting radiologist can make the most of a CT to rule out PE.

  2. Morphine in the treatment of acute pulmonary oedema--Why?

    Science.gov (United States)

    Ellingsrud, C; Agewall, S

    2016-01-01

    Morphine has for a long time, been used in patients with acute pulmonary oedema due to its anticipated anxiolytic and vasodilatory properties, however a discussion about the benefits and risks has been raised recently. A literature search in Medline and Embase using the keywords "pulmonary oedema" OR "lung oedema" OR "acute heart failure" AND "morphine" was performed. A certain vasodilation has been described after morphine administration, but the evidence for this mechanism is relatively poor and morphine-induced anxiolysis may possibly be the most important factor of morphine in pulmonary oedema and therefore some authors have suggested benzodiazepines as an alternative treatment. Respiratory depression seems to be a less relevant clinical problem according to the literature, whereas vomiting is common, which may cause aspiration. In the largest outcome study, based on the ADHERE registry, morphine given in acute decompensated heart failure was an independent predictor of increased hospital mortality, with an odds ratio of 4.8 (95% CI: 4.52-5.18, pmorphine administration and mortality, which was lost after adjusting for confounding factors. Morphine is still used for pulmonary oedema in spite of poor scientific background data. A randomised, controlled study is necessary in order to determine the effect--and especially the risk--when using morphine for pulmonary oedema. Since the positive effects are not sufficiently documented, and since the risk for increased mortality cannot be ruled out, one can advocate that the use should be avoided.

  3. Effect of salbutamol on pulmonary responsiveness in chronic pulmonary allergic inflammation in guinea pigs

    Directory of Open Access Journals (Sweden)

    Kasahara D.I.

    2005-01-01

    Full Text Available Beta-2-agonists have been widely used by asthmatic subjects to relieve their obstructive symptoms. However, there are reports that continuous use could lead to loss of bronchial protection and exacerbation of asthma symptoms. We evaluated the effect of two regimens of salbutamol administration (twice and five times a week in a model of chronic airway inflammation in male Hartley guinea pigs (protocol starting weight: 286 ± 30 g induced by repeated exposures to aerosols of ovalbumin (OVA. After sensitization, guinea pigs were exposed to aerosols of 0.1 mg/ml salbutamol solution twice a week (OVA + S2x, N = 7 or five times a week (OVA + S5x, N = 8. We studied allergen-specific (OVA inhalation time and -nonspecific (response to methacholine respiratory system responsiveness. Seventy-two hours after the last OVA challenge, guinea pigs were anesthetized and tracheostomized, respiratory system resistance and elastance were measured and a dose-response curve to inhaled methacholine chloride was obtained. Specific IgG1 was also quantified by the passive cutaneous anaphylactic technique. OVA-sensitized guinea pigs (N = 8 showed reduction of the time of OVA exposure before the onset of respiratory distress, at the 5th, 6th and 7th exposures (P < 0.001. The OVA + S2x group (but not the OVA + S5x group showed a significant increase in OVA inhalation time. There were no significant differences in pulmonary responsiveness to methacholine among the experimental groups. OVA + S2x (but not OVA + S5x animals showed a decrease in the levels of IgG1-specific anaphylactic antibodies compared to the OVA group (P < 0.05. Our results suggest that, in this experimental model, frequent administration of ß2-agonists results in a loss of some of their protective effects against the allergen.

  4. Pathophysiology of acute mountain sickness and high altitude pulmonary oedema

    DEFF Research Database (Denmark)

    Sutton, J R; Lassen, N

    1979-01-01

    We review the evidence that acute mountain sickness (AMS) and high altitude pulmonary oedema (HAPO) occur together more often than is realized. We hypothesize that AMS and HAPO have a common pathophysiological basis: both are due to increased pressure and flow in the microcirculation, causing...

  5. Protein C and acute inflammation: a clinical and biological perspective.

    Science.gov (United States)

    Christiaans, Sarah C; Wagener, Brant M; Esmon, Charles T; Pittet, Jean Francois

    2013-10-01

    The protein C system plays an active role in modulating severe systemic inflammatory processes such as sepsis, trauma, and acute respiratory distress syndrome (ARDS) via its anticoagulant and anti-inflammatory properties. Plasma levels of activated protein C (aPC) are lower than normal in acute inflammation in humans, except early after severe trauma when high plasma levels of aPC may play a mechanistic role in the development of posttraumatic coagulopathy. Thus, following positive results of preclinical studies, a clinical trial (PROWESS) with high continuous doses of recombinant human aPC given for 4 days demonstrated a survival benefit in patients with severe sepsis. This result was not confirmed by subsequent clinical trials, including the recently published PROWESS-SHOCK trial in patients with septic shock and a phase II trial with patients with nonseptic ARDS. A possible explanation for the major difference in outcome between PROWESS and PROWESS-SHOCK trials is that lung-protective ventilation was used for the patients included in the recent PROWESS-SHOCK, but not in the original PROWESS trial. Since up to 75% of sepsis originates from the lung, aPC treatment may not have added enough to the beneficial effect of lung-protective ventilation to show lower mortality. Thus whether aPC will continue to be used to modulate the acute inflammatory response in humans remains uncertain. Because recombinant human aPC has been withdrawn from the market, a better understanding of the complex interactions between coagulation and inflammation is needed before considering the development of new drugs that modulate both coagulation and acute inflammation in humans.

  6. Tenecteplase in the treatment of acute pulmonary thrombo-embolism.

    Science.gov (United States)

    Bhuvaneswaran, J S; Premchand, Rajendra Kumar; Iyengar, S S; Rajeev Khare; Chabra, C B; Padmanabhan, T N C; Sharma, S K; Jain, Alkesh; Pandian, S A; Rajdev, S; Modi, N; Kumar, V

    2011-05-01

    This is a retrospective study documenting the use of tenecteplase in 41 cases of suspected or confirmed pulmonary embolism receiving in-hospital tenecteplase as per weight-adjusted dosing in addition to standard heparin and oral anticoagulant therapy. The presenting symptoms of dyspnoea, chest pain, hemoptysis and syncope were found in 40 (97.56%), 19 (46.34%), 6 (14.63%) and 9 (21.95%) patients, respectively. There was one case of mortality who was a 26 yrs old female of postpartum pulmonary thrombo-embolism with severe hypotension, cyanosis, bilateral crepitations in lungs and pulmonary hypertension. In the 40 survived patients, there was alleviation of dyspnoea and hemoptysis in all patients. Significant reduction in tachycardia (P tenecteplase therapy. Resolution of pulmonary embolism on CT pulmonary angiography was documented in only two patients. No bleeding events or any other adverse events were reported during this study. The present study suggests favourable efficacy of tenecteplase in patients with suspected or confirmed acute pulmonary embolism. Although no major adverse events were noted, a large prospective study on the use of tenecteplase in pulmonary embolism is suggested.

  7. Effect of infliximab on local and systemic inflammation in chronic obstructive pulmonary disease : A pilot study

    NARCIS (Netherlands)

    Dentener, Mieke A.; Creutzberg, Eva C.; Pennings, Herman-Jan; Rijkers, Ger T.; Mercken, Evi; Wouters, Emiel F. M.

    2008-01-01

    Background: Chronic obstructive pulmonary disease ( COPD) with cachexia is characterized by inflammation reflected by increased levels of tumor necrosis factor-alpha (TNF-alpha). Objectives: In this study, infliximab, an anti-TNF-alpha antibody, was evaluated for its effects on systemic ( plasma) an

  8. Global analysis of gene expression in pulmonary fibrosis reveals distinct programs regulating lung inflammation and fibrosis

    Science.gov (United States)

    Kaminski, Naftali; Allard, John D.; Pittet, Jean F.; Zuo, Fengrong; Griffiths, Mark J. D.; Morris, David; Huang, Xiaozhu; Sheppard, Dean; Heller, Renu A.

    2000-02-01

    The molecular mechanisms of pulmonary fibrosis are poorly understood. We have used oligonucleotide arrays to analyze the gene expression programs that underlie pulmonary fibrosis in response to bleomycin, a drug that causes lung inflammation and fibrosis, in two strains of susceptible mice (129 and C57BL/6). We then compared the gene expression patterns in these mice with 129 mice carrying a null mutation in the epithelial-restricted integrin 6 subunit (6/-), which develop inflammation but are protected from pulmonary fibrosis. Cluster analysis identified two distinct groups of genes involved in the inflammatory and fibrotic responses. Analysis of gene expression at multiple time points after bleomycin administration revealed sequential induction of subsets of genes that characterize each response. The availability of this comprehensive data set should accelerate the development of more effective strategies for intervention at the various stages in the development of fibrotic diseases of the lungs and other organs.

  9. CT pulmonary angiography findings that predict 30-day mortality in patients with acute pulmonary embolism.

    Science.gov (United States)

    Bach, Andreas Gunter; Nansalmaa, Baasai; Kranz, Johanna; Taute, Bettina-Maria; Wienke, Andreas; Schramm, Dominik; Surov, Alexey

    2015-02-01

    Standard computed tomography pulmonary angiography (CTPA) can be used to diagnose acute pulmonary embolism. In addition, multiple findings at CTPA have been proposed as potential tools for risk stratification. Therefore, the aim of the present study is to examine the prognostic value of (I) thrombus distribution, (II) morphometric parameters of right ventricular dysfunction, and (III) contrast reflux in inferior vena cava on 30-day mortality. In a retrospective, single-center study from 06/2005 to 01/2010 365 consecutive patients were included. Inclusion criteria were: presence of acute pulmonary embolism, and availability of 30-day follow-up. A review of patient charts and images was performed. There were no significant differences between the group of 326 survivors and 39 non-survivors in (I) thrombus distribution, and (II) morphometric measurements of right ventricular dysfunction. However, (III) contrast reflux in inferior vena cava was significantly stronger in non-survivors (odds ratio 3.29; p<0.001). Results were independent from comorbidities like heart insufficiency and pulmonary hypertension. Measurement of contrast reflux is a new and robust method for predicting 30-day mortality in patients with acute pulmonary embolism. Obstruction scores and morphometric measurements of right ventricular dysfunction perform poor as risk stratification tools. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

  10. Pharmacological inhibition of GSK-3 in a guinea pig model of LPS-induced pulmonary inflammation : II. Effects on skeletal muscle atrophy

    NARCIS (Netherlands)

    Verhees, Koen J P; Pansters, Nicholas A M; Baarsma, Hoeke A; Remels, Alexander H V; Haegens, Astrid; de Theije, Chiel C; Schols, Annemie M W J; Gosens, Reinoud; Langen, Ramon C J

    2013-01-01

    BACKGROUND: Chronic obstructive pulmonary disease (COPD) is accompanied by pulmonary inflammation and associated with extra-pulmonary manifestations, including skeletal muscle atrophy. Glycogen synthase kinase-3 (GSK-3) has been implicated in the regulation of muscle protein- and myonuclear turnover

  11. Midterm benefits of surgical pulmonary embolectomy for acute pulmonary embolus on right ventricular function.

    Science.gov (United States)

    Keeling, William Brent; Leshnower, Bradley G; Lasajanak, Yi; Binongo, Jose; Guyton, Robert A; Halkos, Michael E; Thourani, Vinod H; Lattouf, Omar M

    2016-09-01

    Surgical pulmonary embolectomy has been used for the successful treatment of massive and submassive pulmonary emboli. The purpose of this study is to document the short- and midterm echocardiographic follow-up of right ventricular function after surgical pulmonary embolectomy for acute pulmonary embolus. A retrospective review of the local Society of Thoracic Surgeons database of patients who underwent surgical pulmonary embolectomy for acute pulmonary embolectomy was conducted from 1998 to 2014 at a US academic center. Patients with chronic thrombus were excluded. The institutional echocardiographic database was searched for follow-up studies to compare markers of right ventricular function. Unadjusted outcomes were described, and quantitative comparisons were made of short- and long-term echocardiographic data. A total of 44 patients were included for analysis; 35 patients (79.5%) had a submassive pulmonary embolectomy, and 9 patients (20.5%) had a massive pulmonary embolectomy and required preoperative inotropy. Mean cardiopulmonary bypass time was 68.0 ± 40.2 minutes, and 30 patients (68.2%) underwent procedures without aortic crossclamping. There was 1 in-hospital mortality (2.3%), and there were no permanent neurologic deficits. A total of 21 patients had echocardiography results available for follow-up. Perioperative echocardiographic data showed an immediate decrease in tricuspid regurgitant velocity and right ventricular pressure (P < .05). Mean midterm echocardiographic follow-up was 30 months in 12 patients. At midterm follow-up, improvements in right ventricular function observed postoperatively persisted. Only 1 patient had moderate right ventricular dysfunction, and no patient had worse than mild tricuspid regurgitation. Mean tricuspid valve regurgitant velocity was 2.4 ± 0.7 m/s, and mean pulmonary artery systolic pressure was 37.2 ± 14.2 mm Hg. Surgical pulmonary embolectomy may represent optimal therapy in selected patients for

  12. Acute pulmonary embolism: from morphology to function.

    Science.gov (United States)

    Mayo, John; Thakur, Yogesh

    2014-02-01

    This article reviews the current diagnostic strategies for patients with suspected pulmonary embolism (PE) focusing on the current first choice imaging modality, computed tomographic pulmonary angiography (CTPA). Diagnostic strengths and weaknesses and associated cost-effectiveness of the diagnostic pathways will be discussed. The radiation dose risk of these pathways will be described and techniques to minimize dose will be reviewed. Finally the impact of new dual energy applications which have the potential to provide additional functional information will be briefly reviewed. Imaging plays a vital role in the diagnostic pathway for clinically suspected PE. CT has been established as the most robust morphologic imaging tool for the evaluation of patients with suspected PE. This conclusion is based on the high diagnostic utility of CT for the detection of PE and its unique capacity for accurate diagnosis of conditions that can mimic the clinical presentation of PE. Although current cost-effectiveness evaluations have established CT as integral in the PE diagnostic pathway, failure to acknowledge the impact of alternate diagnosis represents a current knowledge gap. The emerging dual energy capacity of current CT scanners offers the potential to evaluate both pulmonary vascular morphology and ventilation perfusion relationships within the lung parenchyma at high spatial resolution. This dual assessment of lung morphology and lung function at low (< 5 millisievert) radiation dose represents a substantial advance in PE imaging.

  13. Acute Pulmonary Reperfusion Hemorrhage: A Rare Complication After Oversized Percutaneous Balloon Valvuloplasty for Pulmonary Valve Stenosis

    Directory of Open Access Journals (Sweden)

    Hao-I Cheng

    2009-11-01

    Full Text Available Balloon valvuloplasty became the treatment of choice for valvular pulmonary stenosis following its first description in 1982 by Kan et al, and has almost replaced surgical pulmonary valvotomy in the present day. It is a safe and effective method for children for relief of right ventricular obstruction. The results of the procedure are excellent, without significant complications. This report describes the case of a 12-year-old boy who received successful balloon valvuloplasty for critical pulmonary valve stenosis complicated by an episode of acute pulmonary hemorrhage. Because of cyanosis, hypotension and bradycardia, he received emergent endotracheal intubation with 100% oxygen supplement and the highest infusion rate of inotropic agents. Venoarterial mode extracorporeal membrane oxygenation was indicated for life support due to the persistent high oxygenation index. Extracorporeal membrane oxygenation played a key role in the survival of this patient during the course of treatment.

  14. A case of severe preeclampsia presenting as acute pulmonary oedema

    Directory of Open Access Journals (Sweden)

    D. Sumangala Devi

    2016-03-01

    Full Text Available Pulmonary edema refers to an excessive accumulation of fluid in the pulmonary interstitial and alveolar spaces. It may occur in low risk pregnancies but one very important predisposing factor is association with preeclampsia. We are reporting a case of severe preeclampsia presenting as acute pulmonary oedema. 21 year old primi, a known case of gestational hypertension on drugs had pedal edema which was progressively increasing. She was admitted at 29w5d as her BP was still high. Since her preeclampsia profile was normal and her BP was controlled she was continued on conservative management. After 2 days she developed cough, tachypnoea and tachycardia with clinical findings suggestive of A/c pulmonary oedema. Shifted to HDU and started on diuretics and other symptomatic management. After 1 hour as patient's condition was worsening with O2 saturation fall, decided for LSCS + elective post operative ventilatory support. LSCS done showed evidence of Grade 3 abruption with couvelaire changes on uterus. Baby weighed 1.24 kg, severely asphyxiated, died after 3 days. Patient was put on ventillatory support and she improved postoperatively. Acute pulmonary oedema in pregnant women is a life-threatening event. Prompt diagnosis and management is very important for the survival of the patient. [Int J Reprod Contracept Obstet Gynecol 2016; 5(3.000: 899-902

  15. CT imaging in acute pulmonary embolism: diagnostic strategies

    Energy Technology Data Exchange (ETDEWEB)

    Wildberger, Joachim E.; Mahnken, Andreas H.; Das, Marco; Guenther, Rolf W. [University of Technology (RWTH), Department of Diagnostic Radiology, University Hospital, Aachen (Germany); Kuettner, Axel [Eberhard Karls University, Department of Diagnostic Radiology, Tuebingen (Germany); Lell, Michael [Friedrich Alexander University, Department of Diagnostic Radiology, Erlangen (Germany)

    2005-05-01

    Computed tomography pulmonary angiography (CTA) has increasingly become accepted as a widely available, safe, cost-effective, and accurate method for a quick and comprehensive diagnosis of acute pulmonary embolism (PE). Pulmonary catheter angiography is still considered the gold standard and final imaging method in many diagnostic algorithms. However, spiral CTA has become established as the first imaging test in clinical routine due to its high negative predictive value for clinically relevant PE. Despite the direct visualization of clot material, depiction of cardiac and pulmonary function in combination with the quantification of pulmonary obstruction helps to grade the severity of PE for further risk stratification and to monitor the effect of thrombolytic therapy. Because PE and deep venous thrombosis are two different aspects of the same disease, additional indirect CT venography may be a valuable addition to the initial diagnostic algorithm - if this was positive for PE - and demonstration of the extent and localization of deep venous thrombosis has an impact on clinical management. Additional and alternate diagnoses add to the usefulness of this method. Using advanced multislice spiral CT technology, some practitioners have advocated CTA as the sole imaging tool for routine clinical assessment in suspected acute PE. This will simplify standards of practice in the near future. (orig.)

  16. Enlarged Right Ventricle Without Shock in Acute Pulmonary Embolism: Prognosis

    Science.gov (United States)

    Stein, Paul D.; Beemath, Afzal; Matta, Fadi; Goodman, Lawrence R.; Weg, John G.; Hales, Charles A.; Hull, Russell D.; Leeper, Kenneth V.; Dirk Sostman, H; Woodard, Pamela K.

    2008-01-01

    Background An unsettled issue is use of thrombolytic agents in patients with acute pulmonary embolism who are hemodynamically stable, but have right ventricular enlargement. Purpose To assess in-hospital mortality of hemodynamically stable patients with pulmonary embolism and right ventricular enlargement. Methods Patients were enrolled in the Prospective Investigation of Pulmonary Embolism Diagnosis II (PIOPED II). Exclusions included shock, critically ill, ventilatory support, myocardial infarction within 1 month, or ventricular tachycardia or ventricular fibrillation within 24 hours. We evaluated the ratio of the right ventricular minor axis to the left ventricular minor axis measured on transverse images during computed tomographic angiography. Results Among 76 patients with right ventricular enlargement treated with anticoagulants and/or inferior vena cava filters, in–hospital deaths from pulmonary embolism were 0 of 76 (0%) and all-cause mortality was 2 of 76 (2.6%). No septal motion abnormality was observed in 49 (64%), septal flattening in 25 (33%) and septal deviation in 2 (3%). None required ventilatory support, vasopressor therapy, rescue thrombolytic therapy, or catheter embolectomy. There were no in-hospital deaths due to pulmonary embolism. There was no difference in all-cause mortality comparing patients with and without right ventricular enlargement (relative risk = 1.04) Conclusion In-hospital prognosis is good in patients with pulmonary embolism and right ventricular enlargement if not in shock, acutely ill, on ventilatory support, recent myocardial infarction or life threatening arrhythmia. Right ventricular enlargement alone in patients with pulmonary embolism, therefore, does not appear to indicate a poor prognosis or an indication for thrombolytic therapy. PMID:18187071

  17. Mechanistic aspects of inflammation and clinical management of inflammation in acute gouty arthritis.

    Science.gov (United States)

    Cronstein, Bruce N; Sunkureddi, Prashanth

    2013-01-01

    It has been recently demonstrated that interleukin 1β (IL-1β) plays a central role in monosodium urate crystal-induced inflammation and that the NALP3 inflammasome plays a major role in IL-1β production. These discoveries have offered new insights into the pathogenesis of acute gouty arthritis. In this review, we discuss the molecular mechanisms by which monosodium urate crystals induce acute inflammation and examine the mechanisms of action (MOAs) of traditional anti-inflammatory drugs (e.g., nonsteroidal anti-inflammatory drugs, colchicine, and glucocorticoids) and biologic agents (e.g., the IL-1β antagonists anakinra, rilonacept, and canakinumab) to understand how their MOAs contribute to their safety profiles. Traditional anti-inflammatory agents may act on the IL-1β pathway at some level; however, their MOAs are broad-ranging, unspecific, and biologically complex. This lack of specificity may explain the range of systemic adverse effects associated with them. The therapeutic margins of nonsteroidal anti-inflammatory drugs, colchicine, and glucocorticoids are particularly low in elderly patients and in patients with cardiovascular, metabolic, or renal comorbidities that are frequently associated with gouty arthritis. In contrast, the IL-1β antagonists act on very specific targets of inflammation, which may decrease the potential for systemic adverse effects, although infrequent but serious adverse events (including infection and administration reactions) have been reported. Because these IL-1β antagonists target an early event immediately downstream from NALP3 inflammasome activation, they may provide effective alternatives to traditional agents with minimal systemic adverse effects. Results of ongoing trials of IL-1β antagonists will likely provide clarification of their potential role in the management of acute gouty arthritis.

  18. Acute chlorine gas exposure produces transient inflammation and a progressive alteration in surfactant composition with accompanying mechanical dysfunction

    Energy Technology Data Exchange (ETDEWEB)

    Massa, Christopher B.; Scott, Pamela; Abramova, Elena; Gardner, Carol; Laskin, Debra L.; Gow, Andrew J., E-mail: Gow@rci.rutgers.edu

    2014-07-01

    Acute Cl{sub 2} exposure following industrial accidents or military/terrorist activity causes pulmonary injury and severe acute respiratory distress. Prior studies suggest that antioxidant depletion is important in producing dysfunction, however a pathophysiologic mechanism has not been elucidated. We propose that acute Cl{sub 2} inhalation leads to oxidative modification of lung lining fluid, producing surfactant inactivation, inflammation and mechanical respiratory dysfunction at the organ level. C57BL/6J mice underwent whole-body exposure to an effective 60 ppm-hour Cl{sub 2} dose, and were euthanized 3, 24 and 48 h later. Whereas pulmonary architecture and endothelial barrier function were preserved, transient neutrophilia, peaking at 24 h, was noted. Increased expression of ARG1, CCL2, RETLNA, IL-1b, and PTGS2 genes was observed in bronchoalveolar lavage (BAL) cells with peak change in all genes at 24 h. Cl{sub 2} exposure had no effect on NOS2 mRNA or iNOS protein expression, nor on BAL NO{sub 3}{sup −} or NO{sub 2}{sup −}. Expression of the alternative macrophage activation markers, Relm-α and mannose receptor was increased in alveolar macrophages and pulmonary epithelium. Capillary surfactometry demonstrated impaired surfactant function, and altered BAL phospholipid and surfactant protein content following exposure. Organ level respiratory function was assessed by forced oscillation technique at 5 end expiratory pressures. Cl{sub 2} exposure had no significant effect on either airway or tissue resistance. Pulmonary elastance was elevated with time following exposure and demonstrated PEEP refractory derecruitment at 48 h, despite waning inflammation. These data support a role for surfactant inactivation as a physiologic mechanism underlying respiratory dysfunction following Cl{sub 2} inhalation. - Highlights: • Effect of 60 ppm*hr Cl{sub 2} gas on lung inflammation and mechanical function examined. • Pulmonary inflammation is transient and minor.

  19. Computed tomography of acute pulmonary embolism: state-of-the-art

    Energy Technology Data Exchange (ETDEWEB)

    Zhang, Long Jiang; Lu, Guang Ming [Medical School of Nanjing University, Department of Medical Imaging, Jinling Hospital, Nanjing, Jiangsu (China); Meinel, Felix G.; McQuiston, Andrew D.; Ravenel, James G. [Medical University of South Carolina, Department of Radiology and Radiological Science, Charleston, SC (United States); Schoepf, U.J. [Medical School of Nanjing University, Department of Medical Imaging, Jinling Hospital, Nanjing, Jiangsu (China); Medical University of South Carolina, Department of Radiology and Radiological Science, Charleston, SC (United States)

    2015-09-15

    Multidetector computed tomography (CT) plays an important role in the detection, risk stratification and prognosis evaluation of acute pulmonary embolism. This review will discuss the technical improvements for imaging peripheral pulmonary arteries, the methods of assessing pulmonary embolism severity based on CT findings, a multidetector CT technique for pulmonary embolism detection, and lastly, how to avoid overutilization of CT pulmonary angiography and overdiagnosis of pulmonary embolism. (orig.)

  20. Pulmonary pathology of acute respiratory distress syndrome.

    Science.gov (United States)

    Tomashefski, J F

    2000-09-01

    Lung morphology in ARDS reflects the rapid evolution from interstitial and alveolar edema to end-stage fibrosis consequent to injury of the alveolocapillary unit. This morphologic progression, termed diffuse alveolar damage, has been subdivided into sequentially occurring exudative, proliferative, and fibrotic phases. Pulmonary lesions correlate with the phase of alveolar damage rather than its specific cause. The pathologic features are consistent with the effects of a host of injurious stimuli and the complex interaction of inflammatory mediators on alveolar epithelial and capillary endothelial cells. Although ARDS frequently culminates in "interstitial" fibrosis, the organization of intraluminal exudate dominates the histologic picture in the proliferative phase and establishes the framework for subsequent fibrous remodeling of the lung. Involvement of the pulmonary vasculature is an important aspect of ARDS, from the initial phase of edema to the terminal stage of intractable pulmonary hypertension. Vascular lesions include thrombotic, fibroproliferative, and obliterative changes that, like the parenchymal lesions, correlate with the temporal phase of DAD. Although ARDS is characterized by extensive bilateral lung involvement, alveolar damage can also affect the lung in a localized fashion. RAD is associated with the same clinical risk factors as DAD, suggesting that there is a spectrum in the extent of lung involvement and disease severity in patients at risk for ARDS. The factors that govern which patients will develop the fulminant syndrome are poorly understood. It must be re-emphasized that the lung is stereotyped in its response to injury and, consequently, descriptive, or even quantitative, studies of lung morphology can only provide clues regarding the initiating factors and pathogenetic mechanisms of ARDS. Progress in understanding the pathogenesis of ARDS and development of rational approaches to therapy will ultimately depend on careful clinical and

  1. Macrophage Migration Inhibitory Factor in Acute Adipose Tissue Inflammation.

    Directory of Open Access Journals (Sweden)

    Bong-Sung Kim

    Full Text Available Macrophage migration inhibitory factor (MIF is a pleiotropic cytokine and has been implicated in inflammatory diseases. However, little is known about the regulation of MIF in adipose tissue and its impact on wound healing. The aim of this study was to investigate MIF expression in inflamed adipose and determine its role in inflammatory cell recruitment and wound healing. Adipose tissue was harvested from subcutaneous adipose tissue layers of 24 healthy subjects and from adipose tissue adjacent to acutely inflamed wounds of 21 patients undergoing wound debridement. MIF protein and mRNA expression were measured by ELISA and RT-PCR. Cell-specific MIF expression was visualized by immunohistochemistry. The functional role of MIF in cell recruitment was investigated by a chemotaxis assay and by flow cytometry of labeled macrophages that were injected into Mif-/-and wildtype mice. Wound healing was evaluated by an in vitro scratch assay on human fibroblast monolayers. MIF protein levels of native adipose tissue and supernatants from acutely inflamed wounds were significantly elevated when compared to healthy controls. MIF mRNA expression was increased in acutely inflamed adipose tissue indicating the activation of MIF gene transcription in response to adipose tissue inflammation. MIF is expressed in mature adipocytes and in infiltrated macrophages. Peripheral blood mononuclear cell migration was significantly increased towards supernatants derived from inflamed adipose tissue. This effect was partially abrogated by MIF-neutralizing antibodies. Moreover, when compared to wildtype mice, Mif-/-mice showed reduced infiltration of labeled macrophages into LPS-stimulated epididymal fat pads in vivo. Finally, MIF antibodies partially neutralized the detrimental effect of MIF on fibroblast wound healing. Our results indicate that increased MIF expression and rapid activation of the MIF gene in fat tissue adjacent to acute wound healing disorders may play a

  2. Sesame Oil Attenuates Ovalbumin-Induced Pulmonary Edema and Bronchial Neutrophilic Inflammation in Mice

    Directory of Open Access Journals (Sweden)

    Dur-Zong Hsu

    2013-01-01

    Full Text Available Background. Allergic asthma is one of the most common chronic inflammatory diseases of airways. Severe asthma may lead to hospitalization and death. Sesame oil is a natural product with anti-inflammatory property. However, the effect of sesame oil on allergic asthma has never been studied. Objective. We investigate the effect of sesame oil on pulmonary inflammation in allergic asthma model. Methods. Allergic airway inflammation was induced by sensitizing with two doses of 10 mg ovalbumin (OVA and then challenged with 1% OVA nebulizer exposure (1 h/day for 3 days. Sesame oil (0.25, 0.5, or 1 mL/kg/day was given orally 30 min before each challenge. Samples were collected 24 h after the last challenge. Results. Data showed that sesame oil inhibited pulmonary edema and decreased interleukin (IL-1β and IL-6 levels in bronchoalveolar lavage fluid in OVA-treated mice. Sesame oil also decreased pulmonary nitrite level, inducible nitric oxide synthase expression, and neutrophil infiltration induced by OVA. Further, sesame oil decreased serum IgE level in OVA-treated mice. Conclusion. Sesame oil may attenuate pulmonary edema and bronchial neutrophilic inflammation by inhibiting systemic IgE level in allergic asthma.

  3. Inhibition of lipopolysaccharide induced acute inflammation in lung by chlorination

    Energy Technology Data Exchange (ETDEWEB)

    Zhang, Jinshan; Xue, Jinling; Xu, Bi; Xie, Jiani [Environmental Simulation and Pollution Control State Key Joint Laboratory, School of Environment, Tsinghua University, Beijing 100084 (China); Qiao, Juan, E-mail: qjuan@tsinghua.edu.cn [Department of Chemistry, Tsinghua University, Beijing 100084 (China); Lu, Yun, E-mail: luyun@tsinghua.edu.cn [Environmental Simulation and Pollution Control State Key Joint Laboratory, School of Environment, Tsinghua University, Beijing 100084 (China)

    2016-02-13

    Highlights: • Chlorination is effective to reduce the inflammation inducing capacity of LPS in lung. • LAL-detected endotoxin activity is not correlated to the potency of inflammation induction. • Alkyl chain of LPS was chlorinated in chlorination process. • LPS aggregate size decreases after chlorination. - Abstract: Lipopolysaccharide (LPS, also called endotoxin) is a pro-inflammatory constituent of gram negative bacteria and cyanobacteria, which causes a potential health risk in the process of routine urban application of reclaimed water, such as car wash, irrigation, scenic water refilling, etc. Previous studies indicated that the common disinfection treatment, chlorination, has little effect on endotoxin activity removal measured by Limulus amebocyte lysate (LAL) assay. However, in this study, significant decrease of acute inflammatory effects was observed in mouse lung, while LAL assay still presented a moderate increase of endotoxin activity. To explore the possible mechanisms, the nuclear magnetic resonance (NMR) results showed the chlorination happened in alkyl chain of LPS molecules, which could affect the interaction between LPS and LPS-binding protein. Also the size of LPS aggregates was found to drop significantly after treatment, which could be another results of chlorination caused polarity change. In conclusion, our observation demonstrated that chlorination is effective to reduce the LPS induced inflammation in lung, and it is recommended to use health effect-based methods to assess risk removal of water treatment technologies.

  4. IL-18 induces airway hyperresponsiveness and pulmonary inflammation via CD4+ T cell and IL-13.

    Directory of Open Access Journals (Sweden)

    Masanori Sawada

    Full Text Available IL-18 plays a key role in the pathogenesis of pulmonary inflammatory diseases including pulmonary infection, pulmonary fibrosis, lung injury and chronic obstructive pulmonary disease (COPD. However, it is unknown whether IL-18 plays any role in the pathogenesis of asthma. We hypothesized that overexpression of mature IL-18 protein in the lungs may exacerbate disease activities of asthma. We established lung-specific IL-18 transgenic mice on a Balb/c genetic background. Female mice sensitized- and challenged- with antigen (ovalbumin were used as a mouse asthma model. Pulmonary inflammation and emphysema were not observed in the lungs of naïve transgenic mice. However, airway hyperresponsiveness and airway inflammatory cells accompanied with CD4(+ T cells, CD8(+ T cells, eosinophils, neutrophils, and macrophages were significantly increased in ovalbumin-sensitized and challenged transgenic mice, as compared to wild type Balb/c mice. We also demonstrate that IL-18 induces IFN-γ, IL-13, and eotaxin in the lungs of ovalbumin-sensitized and challenged transgenic mice along with an increase in IL-13 producing CD4(+ T cells. Treatment with anti-CD4 monoclonal antibody or deletion of the IL-13 gene improves ovalbumin-induced airway hyperresponsiveness and reduces airway inflammatory cells in transgenic mice. Overexpressing the IL-18 protein in the lungs induces type 1 and type 2 cytokines and airway inflammation, and results in increasing airway hyperresponsiveness via CD4(+ T cells and IL-13 in asthma.

  5. Acute Exacerbation of Chronic Obstructive Pulmonary Disease: Cardiovascular Links

    Directory of Open Access Journals (Sweden)

    Cheryl R. Laratta

    2014-01-01

    Full Text Available Chronic obstructive pulmonary disease (COPD is a chronic, progressive lung disease resulting from exposure to cigarette smoke, noxious gases, particulate matter, and air pollutants. COPD is exacerbated by acute inflammatory insults such as lung infections (viral and bacterial and air pollutants which further accelerate the steady decline in lung function. The chronic inflammatory process in the lung contributes to the extrapulmonary manifestations of COPD which are predominantly cardiovascular in nature. Here we review the significant burden of cardiovascular disease in COPD and discuss the clinical and pathological links between acute exacerbations of COPD and cardiovascular disease.

  6. Acute Pulmonary Edema Caused by a Giant Atrial Myxoma

    Directory of Open Access Journals (Sweden)

    Andrea Fisicaro

    2013-01-01

    Full Text Available Atrial myxoma is the most common primary cardiac tumor. Its clinical presentation spreads from asymptomatic incidental mass to serious life-threatening cardiovascular complications. We report the case of a 44-year-old man with evening fever and worsening dyspnea in the last weeks, admitted to our hospital for acute pulmonary edema. The cardiac auscultation was very suspicious for mitral valve stenosis, but the echocardiography revealed a huge atrial mass with a diastolic prolapse into mitral valve orifice causing an extremely high transmitral gradient pressure. Awareness of this uncommon acute presentation of atrial myxoma is necessary for timely diagnosis and prompt surgical intervention.

  7. Acute pulmonary edema secondary to hyperbaric oxygen therapy

    Science.gov (United States)

    Obiagwu, Chukwudi; Paul, Vishesh; Chadha, Sameer; Hollander, Gerald; Shani, Jacob

    2015-01-01

    Hyperbaric oxygen therapy (HBOT) has been shown to be effective in the treatment of diabetic ulcers, air embolism, carbon monoxide poisoning and gas gangrene with minimal adverse effects. Very few cases of HBOT causing acute pulmonary edema (PE) has been described; with a study on dogs suggesting that a complication of this therapy could be PE. We describe the case of an 80-year-old man with a history of stable systolic heart failure and diabetes mellitus presenting with acute PE following treatment with HBOT for diabetic foot. PMID:25988073

  8. Effects of hydrogen sulfide on inflammation in caerulein-induced acute pancreatitis

    Directory of Open Access Journals (Sweden)

    Bhatia Madhav

    2009-12-01

    Full Text Available Abstract Background Hydrogen sulfide (H2S, a gaseous mediator plays an important role in a wide range of physiological and pathological processes. H2S has been extensively studied for its various roles in cardiovascular and neurological disorders. However, the role of H2S in inflammation is still controversial. The current study was aimed to investigate the therapeutic potential of sodium hydrosulfide (NaHS, an H2S donor in in vivo model of acute pancreatitis in mice. Methods Acute pancreatitis was induced in mice by hourly caerulein injections (50 μg/kg for 10 hours. Mice were treated with different dosages of NaHS (5 mg/kg, 10 mg/kg or 15 mg/kg or with vehicle, distilled water (DW. NaHS or DW was administered 1 h before induction of pancreatitis. Mice were sacrificed 1 h after the last caerulein injection. Blood, pancreas and lung tissues were collected and were processed to measure the plasma amylase, myeloperoxidase (MPO activities in pancreas and lung and chemokines and adhesion molecules in pancreas and lung. Results It was revealed that significant reduction of inflammation, both in pancreas and lung was associated with NaHS 10 mg/kg. Further the anti-inflammatory effects of NaHS 10 mg/kg were associated with reduction of pancreatic and pulmonary inflammatory chemokines and adhesion molecules. NaHS 5 mg/kg did not cause significant improvement on inflammation in pancreas and associated lung injury and NaHS 15 mg/kg did not further enhance the beneficial effects seen with NaHS 10 mg/kg. Conclusion In conclusion, these data provide evidence for anti-inflammatory effects of H2S based on its dosage used.

  9. Variability in Ozone-Induced Pulmonary Injury and Inflammation in Healthy and Cardiovascular Compromised Rat Models

    Science.gov (United States)

    The molecular bases for variability in air pollutant-induced pulmonary injury due to underlying cardiovascular (CVD) and/or metabolic diseases are unknown. We hypothesized that healthy and genetic CVD-prone rat models will exhibit exacerbated response to acute ozone exposure depe...

  10. Vanadium pentoxide induces pulmonary inflammation and tumor promotion in a strain-dependent manner

    Directory of Open Access Journals (Sweden)

    Bauer Alison K

    2010-04-01

    Full Text Available Abstract Background Elevated levels of air pollution are associated with increased risk of lung cancer. Particulate matter (PM contains transition metals that may potentiate neoplastic development through the induction of oxidative stress and inflammation, a lung cancer risk factor. Vanadium pentoxide (V2O5 is a component of PM derived from fuel combustion as well as a source of occupational exposure in humans. In the current investigation we examined the influence of genetic background on susceptibility to V2O5-induced inflammation and evaluated whether V2O5 functions as a tumor promoter using a 2-stage (initiation-promotion model of pulmonary neoplasia in mice. Results A/J, BALB/cJ (BALB, and C57BL/6J (B6 mice were treated either with the initiator 3-methylcholanthrene (MCA; 10 μg/g; i.p. or corn oil followed by 5 weekly aspirations of V2O5 or PBS and pulmonary tumors were enumerated 20 weeks following MCA treatment. Susceptibility to V2O5-induced pulmonary inflammation was assessed in bronchoalveolar lavage fluid (BALF, and chemokines, transcription factor activity, and MAPK signaling were quantified in lung homogenates. We found that treatment of animals with MCA followed by V2O5 promoted lung tumors in both A/J (10.3 ± 0.9 tumors/mouse and BALB (2.2 ± 0.36 mice significantly above that observed with MCA/PBS or V2O5 alone (P 2O5 were also found to be more susceptible to V2O5-induced pulmonary inflammation and hyperpermeability (A/J>BALB>B6. Differential strain responses in inflammation were positively associated with elevated levels of the chemokines KC and MCP-1, higher NFκB and c-Fos binding activity, as well as sustained ERK1/2 activation in lung tissue. Conclusions In this study we demonstrate that V2O5, an occupational and environmentally relevant metal oxide, functions as an in vivo lung tumor promoter among different inbred strains of mice. Further, we identified a positive relationship between tumor promotion and susceptibility

  11. Pharm GKB: Acute bovine pulmonary emphysema AND edema [PharmGKB

    Lifescience Database Archive (English)

    Full Text Available Overview Alternate Names: Synonym ABPE; Acute bovine pulmonary emphysema and edema;...63 External Vocabularies MeSH: Pneumonia, Atypical Interstitial, of Cattle (D011016) SnoMedCT: Acute bovine ...ia, Atypical Interstitial, of Cattle [Disease/Finding] (N0000010988) Common Searches Search Medline Plus Search CTD Pharm GKB: Acute bovine pulmonary emphysema AND edema ...

  12. Acute pulmonary admissions following implementation of a national workplace smoking ban.

    LENUS (Irish Health Repository)

    Kent, Brian D

    2012-09-01

    The implementation of workplace smoking bans has contributed to a significant reduction in the incidence of acute coronary syndrome admissions, but their influence on adult acute pulmonary disease admissions is unclear. We sought to assess the impact of a national smoking ban on nationwide admissions of individuals of working age with acute pulmonary illness.

  13. Microbiota Promotes Chronic Pulmonary Inflammation by Enhancing IL-17A and Autoantibodies.

    Science.gov (United States)

    Yadava, Koshika; Pattaroni, Céline; Sichelstiel, Anke K; Trompette, Aurélien; Gollwitzer, Eva S; Salami, Olawale; von Garnier, Christophe; Nicod, Laurent P; Marsland, Benjamin J

    2016-05-01

    Changes in the pulmonary microbiota are associated with progressive respiratory diseases including chronic obstructive pulmonary disease (COPD). Whether there is a causal relationship between these changes and disease progression remains unknown. To investigate the link between an altered microbiota and disease, we used a murine model of chronic lung inflammation that is characterized by key pathological features found in COPD and compared responses in specific pathogen-free (SPF) mice and mice depleted of microbiota by antibiotic treatment or devoid of a microbiota (axenic). Mice were challenged with LPS/elastase intranasally over 4 weeks, resulting in a chronically inflamed and damaged lung. The ensuing cellular infiltration, histological damage, and decline in lung function were quantified. Similar to human disease, the composition of the pulmonary microbiota was altered in diseased animals. We found that the microbiota richness and diversity were decreased in LPS/elastase-treated mice, with an increased representation of the genera Pseudomonas and Lactobacillus and a reduction in Prevotella. Moreover, the microbiota was implicated in disease development as mice depleted, or devoid, of microbiota exhibited an improvement in lung function, reduced inflammation, and lymphoid neogenesis. The absence of microbial cues markedly decreased the production of IL-17A, whereas intranasal transfer of fluid enriched with the pulmonary microbiota isolated from diseased mice enhanced IL-17A production in the lungs of antibiotic-treated or axenic recipients. Finally, in mice harboring a microbiota, neutralizing IL-17A dampened inflammation and restored lung function. Collectively, our data indicate that host-microbial cross-talk promotes inflammation and could underlie the chronicity of inflammatory lung diseases.

  14. Protection against fine particle-induced pulmonary and systemic inflammation by omega-3 polyunsaturated fatty acids.

    Science.gov (United States)

    Li, Xiang-Yong; Hao, Lei; Liu, Ying-Hua; Chen, Chih-Yu; Pai, Victor J; Kang, Jing X

    2017-03-01

    Exposure to fine particulate matter, such as through air pollution, has been linked to the increased incidence of chronic diseases. However, few measures have been taken to reduce the health risks associated with fine particle exposure. The identification of safe and effective methods to protect against fine particle exposure-related damage is urgently needed. We used synthetic, non-toxic, fluorescent fine particles to investigate the physical distribution of inhaled fine particles and their effects on pulmonary and systemic inflammation in mice. Tissue levels of omega-3 fatty acids were elevated via dietary supplementation or the fat-1 transgenic mouse model. Markers of pulmonary and systemic inflammation were assessed. We discovered that fine particulate matter not only accumulates in the lungs but can also penetrate the pulmonary barrier and travel into other organs, including the brain, liver, spleen, kidney, and testis. These particles induced both pulmonary and systemic inflammation and increased oxidative stress. We also show that elevating tissue levels of omega-3 fatty acids was effective in reducing fine particle-induced inflammation, whether as a preventive method (prior to exposure) or as an intervention (after exposure). These results advance our understanding of how fine particles contribute to disease development and suggest that increasing tissue omega-3 levels may be a promising nutritional means for reducing the risk of diseases induced by particle exposure. Our findings demonstrate that elevating tissue omega-3 levels can prevent and treat fine particle-induced health problems and thereby present an immediate, practical solution for reducing the disease burden of air pollution. Copyright © 2016 The Authors. Published by Elsevier B.V. All rights reserved.

  15. Modified PISAPED Criteria in Combination with Ventilation Scintigraphic Finding for Predicting Acute Pulmonary Embolism

    OpenAIRE

    Watanabe, Naoyuki; Fettich, Jure; Küçük, Nurie Özlem; Kraft, Otakar; Mut, Fernando; Choudhury, Partha; Sharma, Surendra K.; Endo, Keigo; Dondi, Maurizio

    2015-01-01

    This prospective clinical study aimed at assessing three pulmonary scintigraphic algorithms to detect acute pulmonary embolism (PE): Lung ventilation/perfusion (V/Q) scintigraphy along with modified prospective investigation of pulmonary embolism diagnosis (PIOPED) criteria; lung perfusion scintigraphy along with prospective investigative study of acute pulmonary embolism diagnosis (PISAPED) criteria; and lung perfusion scan in combination with ventilation scan, along with modified PISAPED cr...

  16. Noninvasive mechanical ventilation in chronic obstructive pulmonary disease and in acute cardiogenic pulmonary edema.

    Science.gov (United States)

    Rialp Cervera, G; del Castillo Blanco, A; Pérez Aizcorreta, O; Parra Morais, L

    2014-03-01

    Noninvasive ventilation (NIV) with conventional therapy improves the outcome of patients with acute respiratory failure due to hypercapnic decompensation of chronic obstructive pulmonary disease (COPD) or acute cardiogenic pulmonary edema (ACPE). This review summarizes the main effects of NIV in these pathologies. In COPD, NIV improves gas exchange and symptoms, reducing the need for endotracheal intubation, hospital mortality and hospital stay compared with conventional oxygen therapy. NIV may also avoid reintubation and may decrease the length of invasive mechanical ventilation. In ACPE, NIV accelerates the remission of symptoms and the normalization of blood gas parameters, reduces the need for endotracheal intubation, and is associated with a trend towards lesser mortality, without increasing the incidence of myocardial infarction. The ventilation modality used in ACPE does not affect the patient prognosis.

  17. Human C-C chemokine receptor 3 monoclonal antibody inhibits pulmonary inflammation in allergic mice

    Institute of Scientific and Technical Information of China (English)

    Kai WANG; Hua-hao SHEN; Wen LI; Hua-qiong HUANG

    2007-01-01

    Aim:To evaluate the effect of C-C chemokine receptor 3 (CCR3) blockade on pulmonary inflammation and mucus production in allergic mice. Methods:We used the synthetic peptide of the CCR3 NH2-terminal as the immunizing antigen and generated murine monoclonal antibody against the human CCR3. In addition,the generated antibody was administered to mice sensitized and challenged with ovalbumin. The inflammatory cells in bronchoalveolar lavage,cytokine levels,pulmonary histopathology,and mucus secretion were examined. Results:The Western blotting analysis indicated that the generated antibody bound to CCR3 specifically. The allergic mice treated with the antihuman CCR3 antibody exhibited a significant reduction of pulmonary inflammation accompanied with the alteration of cytokine. Conclusion:The antibody we generated was specific to CCR3. The inhibition of airway inflammation and mucus overproduction by the antibody suggested that the blockade of CCR3 is an appealing therapeutical target for asthma. The present research may provide an experimental basis for the further study of this agent.

  18. Bufei Huoxue Capsule Attenuates PM2.5-Induced Pulmonary Inflammation in Mice

    Directory of Open Access Journals (Sweden)

    Yue Jing

    2017-01-01

    Full Text Available Atmospheric fine particulate matter 2.5 (PM 2.5 may carry many toxic substances on its surface and this may pose a public health threat. Epidemiological research indicates that cumulative ambient PM2.5 is correlated to morbidity and mortality due to pulmonary and cardiovascular diseases and cancer. Mitigating the toxic effects of PM2.5 is therefore highly desired. Bufei Huoxue (BFHX capsules have been used in China to treat pulmonary heart disease (cor pulmonale. Thus, we assessed the effects of BFHX capsules on PM2.5-induced pulmonary inflammation and the underlying mechanisms of action. Using Polysearch and Cytoscape 3.2.1 software, pharmacological targets of BFHX capsules in atmospheric PM2.5-related respiratory disorders were predicted and found to be related to biological pathways of inflammation and immune function. In a mouse model of PM2.5-induced inflammation established with intranasal instillation of PM2.5 suspension, BFHX significantly reduced pathological response and inflammatory mediators including IL-4, IL-6, IL-10, IL-8, TNF-α, and IL-1β. BFHX also reduced keratinocyte growth factor (KGF, secretory immunoglobulin A (sIgA, and collagen fibers deposition in lung and improved lung function. Thus, BFHX reduced pathological responses induced by PM2.5, possibly via regulation of inflammatory mediators in mouse lungs.

  19. Bufei Huoxue Capsule Attenuates PM2.5-Induced Pulmonary Inflammation in Mice

    Science.gov (United States)

    Jing, Yue; Cai, Zhe; Zhao, Yukun; Wu, Ye; Zheng, Xuan; Liu, Ying; Qin, Yuying; Gu, Mingjie; Jin, Jin

    2017-01-01

    Atmospheric fine particulate matter 2.5 (PM 2.5) may carry many toxic substances on its surface and this may pose a public health threat. Epidemiological research indicates that cumulative ambient PM2.5 is correlated to morbidity and mortality due to pulmonary and cardiovascular diseases and cancer. Mitigating the toxic effects of PM2.5 is therefore highly desired. Bufei Huoxue (BFHX) capsules have been used in China to treat pulmonary heart disease (cor pulmonale). Thus, we assessed the effects of BFHX capsules on PM2.5-induced pulmonary inflammation and the underlying mechanisms of action. Using Polysearch and Cytoscape 3.2.1 software, pharmacological targets of BFHX capsules in atmospheric PM2.5-related respiratory disorders were predicted and found to be related to biological pathways of inflammation and immune function. In a mouse model of PM2.5-induced inflammation established with intranasal instillation of PM2.5 suspension, BFHX significantly reduced pathological response and inflammatory mediators including IL-4, IL-6, IL-10, IL-8, TNF-α, and IL-1β. BFHX also reduced keratinocyte growth factor (KGF), secretory immunoglobulin A (sIgA), and collagen fibers deposition in lung and improved lung function. Thus, BFHX reduced pathological responses induced by PM2.5, possibly via regulation of inflammatory mediators in mouse lungs.

  20. Diabetic Microvascular Disease and Pulmonary Fibrosis: The Contribution of Platelets and Systemic Inflammation

    Directory of Open Access Journals (Sweden)

    Rekha Jagadapillai

    2016-11-01

    Full Text Available Diabetes is strongly associated with systemic inflammation and oxidative stress, but its effect on pulmonary vascular disease and lung function has often been disregarded. Several studies identified restrictive lung disease and fibrotic changes in diabetic patients and in animal models of diabetes. While microvascular dysfunction is a well-known complication of diabetes, the mechanisms leading to diabetes-induced lung injury have largely been disregarded. We described the potential involvement of diabetes-induced platelet-endothelial interactions in perpetuating vascular inflammation and oxidative injury leading to fibrotic changes in the lung. Changes in nitric oxide synthase (NOS activation and decreased NO bioavailability in the diabetic lung increase platelet activation and vascular injury and may account for platelet hyperreactivity reported in diabetic patients. Additionally, the Janus kinase/signal transducer and activator of transcription (JAK/STAT pathway has been reported to mediate pancreatic islet damage, and is implicated in the onset of diabetes, inflammation and vascular injury. Many growth factors and diabetes-induced agonists act via the JAK/STAT pathway. Other studies reported the contribution of the JAK/STAT pathway to the regulation of the pulmonary fibrotic process but the role of this pathway in the development of diabetic lung fibrosis has not been considered. These observations may open new therapeutic perspectives for modulating multiple pathways to mitigate diabetes onset or its pulmonary consequences.

  1. Inflammation in pulmonary hypertension: what we know and what we could logically and safely target first.

    Science.gov (United States)

    Cohen-Kaminsky, Sylvia; Hautefort, Aurélie; Price, Laura; Humbert, Marc; Perros, Frédéric

    2014-08-01

    Inflammation is important for the initiation and the maintenance of vascular remodeling in most of the animal models of pulmonary arterial hypertension (PAH), and therapeutic targeting of inflammation in these models blocks PAH development. In humans, pulmonary vascular lesions of PAH are the source of cytokine and chemokine production, related to inflammatory cell recruitment and lymphoid neogenesis. Circulating autoantibodies to endothelial cells and to fibroblasts have been reported in 10-40% of patients with idiopathic PAH, suggesting a possible role for autoimmunity in the pathogenesis of pulmonary vascular lesions. Current specific PAH treatments have immunomodulatory properties, and some studies have demonstrated a correlation between levels of circulating inflammatory mediators and patient survival. New immunopathological approaches to PAH should enable the development of innovative treatments for this severe condition.

  2. Lung inflammation and genotoxicity following pulmonary exposure to nanoparticles in ApoE-/- mice

    DEFF Research Database (Denmark)

    Raun Jacobsen, Nicklas; Møller, Peter; Alstrup Jensen, Keld

    2009-01-01

    Background: The toxic and inflammatory potential of 5 different types of nanoparticles were studied in a sensitive model for pulmonary effects in apolipoprotein E knockout mice (ApoE(-/-)). We studied the effects instillation or inhalation Printex 90 of carbon black ( CB) and compared CB instilla......Background: The toxic and inflammatory potential of 5 different types of nanoparticles were studied in a sensitive model for pulmonary effects in apolipoprotein E knockout mice (ApoE(-/-)). We studied the effects instillation or inhalation Printex 90 of carbon black ( CB) and compared CB...... instillation in ApoE-/- and C57 mice. Three and 24 h after pulmonary exposure, inflammation was assessed by mRNA levels of cytokines in lung tissue, cell composition, genotoxicity, protein and lactate dehydrogenase activity in broncho-alveolar lavage (BAL) fluid. Results: Firstly, we found that intratracheal...... instillation of CB caused far more pulmonary toxicity in ApoE-/- mice than in C57 mice. Secondly, we showed that instillation of CB was more toxic than inhalation of a presumed similar dose with respect to inflammation in the lungs of ApoE(-/-) mice. Thirdly, we compared effects of instillation in ApoE-/- mice...

  3. Pulmonary CT findings in acute mercury vapour exposure

    Energy Technology Data Exchange (ETDEWEB)

    Hashimoto, Manabu; Sato, Kimihiko; Heianna, Jyouiti; Hirano, Yoshinori; Omachi, Kohiti; Izumi, Jyunichi; Watarai, Jiro

    2001-01-01

    AIM: We describe the pulmonary computed tomography (CT) findings in acute mercury poisoning. MATERIALS AND METHODS: Initial (n= 8) and follow-up (n= 6) chest CT examinations in eight patients exposed to mercury vapour while cutting pipes in a sulphuric acid plant were reviewed. Of the eight patients, two were asymptomatic and had normal CT results, two were asymptomatic but had abnormalities on CT, and four had both acute symptoms and positive CT results. The patients were all men whose ages ranged from 37 to 54 years (mean, 49 years). RESULTS: Poorly defined nodules were present in five of six patients with positive CT findings, present alone in two patients or as part of a mixed pattern in three. They were random in distribution. Alveolar consolidation (n= 3) and areas of ground-glass opacity (n= 4) were observed and were more prominent in the most severely affected patients with the highest blood and urine level of mercury, predominantly in the upper and/or middle zone. These abnormal findings on CT resolved with (n= 1) or without (n= 5) steroid therapy. Pathological findings (n= 1) demonstrated acute interstitial changes predominantly with oedema. CONCLUSION: We report CT findings in eight patients acutely exposed to mercury vapour. The pulmonary injury was reversible on CT in these cases. Hashimoto, M. (2001)

  4. Acute effects of cigarette smoke on inflammation and oxidative stress : a review

    NARCIS (Netherlands)

    van der Vaart, H; Postma, DS; Timens, W; Ten Hacken, NHT

    2004-01-01

    Compared with the effects of chronic smoke exposure on lung function and airway inflammation, there are few data on the acute effects of smoking. A review of the literature identified 123 studies investigating the acute effects of cigarette smoking on inflammation and oxidative stress in human, anim

  5. Tinea corporis with acute inflammation caused by Trichophyton tonsurans.

    Science.gov (United States)

    Ohno, Sayoko; Tanabe, Hiroshi; Kawasaki, Masako; Horiguchi, Yuji

    2008-09-01

    A 13-year-old Japanese boy presented with acute skin inflammation on the extremities. He belonged to a judo club of a junior high school in which club tinea capitis and tinea corporis seemed to be prevalent. Vesicles and pustules appeared on his right forearm and right leg. They increased in numbers and formed annular lesions. Pruritic erythema appeared surrounding these lesions. Direct microscopic examination of the lesions detected hyphae, and culture for the fungi yielded yellowish colonies. The result of culture from pustules revealed Staphylococcus aureus. At first, a topical antifungal drug and systemic antibiotics seemed to cure annular lesions, but pustules arose again. A large surrounding erythema was cured by topical treatment with a steroid agent. A biopsy specimen from a pustule showed hyphae of fungi within a hair shaft and in the bulb. The restriction fragment length polymorphism in the internal transcribed spacer regions of the ribosomal gene (polymerase chain reaction restriction fragment length polymorphism) revealed a banding pattern compatible with Trichophyton tonsurans. Treatment with systemic itraconazole was begun and lesions disappeared immediately. Systemic antifungal therapy was needed in our case. Tinea corporis with inflammation necessitates systemic antifungal therapy.

  6. Pulmonary contusion and acute respiratory distress syndrome (ARDS) as complications of blunt chest trauma

    National Research Council Canada - National Science Library

    Michalska, Agata; Jurczyk, Agnieszka P; Machała, Waldemar; Szram, Stefan; Berent, Jarosław

    2009-01-01

    .... The authors of the article would like to emphasize the pathophysiology and diagnostic difficulties in such blunt chest trauma complications as pulmonary contusions and acute respiratory distress...

  7. The role of iron in Libby amphibole-induced acute lung injury and inflammation.

    Science.gov (United States)

    Shannahan, Jonathan H; Ghio, Andrew J; Schladweiler, Mette C; McGee, John K; Richards, Judy H; Gavett, Stephen H; Kodavanti, Urmila P

    2011-05-01

    Complexation of host iron (Fe) on the surface of inhaled asbestos fibers has been postulated to cause oxidative stress contributing to in vivo pulmonary injury and inflammation. We examined the role of Fe in Libby amphibole (LA; mean length 4.99 µm ± 4.53 and width 0.28 µm ± 0.19) asbestos-induced inflammogenic effects in vitro and in vivo. LA contained acid-leachable Fe and silicon. In a cell-free media containing FeCl(3), LA bound #17 µg of Fe/mg of fiber and increased reactive oxygen species generation #3.5 fold, which was reduced by deferoxamine (DEF) treatment. In BEAS-2B cells exposure to LA, LA loaded with Fe (FeLA), or LA with DEF did not increase HO-1 or ferritin mRNA expression. LA increased IL-8 expression, which was reduced by Fe loading but increased by DEF. To determine the role of Fe in LA-induced lung injury in vivo, spontaneously hypertensive rats were exposed intratracheally to either saline (300 µL), DEF (1 mg), FeCl(3) (21 µg), LA (0.5 mg), FeLA (0.5 mg), or LA + DEF (0.5 mg). LA caused BALF neutrophils to increase 24 h post-exposure. Loading of Fe on LA but not chelation slightly decreased neutrophilic influx (LA + DEF > LA > FeLA). At 4 h post-exposure, LA-induced lung expression of MIP-2 was reduced in rats exposed to FeLA but increased by LA + DEF (LA + DEF > LA > FeLA). Ferritin mRNA was elevated in rats exposed to FeLA compared to LA. In conclusion, the acute inflammatory response to respirable fibers and particles may be inhibited in the presence of surface-complexed or cellular bioavailable Fe. Cell and tissue Fe-overload conditions may influence the pulmonary injury and inflammation caused by fibers.

  8. Pulmonary and extrapulmonary acute respiratory distress syndrome: are they different?

    Science.gov (United States)

    Garcia, Cristiane S N Baez; Pelosi, Paolo; Rocco, Patricia R M

    2008-06-01

    The pathogenesis of acute respiratory distress syndrome (ARDS) has been described by the presence of direct (pulmonary) and/or indirect (extrapulmonary) insult to the lung parenchyma. Evidence indicates that the pathophysiology of ARDS may differ according to the type of primary insult. This article presents a brief overview of differences between pulmonary and extrapulmonary ARDS, and discusses the interactions between morpho-functional aspects and response to differents therapies, both in experimental and clinical studies. This systematic review included clinical and experimental ARDS studies found in MedLine and SciElo databases in the last 20 years. Many researchers acknowledge that experimental pulmonary and extrapulmonary ARDS are not identical with regard to morpho-functional aspects, the response to positive end-expiratory pressure (PEEP), recruitment manoeuvre, prone position and other adjunctive therapies. However, contradictory results have been reported in different clinical studies, which could be attributed to the difficulty of classifying ARDS in one or the other category, and to the assurance regarding the onset, phase and severity of ARDS in all patients. Heterogeneous ARDS patients are still considered as belonging to one syndrome, and are therefore treated in a similar manner. Thus, it is important to understand the pathophysiology of pulmonary and extrapulmonary ARDS in an attempt to better treat these patients.

  9. Acute lung inflammation in Klebsiella pneumoniae B5055-induced pneumonia and sepsis in BALB/c mice: a comparative study.

    Science.gov (United States)

    Kumar, Vijay; Chhibber, Sanjay

    2011-10-01

    Lungs play an important role in the body's defense against a variety of pathogens, but this network of immune system-mediated defense can be deregulated during acute pulmonary infections. The present study compares acute lung inflammation occurring during Klebsiella pneumoniae B5055-induced pneumonia and sepsis in BALB/c mice. Pneumonia was induced by intranasal instillation of bacteria (10(4) cfu), while sepsis was developed by placing the fibrin-thrombin clot containing known amount of bacteria (10(2) cfu) into the peritoneal cavity of animals. Mice with sepsis showed 100% mortality within five post-infection days, whereas all the animals with pneumonia survived. In animals suffering from K. pneumoniae B5055-induced pneumonia, all the inflammatory parameters (TNF-α, IL-1α, MPO, MDA, and NO) were found to be maximum till third post-infection day, after that, a decline was observed, whereas in septic animals, all the above-mentioned markers of inflammation kept on increasing. Histopathological study showed presence of alternatively activated alveolar macrophages (or foam cells) in lungs of mice with pneumonia after third post-infection day, which might have contributed to the induction of resolution of inflammation, but no such observation was made in lungs of septic mice. Hence, during pneumonia, controlled activation of macrophages may lead to resolution of inflammation.

  10. Acute responses to inhalation of Iloprost in patients with pulmonary hypertension.

    Science.gov (United States)

    Zhang, Hong-Liang; Liu, Zhi-Hong; Wang, Yong; Xiong, Chang-Ming; Ni, Xin-Hai; He, Jian-Guo; Luo, Qin; Zhao, Zhi-Hui; Zhao, Qing; Sun, Xing-Guo

    2012-08-01

    Iloprost has been used to test acute pulmonary vasoreactivity in idiopathic pulmonary arterial hypertension (PAH). We aimed to investigate the acute hemodynamic and oxygenation responses and tolerability to 20 µg aerosolized Iloprost in Chinese patients with pulmonary hypertension. Between March 2005 and May 2010, 212 pulmonary hypertension patients inhaled a single dose of 20 µg Iloprost over 10 - 15 minutes for vasoreactivity testing. The acute hemodynamic and oxygenation responses and adverse events were recorded. Iloprost decreased total pulmonary resistance ((1747 ± 918) dyn×s×cm(-5) vs. (1581 ± 937) dyn×s×cm(-5), P Iloprost. No adverse events requiring medical care or leading to termination of inhalation occurred. Inhalation of 20 µg Iloprost showed potent and selective pulmonary hemodynamic effects and was well tolerated in the Chinese pulmonary hypertension patients. Patients with idiopathic PAH and less severe pulmonary hypertension responded more favorably to inhalation of Iloprost.

  11. Conserved gene regulation during acute inflammation between zebrafish and mammals

    Science.gov (United States)

    Forn-Cuní, G.; Varela, M.; Pereiro, P.; Novoa, B.; Figueras, A.

    2017-01-01

    Zebrafish (Danio rerio), largely used as a model for studying developmental processes, has also emerged as a valuable system for modelling human inflammatory diseases. However, in a context where even mice have been questioned as a valid model for these analysis, a systematic study evaluating the reproducibility of human and mammalian inflammatory diseases in zebrafish is still lacking. In this report, we characterize the transcriptomic regulation to lipopolysaccharide in adult zebrafish kidney, liver, and muscle tissues using microarrays and demonstrate how the zebrafish genomic responses can effectively reproduce the mammalian inflammatory process induced by acute endotoxin stress. We provide evidence that immune signaling pathways and single gene expression is well conserved throughout evolution and that the zebrafish and mammal acute genomic responses after lipopolysaccharide stimulation are highly correlated despite the differential susceptibility between species to that compound. Therefore, we formally confirm that zebrafish inflammatory models are suited to study the basic mechanisms of inflammation in human inflammatory diseases, with great translational impact potential. PMID:28157230

  12. Preferential recruitment of neutrophils by endothelin-1 in acute lung inflammation induced by lipopolysaccharide or cigarette smoke

    Science.gov (United States)

    Bhavsar, Tapan; Liu, Xing Jian; Patel, Hardik; Stephani, Ralph; Cantor, Jerome O

    2008-01-01

    This study examined the role of endothelin-1 (ET-1) in recruiting inflammatory cells to the lung after induction of injury with either lipopolysaccharide (LPS) or cigarette smoke. Hamsters injected with either ET-1 or its precursor peptide (Big ET-1) prior to treatment with LPS or cigarette smoke had markedly increased concentrations of neutrophils in bronchoalveolar lavage fluid (BALF) despite a reduction in total numbers of BALF leukocytes. Furthermore, the effect of ET-1 on smoke-exposed animals was reversed by addition of an endothelin-A receptor antagonist. These results are consistent with preferential recruitment of neutrophils by ET-1, and suggest that inhibition of this proinflammatory mediator may decrease acute pulmonary inflammation associated with cigarette smoke and other pulmonary toxins. PMID:18990977

  13. Acute hemodynamic response to vasodilators in primary pulmonary hypertension.

    Directory of Open Access Journals (Sweden)

    Kulkarni H

    1996-01-01

    Full Text Available Acute hemodynamic effects of high flow oxygen (O2 inhalation, sublingual isosorbide dinitrate (ISDN, intravenous aminophylline (AMN and sublingual nifedipine (NIF were studied in 32 patients with primary pulmonary hypertension (PPH. In 30 out of 32 patients the basal ratio of pulmonary to systemic vascular resistance (Rp/Rs was > 0.5 (mean = 0.77 +/- 0.20. Oxygen caused significant decrease in the mean resistance ratio to 0.68 +/- 0.20 (p = 0.005. ISDN, AMN and NIF caused increase in the resistance ratio to 0.79 +/- 0.26; 0.78 +/- 0.26; and 0.80 +/- 0.23 respectively. O2, ISDN, AMN and NIF caused a fall of Rp/Rs in 21 (65.6%, 10 (31.2%, 10(31.2% and 9(28.1% patients respectively. Thus, of the four drugs tested high flow O2 inhalation resulted in fall of Rp/Rs in two thirds of patients whereas ISDN, AMN and NIF caused a mean rise in Rp/Rs. One third of patients did respond acutely to the latter three drugs. Acute hemodynamic studies are useful before prescribing vasodilators in patients with PPH since more of the commonly used drugs like ISDN, AMN, NIF could have detrimental hemodynamic responses in some patients. However, great caution should be exercised before performing hemodynamic study as the procedure has definite mortality and morbidity.

  14. P2Y6 Receptor Activation Promotes Inflammation and Tissue Remodeling in Pulmonary Fibrosis

    Directory of Open Access Journals (Sweden)

    Tobias Müller

    2017-08-01

    Full Text Available Idiopathic pulmonary fibrosis (IPF is a disease with a poor prognosis and very few available treatment options. The involvement of the purinergic receptor subtypes P2Y2 and P2X7 in fibrotic lung disease has been demonstrated recently. In this study, we investigated the role of P2Y6 receptors in the pathogenesis of IPF in humans and in the animal model of bleomycin-induced lung injury. P2Y6R expression was upregulated in lung structural cells but not in bronchoalveolar lavage (BAL cells derived from IPF patients as well as in animals following bleomycin administration. Furthermore, BAL fluid levels of the P2Y6R agonist uridine-5′-diphosphate were elevated in animals with bleomycin-induced pulmonary fibrosis. Inflammation and fibrosis following bleomycin administration were reduced in P2Y6R-deficient compared to wild-type animals confirming the pathophysiological relevance of P2Y6R subtypes for fibrotic lung diseases. Experiments with bone marrow chimeras revealed the importance of P2Y6R expression on lung structural cells for pulmonary inflammation and fibrosis. Similar effects were obtained when animals were treated with the P2Y6R antagonist MRS2578. In vitro studies demonstrated that proliferation and secretion of the pro-inflammatory/pro-fibrotic cytokine IL-6 by lung fibroblasts are P2Y6R-mediated processes. In summary, our results clearly demonstrate the involvement of P2Y6R subtypes in the pathogenesis of pulmonary fibrosis. Thus, blocking pulmonary P2Y6 receptors might be a new target for the treatment of IPF.

  15. Delayed Pneumoperitoneum and Acute Pulmonary Edema Secondary to Acute Gastric Dilatation

    Science.gov (United States)

    Ahn, Jae Yun; Kim, Jong Kun

    2015-01-01

    Pneumoperitoneum caused by acute gastric dilatation (AGD) is a very rare complication. We report a case of pneumoperitoneum and acute pulmonary edema caused by AGD in a patient with Parkinson’s disease. A 78-year-old woman presented with pneumonia and AGD. We inserted a nasogastric tube and administered empirical antibiotics. We performed an endoscopy, and perforation or necrosis of the stomach and pyloric stenosis were not observed. Thirty-six hours after admission, the patient suddenly developed dyspnea and shock, and eventually died. We suspected the cause of death was pneumoperitoneum and acute pulmonary edema caused by AGD during the conservative treatment period. Immunocompromised patients with chronic illness require close observation even if they do not show any symptoms suggestive of complications. Even if the initial endoscopic or abdominal radiologic findings do not show gastric necrosis or perforation, follow-up with endoscopy is essential to recognize complications of AGD early. PMID:26668807

  16. Surgical treatment of acute pulmonary embolism--a 12-year retrospective analysis

    DEFF Research Database (Denmark)

    Lehnert, Per; Møller, Christian H; Carlsen, Jørn

    2012-01-01

    Surgical embolectomy for acute pulmonary embolism (PE) is considered to be a high risk procedure and therefore a last treatment option. We wanted to evaluate the procedures role in modern treatment of acute PE....

  17. Role of macrophage chemoattractant protein-1 in acute inflammation after lung contusion.

    Science.gov (United States)

    Suresh, Madathilparambil V; Yu, Bi; Machado-Aranda, David; Bender, Matthew D; Ochoa-Frongia, Laura; Helinski, Jadwiga D; Davidson, Bruce A; Knight, Paul R; Hogaboam, Cory M; Moore, Bethany B; Raghavendran, Krishnan

    2012-06-01

    Lung contusion (LC), commonly observed in patients with thoracic trauma is a leading risk factor for development of acute lung injury/acute respiratory distress syndrome. Previously, we have shown that CC chemokine ligand (CCL)-2, a monotactic chemokine abundant in the lungs, is significantly elevated in LC. This study investigated the nature of protection afforded by CCL-2 in acute lung injury/acute respiratory distress syndrome during LC, using rats and CC chemokine receptor (CCR) 2 knockout (CCR2(-/-)) mice. Rats injected with a polyclonal antibody to CCL-2 showed higher levels of albumin and IL-6 in the bronchoalveolar lavage and myeloperoxidase in the lung tissue after LC. Closed-chest bilateral LC demonstrated CCL-2 localization in alveolar macrophages (AMs) and epithelial cells. Subsequent experiments performed using a murine model of LC showed that the extent of injury, assessed by pulmonary compliance and albumin levels in the bronchoalveolar lavage, was higher in the CCR2(-/-) mice when compared with the wild-type (WT) mice. We also found increased release of IL-1β, IL-6, macrophage inflammatory protein-1, and keratinocyte chemoattractant, lower recruitment of AMs, and higher neutrophil infiltration and phagocytic activity in CCR2(-/-) mice at 24 hours. However, impaired phagocytic activity was observed at 48 hours compared with the WT. Production of CCL-2 and macrophage chemoattractant protein-5 was increased in the absence of CCR2, thus suggesting a negative feedback mechanism of regulation. Isolated AMs in the CCR2(-/-) mice showed a predominant M1 phenotype compared with the predominant M2 phenotype in WT mice. Taken together, the above results show that CCL-2 is functionally important in the down-modulation of injury and inflammation in LC.

  18. Acute and subacute pulmonary toxicity caused by a single intratracheal instillation of colloidal silver nanoparticles in mice: pathobiological changes and metallothionein responses.

    Science.gov (United States)

    Kaewamatawong, Theerayuth; Banlunara, Wijit; Maneewattanapinyo, Pattwat; Thammachareon, Chuchaat; Ekgasit, Sanong

    2014-01-01

    To study the acute and subacute pulmonary toxicity of colloidal silver nanoparticles (Ag-NPs), 0 or 100 ppm of Ag-NPs were instilled intratracheally in mice. Cellular and biochemical parameters in bronchoalveolar lavage fluid (BALF) and histological alterations were determined 1, 3, 7, 15, and 30 days after instillation. Ag-NPs induced moderate pulmonary inflammation and injury on BALF indices during the acute period; however, these changes gradually regressed in a time-dependent manner. Concomitant histopathological and laminin immunohistochemical findings generally correlated to BALF data. Superoxide dismutase and metallothionein expression occurred in particle-laden macrophages and alveolar epithelial cells, which correlated to lung lesions in mice treated with Ag-NPs. These findings suggest that instillation of Ag-NPs causes transient moderate acute lung inflammation and tissue damage. Oxidative stress may underlie the induction of injury to lung tissue. Moreover, the expression of metallothionein in tissues indicated the protective response to exposure to Ag-NPs.

  19. Acute phase response, inflammation and metabolic syndrome biomarkers of Libby asbestos exposure

    Energy Technology Data Exchange (ETDEWEB)

    Shannahan, Jonathan H. [Curriculum in Toxicology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599 (United States); Alzate, Oscar [Systems Proteomics Center, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599 (United States); Winnik, Witold M.; Andrews, Debora [Proteomics Core, Research Core Unit, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711 (United States); Schladweiler, Mette C. [Cardiopulmonary and Immunotoxicology Branch, Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711 (United States); Ghio, Andrew J. [Clinical Research Branch, Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Chapel Hill, NC 27599 (United States); Gavett, Stephen H. [Cardiopulmonary and Immunotoxicology Branch, Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711 (United States); Kodavanti, Urmila P., E-mail: Kodavanti.Urmila@epa.gov [Cardiopulmonary and Immunotoxicology Branch, Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711 (United States)

    2012-04-15

    Identification of biomarkers assists in the diagnosis of disease and the assessment of health risks from environmental exposures. We hypothesized that rats exposed to Libby amphibole (LA) would present with a unique serum proteomic profile which could help elucidate epidemiologically-relevant biomarkers. In four experiments spanning varied protocols and temporality, healthy (Wistar Kyoto, WKY; and F344) and cardiovascular compromised (CVD) rat models (spontaneously hypertensive, SH; and SH heart failure, SHHF) were intratracheally instilled with saline (control) or LA. Serum biomarkers of cancer, inflammation, metabolic syndrome (MetS), and the acute phase response (APR) were analyzed. All rat strains exhibited acute increases in α-2-macroglobulin, and α1-acid glycoprotein. Among markers of inflammation, lipocalin-2 was induced in WKY, SH and SHHF and osteopontin only in WKY after LA exposure. While rat strain- and age-related changes were apparent in MetS biomarkers, no LA effects were evident. The cancer marker mesothelin was increased only slightly at 1 month in WKY in one of the studies. Quantitative Intact Proteomic profiling of WKY serum at 1 day or 4 weeks after 4 weekly LA instillations indicated no oxidative protein modifications, however APR proteins were significantly increased. Those included serine protease inhibitor, apolipoprotein E, α-2-HS-glycoprotein, t-kininogen 1 and 2, ceruloplasmin, vitamin D binding protein, serum amyloid P, and more 1 day after last LA exposure. All changes were reversible after a short recovery regardless of the acute or long-term exposures. Thus, LA exposure induces an APR and systemic inflammatory biomarkers that could have implications in systemic and pulmonary disease in individuals exposed to LA. -- Highlights: ► Biomarkers of asbestos exposure are required for disease diagnosis. ► Libby amphibole exposure is associated with increased human mortality. ► Libby amphibole increases circulating proteins involved

  20. Severity assessment of acute pulmonary embolism: evaluation using helical CT

    Energy Technology Data Exchange (ETDEWEB)

    Collomb, D.; Paramelle, P.J.; Calaque, O. [Department of Radiology, CHU Grenoble, BP 218, 38043, Grenoble Cedex (France); Bosson, J.L. [Department of Statistics and Vascular diseases, CHU Grenoble, BP 218, 38043, Grenoble Cedex (France); Vanzetto, G. [Department of Cardiology, CHU Grenoble, BP 218, 38043, Grenoble Cedex (France); Barnoud, D. [Department of Medical Intensive Care, CHU Grenoble, BP 218, BP 218, 38043, Grenoble Cedex (France); Pison, C. [Department of Pulmonary Medicine, CHU Grenoble, BP 218, 38043, Grenoble Cedex (France); Coulomb, M.; Ferretti, G.

    2003-07-01

    The objective was to evaluate the helical CT (HCT) criteria that could indicate severe pulmonary embolism (PE). In a retrospective study, 81 patients (mean age 62 years) with clinical suspicion of PE explored by HCT were studied. The patients were separated into three different groups according to clinical severity and treatment decisions: group SPE included patients with severe PE based on clinical data who were treated by fibrinolysis or embolectomy (n=20); group NSPE included patients with non-severe PE who received heparin (n=30); and group WPE included patients without PE (n=31). For each patient we calculated a vascular obstruction index based on the site of obstruction and the degree of occlusion in the pulmonary artery. We noted the HCT signs, i.e., cardiac and pulmonary artery dimensions, that could indicate acute cor pulmonale. According to multivariate analysis, factors significantly correlated with the severity of PE were: the vascular obstruction index (group SPE: 54%; group NSPE: 24%; p<0.001); the maximum minor axis of the left ventricle (group SPE: 30.2 mm; group NSPE: 40.4 mm; p<0.001); the diameter of the central pulmonary artery (group SPE: 32.4 mm; group NSPE: 28.3 mm; p<0.001); the maximum minor axis of the right ventricle (group SPE: 47.5 mm; group NSPE: 42.7 mm; p=0.029); the right ventricle/left ventricle minor axis ratio (group SPE: 1.63; group NSPE: 1.09; p<0.0001). Our data suggest that hemodynamic severity of PE can be assessed on HCT scans by measuring four main criteria: the vascular obstruction index; the minimum diameter of the left ventricle; the RV:LV ratio; and the diameter of the central pulmonary artery. (orig.)

  1. Massive pulmonary embolism at the onset of acute promyelocytic leukemia

    Directory of Open Access Journals (Sweden)

    Federica Sorà

    2016-07-01

    Full Text Available Life-threatening bleeding is a major and early complication of acute promyelocytic leukemia (APL, but in the last years there is a growing evidence of thromboses in  APL. We report the first case of a young woman with dyspnea as the first symptom of APL due to massive pulmonary embolism (PE successfully treated with thrombolysis for PE and heparin. APL has been processed with a combination of all-trans retinoic acid (ATRA and arsenic trioxide (ATO obtaining complete remission.

  2. The importance of serological assays in diagnosing acute pulmonary histoplasmosis

    Directory of Open Access Journals (Sweden)

    RS Freitas

    2009-01-01

    Full Text Available Histoplasmosis is a systemic mycosis caused by inhalation of Histoplasma capsulatum microconidia. The disease does not normally affect immunocompetent individuals after a single, transient inhalation exposure. However, longer exposure may cause chronic or disseminated acute pulmonary infection. Herein, we report the case of a 24-year-old immunocompetent patient, who presented fever, cough and dyspnea for one month. The chest radiography revealed interstitial infiltrate and diffuse micronodules. The patient reported having had close and prolonged contact with bats. Diagnosis was confirmed by positive double immunodifusion and immunoblotting assays. She was treated with ketoconazole (400 mg and there was complete resolution of the disease.

  3. Echocardiographic changes during acute pulmonary edema subsequent to scorpion sting

    Directory of Open Access Journals (Sweden)

    K Delma

    2012-01-01

    Full Text Available Acute pulmonary edema (APE occurring after scorpion sting is the leading cause of death of the victims of scorpion envenomation. The APE origin is still questioned by physicians treating these patients. Based on echocardiographic study of 20 patients with severe envenomation treated in Ouargla Hospital resuscitation ward during the last four years, the APE etiology seems more likely cardiogenic, referring to cardiac symptoms confirmed by echocardiography although other mechanisms may also be involved. This hypothesis is further confirmed by the positive response of patients to the administration of dobutamine.

  4. Acute Pulmonary Edema Associated With Propofol: An Unusual Complication

    Science.gov (United States)

    Waheed, Mian Adnan; Oud, Lavi

    2014-01-01

    Propofol is frequently used in the emergency department to provide procedural sedation for patients undergoing various procedures and is considered to be safe when administered by trained personnel. Pulmonary edema after administration of propofol has rarely been reported. We report a case of a 23-year-old healthy male who developed acute cough, hemoptysis and hypoxia following administration of propofol for splinting of a foot fracture. Chest radiography showed bilateral patchy infiltrates. The patient was treated successfully with supportive care. This report emphasizes the importance of this potentially fatal propofol-associated complication and discusses possible underlying mechanisms and related literature. PMID:25493132

  5. Effect of Naturally Occurring Ozone Air Pollution Episodes on Pulmonary Oxidative Stress and Inflammation

    Directory of Open Access Journals (Sweden)

    Cheryl Pirozzi

    2015-05-01

    Full Text Available This study aimed to determine if naturally occurring episodes of ozone air pollution in the Salt Lake Valley in Utah, USA, during the summer are associated with increased pulmonary inflammation and oxidative stress, increased respiratory symptoms, and decreased lung function in individuals with chronic obstructive pulmonary disease (COPD compared to controls. We measured biomarkers (nitrite/nitrate (NOx, 8-isoprostane in exhaled breath condensate (EBC, spirometry, and respiratory symptoms in 11 former smokers with moderate-to-severe COPD and nine former smokers without airflow obstruction during periods of low and high ozone air pollution. High ozone levels were associated with increased NOx in EBC in both COPD (8.7 (±8.5 vs. 28.6 (±17.6 μmol/L on clean air vs. pollution days, respectively, p < 0.01 and control participants (7.6 (±16.5 vs. 28.5 (±15.6 μmol/L on clean air vs. pollution days, respectively, p = 0.02. There was no difference in pollution effect between COPD and control groups, and no difference in EBC 8-isoprostane, pulmonary function, or respiratory symptoms between clean air and pollution days in either group. Former smokers both with and without airflow obstruction developed airway oxidative stress and inflammation in association with ozone air pollution episodes.

  6. Pulmonary Thromboembolism Complicating Acute Pancreatitis With Pancreatic Ascites: A Series of 4 cases

    OpenAIRE

    Ruchir Patel; Nirav Pipaliya; Prateik Poddar; Vikas Pandey; Meghraj Ingle; Prabha Sawant

    2016-01-01

    Acute pancreatitis is an inflammatory disease often associated with local and systemic complications. Portosplenic and splanchnic vascular complications of acute pancreatitis are common, but extrasplanchnic vessel thrombosis is less commonly seen. Among them, pulmonary thromboembolism is a very rare complication to be encountered with. We report four cases of acute pulmonary thromboembolism in patients with acute pancreatitis superimposed on chronic pancreatitis. All the patients had abdomina...

  7. Lung inflammation and genotoxicity in mice lungs after pulmonary exposure to candle light combustion particles.

    Science.gov (United States)

    Skovmand, Astrid; Damiao Gouveia, Ana Cecilia; Koponen, Ismo Kalevi; Møller, Peter; Loft, Steffen; Roursgaard, Martin

    2017-07-05

    Candle burning produces a large amount of particles that contribute substantially to the exposure to indoor particulate matter. The exposures to various types of combustion particles, such as diesel exhaust particles, have been associated with increased risk of lung cancer by mechanisms that involve oxidative stress, inflammation and genotoxicity. The aim of this study was to compare pulmonary effects of candle light combustion particles (CP) with two benchmark diesel exhaust particles (A-DEP and SRM2975). Intratracheal (i.t.) instillation of CP (5mg/kg bodyweight) in C57BL/6n mice produced a significant influx of alveolar macrophages and polymorphonuclear leukocytes and increased concentrations of proteins and lactate dehydrogenase activity in bronchoalveolar fluid. Lower levels of these markers of inflammation and cytotoxicity were observed after i.t. instillation of the same dose of A-DEP or SRM2975. The i.t. instillation of CP did not generate oxidative damage to DNA in lung tissue, measured as DNA strand breaks and human 8-oxoguanine glycosylase-sensitive sites by the comet assay. The lack of genotoxic response was confirmed in lung epithelial (A549) cells, although the exposure to CP increased intracellular levels of reactive oxygen species. In conclusion, pulmonary exposure to particles from burning candles is associated with inflammation and cytotoxicity in the lungs. Copyright © 2017 Elsevier B.V. All rights reserved.

  8. Acute inflammation in horizontal incompletely impacted third molar with radiolucency in the elderly

    Science.gov (United States)

    Yamaoka, Minoru; Ono, Yusuke; Takahashi, Masahiro; Ishizuka, Masahide; Uchihashi, Takayuki; Yasuda, Kouichi; Uematsu, Takashi; Furusawa, Kiyofumi

    2009-01-01

    Although radiolucency has been shown as a risk of infection, the poorly understood effects of aging on radiolucency correlate with acute pericoronitis, which has a high risk of infection extending any complications. We reviewed the records of 346 consecutive patients aged more than 41 years to evaluate whether pericoronal radiolucency below the crown in mandibular horizontal incompletely impacted third molars is related to acute inflammation. The frequency of acute inflammation in teeth with pericoronal radiolucency below the crown was similar to that in teeth without; however, the odds ratio of acute inflammation exhibited in women aged more than 61 years compared to women aged 41–50 years was 9.77 (95% confidence interval [CI]: 1.67–57.29; P pericoronitis, including the severe forms of acute inflammation that result from pericoronitis, with pericoronal radiolucency below the crown in the elderly. PMID:19696898

  9. Acute pulmonary toxicity following inhalation exposure to aerosolized VX in anesthetized rats.

    Science.gov (United States)

    Peng, Xinqi; Perkins, Michael W; Simons, Jannitt; Witriol, Alicia M; Rodriguez, Ashley M; Benjamin, Brittany M; Devorak, Jennifer; Sciuto, Alfred M

    2014-06-01

    This study evaluated acute toxicity and pulmonary injury in rats at 3, 6 and 24 h after an inhalation exposure to aerosolized O-ethyl S-[2-(diisopropylamino)ethyl] methylphosphonothioate (VX). Anesthetized male Sprague-Dawley rats (250-300 g) were incubated with a glass endotracheal tube and exposed to saline or VX (171, 343 and 514 mg×min/m³ or 0.2, 0.5 and 0.8 LCt₅₀, respectively) for 10 min. VX was delivered by a small animal ventilator at a volume of 2.5 ml × 70 breaths/minute. All VX-exposed animals experienced a significant loss in percentage body weight at 3, 6, and 24 h post-exposure. In comparison to controls, animals exposed to 514 mg×min/m³ of VX had significant increases in bronchoalveolar lavage (BAL) protein concentrations at 6 and 24 h post-exposure. Blood acetylcholinesterase (AChE) activity was inhibited dose dependently at each of the times points for all VX-exposed groups. AChE activity in lung homogenates was significantly inhibited in all VX-exposed groups at each time point. All VX-exposed animals assessed at 20 min and 3, 6 and 24 h post-exposure showed increases in lung resistance, which was prominent at 20 min and 3 h post-exposure. Histopathologic evaluation of lung tissue of the 514 mg×min/m³ VX-exposed animals at 3, 6 and 24 h indicated morphological changes, including perivascular inflammation, alveolar exudate and histiocytosis, alveolar septal inflammation and edema, alveolar epithelial necrosis, and bronchiolar inflammatory infiltrates, in comparison to controls. These results suggest that aerosolization of the highly toxic, persistent chemical warfare nerve agent VX results in acute pulmonary toxicity and lung injury in rats.

  10. Chest sonography: a useful tool to differentiate acute cardiogenic pulmonary edema from acute respiratory distress syndrome

    Directory of Open Access Journals (Sweden)

    Soldati Gino

    2008-04-01

    Full Text Available Abstract Background Differential diagnosis between acute cardiogenic pulmonary edema (APE and acute lung injury/acute respiratory distress syndrome (ALI/ARDS may often be difficult. We evaluated the ability of chest sonography in the identification of characteristic pleuropulmonary signs useful in the diagnosis of ALI/ARDS and APE. Methods Chest sonography was performed on admission to the intensive care unit in 58 consecutive patients affected by ALI/ARDS or by acute pulmonary edema (APE. Results Ultrasound examination was focalised on finding in the two groups the presence of: 1 alveolar-interstitial syndrome (AIS 2 pleural lines abnormalities 3 absence or reduction of "gliding" sign 4 "spared areas" 5 consolidations 6 pleural effusion 7 "lung pulse". AIS was found in 100% of patients with ALI/ARDS and in 100% of patients with APE (p = ns. Pleural line abnormalities were observed in 100% of patients with ALI/ARDS and in 25% of patients with APE (p All signs, except the presence of AIS, presented a statistically significant difference in presentation between the two syndromes resulting specific for the ultrasonographic characterization of ALI/ARDS. Conclusion Pleuroparenchimal patterns in ALI/ARDS do find a characterization through ultrasonographic lung scan. In the critically ill the ultrasound demonstration of a dyshomogeneous AIS with spared areas, pleural line modifications and lung consolidations is strongly predictive, in an early phase, of non-cardiogenic pulmonary edema.

  11. Elimination Half-Lives of Acute Phase Proteins in Rats and Beagle Dogs During Acute Inflammation.

    Science.gov (United States)

    Kuribayashi, Takashi; Seita, Tetsuro; Momotani, Eiichi; Yamazaki, Shunsuke; Hagimori, Kohei; Yamamoto, Shizuo

    2015-08-01

    The half-lives of typical acute phase proteins in rats and beagle dogs during acute inflammation were investigated. Acute inflammation was induced by injection of turpentine oil in rats and administration of indomethacin in beagle dogs. Serum concentrations of α2-macroglobulin (α2M) and C-reactive protein (CRP) were measured by enzyme-linked immunosorbent assay and α1-acid glycoprotein (AAG) was measured by single radial immunodiffusion. Half-life was calculated as 0.693/elimination rate constant (K). The mean half-lives in the terminal elimination phase of α2M and AAG were 68.1 and 164.8 h, respectively. The half-life of AAG was significantly longer than that of α2M. Mean half-lives in the terminal elimination phase of CRP and AAG were 161.9 and 304.4 h, respectively. The half-life of AAG was significantly longer than that of CRP in beagle dogs. No significant differences in the half-life of AAG were observed between rats and beagle dogs. Furthermore, serum concentrations in the terminal elimination phase could be simulated with the K data acquired in this study.

  12. Use of silver nanowires to determine thresholds for fibre length-dependent pulmonary inflammation and inhibition of macrophage migration in vitro

    Directory of Open Access Journals (Sweden)

    Schinwald Anja

    2012-12-01

    macrophage migration at long fibre lengths could account for their well-documented long term retention in the lungs compared to short fibres. Knowledge of the threshold length for acute pulmonary inflammation contributes to hazard identification of nanofibres.

  13. Butylated hydroxytoluene (BHT) induction of pulmonary inflammation: a role in tumor promotion.

    Science.gov (United States)

    Bauer, A K; Dwyer-Nield, L D; Keil, K; Koski, K; Malkinson, A M

    2001-01-01

    Chronic pulmonary inflammatory diseases predispose towards lung cancer by unknown mechanisms. Butylated hydroxytoluene (BHT) administration to mice causes lung injury and a subsequent inflammatory response, and when administered chronically to certain inbred strains following carcinogen treatment, increases lung tumor multiplicity. We hypothesize that inflammation promotes lung tumor growth in this model system and have begun to examine this hypothesis by assessing inflammatory parameters in inbred strains that vary in their susceptibility to promotion. Positive correlations were found between susceptibilities to tumor promotion and BHT induction of alveolar macrophage and lymphocyte infiltration into alveolar airspaces, and increased vascular permeability (P BHT, along with decreased tumorigenesis after macrophage depletion, are consistent with a role of inflammation in promotion. Inflammatory mediators may provide targets for early diagnosis and chemoprevention.

  14. Investigating suspected acute pulmonary embolism - what are hospital clinicians thinking?

    Energy Technology Data Exchange (ETDEWEB)

    McQueen, A.S. [Department of Radiology, Royal Victoria Infirmary, Newcastle upon Tyne (United Kingdom)], E-mail: andrewmcqueen7@hotmail.com; Worthy, S. [Department of Radiology, Royal Victoria Infirmary, Newcastle upon Tyne (United Kingdom); Keir, M.J. [Department of Medical Physics, Royal Victoria Infirmary, Newcastle upon Tyne (United Kingdom)

    2008-06-15

    Aims: To assess local clinical knowledge of the appropriate investigation of suspected acute pulmonary embolism (PE) and this compare with the 2003 British Thoracic Society (BTS) guidelines as a national reference standard. Methods: A clinical questionnaire was produced based on the BTS guidelines. One hundred and eight-six participants completed the questionnaires at educational sessions for clinicians of all grades, within a single NHS Trust. The level of experience amongst participants ranged from final year medical students to consultant physicians. Results: The clinicians were divided into four groups based on seniority: Pre-registration, Junior, Middle, and Senior. Forty-six point eight percent of all the clinicians correctly identified three major risk factors for PE and 25.8% recognized the definition of the recommended clinical probability score from two alternatives. Statements regarding the sensitivity of isotope lung imaging and computed tomography pulmonary angiography (CTPA) received correct responses from 41.4 and 43% of participants, respectively, whilst 81.2% recognized that an indeterminate ventilation-perfusion scintigraphy (V/Q) study requires further imaging. The majority of clinicians correctly answered three clinical scenario questions regarding use of D-dimers and imaging (78, 85, and 57.5%). There was no statistically significant difference between the four groups for any of the eight questions. Conclusions: The recommended clinical probability score was unfamiliar to all four groups of clinicians in the present study, and the majority of doctors did not agree that a negative CTPA or isotope lung scintigraphy reliably excluded PE. However, questions based on clinical scenarios received considerably higher rates of correct responses. The results indicate that various aspects of the national guidelines on suspected acute pulmonary embolism are unfamiliar to many UK hospital clinicians. Further research is needed to identify methods to improve

  15. Chronic obstructive pulmonary disease and obstructive sleep apnea: overlaps in pathophysiology, systemic inflammation, and cardiovascular disease.

    LENUS (Irish Health Repository)

    McNicholas, Walter T

    2012-02-01

    Chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea syndrome represent two of the most prevalent chronic respiratory disorders in clinical practice, and cardiovascular diseases represent a major comorbidity in each disorder. The two disorders coexist (overlap syndrome) in approximately 1% of adults but asymptomatic lower airway obstruction together with sleep-disordered breathing is more prevalent. Although obstructive sleep apnea syndrome has similar prevalence in COPD as the general population, and vice versa, factors such as body mass index and smoking influence relationships. Nocturnal oxygen desaturation develops in COPD, independent of apnea\\/hypopnea, and is more severe in the overlap syndrome, thus predisposing to pulmonary hypertension. Furthermore, upper airway flow limitation contributes to nocturnal desaturation in COPD without apnea\\/hypopnea. Evidence of systemic inflammation in COPD and sleep apnea, involving C-reactive protein and IL-6, in addition to nuclear factor-kappaB-dependent pathways involving tumor necrosis factor-alpha and IL-8, provides insight into potential basic interactions between both disorders. Furthermore, oxidative stress develops in each disorder, in addition to activation and\\/or dysfunction of circulating leukocytes. These findings are clinically relevant because systemic inflammation may contribute to the pathogenesis of cardiovascular diseases and the cell\\/molecular pathways involved are similar to those identified in COPD and sleep apnea. However, the pathophysiological and clinical significance of systemic inflammation in COPD and sleep apnea is not proven, and thus, studies of patients with the overlap syndrome should provide insight into the mechanisms of systemic inflammation in COPD and sleep apnea, in addition to potential relationships with cardiovascular disease.

  16. Trace Levels of Staphylococcal Enterotoxin Bioactivity Are Concealed in a Mucosal Niche during Pulmonary Inflammation.

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    Antoine Ménoret

    Full Text Available Pathogen and cellular by-products released during infection or trauma are critical for initiating mucosal inflammation. The localization of these factors, their bioactivity and natural countermeasures remain unclear. This concept was studied in mice undergoing pulmonary inflammation after Staphylococcal enterotoxin A (SEA inhalation. Highly purified bronchoalveolar lavage fluid (BALF fractions obtained by sequential chromatography were screened for bioactivity and subjected to mass spectrometry. The Inflammatory and inhibitory potentials of the identified proteins were measured using T cells assays. A potent pro-inflammatory factor was detected in BALF, and we hypothesized SEA could be recovered with its biological activity. Highly purified BALF fractions with bioactivity were subjected to mass spectrometry. SEA was the only identified protein with known inflammatory potential, and unexpectedly, it co-purified with immunosuppressive proteins. Among them was lactoferrin, which inhibited SEA and anti-CD3/-CD28 stimulation by promoting T cell death and reducing TNF synthesis. Higher doses of lactoferrin were required to inhibit effector compared to resting T cells. Inhibition relied on the continual presence of lactoferrin rather than a programming event. The data show a fraction of bioactive SEA resided in a mucosal niche within BALF even after the initiation of inflammation. These results may have clinical value in human diagnostic since traces levels of SEA can be detected using a sensitive bioassay, and may help pinpoint potential mediators of lung inflammation when molecular approaches fail.

  17. An Immature Myeloid/Myeloid-Suppressor Cell Response Associated with Necrotizing Inflammation Mediates Lethal Pulmonary Tularemia.

    Science.gov (United States)

    Periasamy, Sivakumar; Avram, Dorina; McCabe, Amanda; MacNamara, Katherine C; Sellati, Timothy J; Harton, Jonathan A

    2016-03-01

    Inhalation of Francisella tularensis (Ft) causes acute and fatal pneumonia. The lung cytokine milieu favors exponential Ft replication, but the mechanisms underlying acute pathogenesis and death remain unknown. Evaluation of the sequential and systemic host immune response in pulmonary tularemia reveals that in contrast to overwhelming bacterial burden or cytokine production, an overt innate cellular response to Ft drives tissue pathology and host mortality. Lethal infection with Ft elicits medullary and extra-medullary myelopoiesis supporting recruitment of large numbers of immature myeloid cells and MDSC to the lungs. These cells fail to mature and die, leading to subsequent necrotic lung damage, loss of pulmonary function, and host death that is partially dependent upon immature Ly6G+ cells. Acceleration of this process may account for the rapid lethality seen with Ft SchuS4. In contrast, during sub-lethal infection with Ft LVS the pulmonary cellular response is characterized by a predominance of mature neutrophils and monocytes required for protection, suggesting a required threshold for lethal bacterial infection. Further, eliciting a mature phagocyte response provides transient, but dramatic, innate protection against Ft SchuS4. This study reveals that the nature of the myeloid cell response may be the primary determinant of host mortality versus survival following Francisella infection.

  18. An Immature Myeloid/Myeloid-Suppressor Cell Response Associated with Necrotizing Inflammation Mediates Lethal Pulmonary Tularemia

    Science.gov (United States)

    Periasamy, Sivakumar; Avram, Dorina; McCabe, Amanda; MacNamara, Katherine C.; Sellati, Timothy J.; Harton, Jonathan A.

    2016-01-01

    Inhalation of Francisella tularensis (Ft) causes acute and fatal pneumonia. The lung cytokine milieu favors exponential Ft replication, but the mechanisms underlying acute pathogenesis and death remain unknown. Evaluation of the sequential and systemic host immune response in pulmonary tularemia reveals that in contrast to overwhelming bacterial burden or cytokine production, an overt innate cellular response to Ft drives tissue pathology and host mortality. Lethal infection with Ft elicits medullary and extra-medullary myelopoiesis supporting recruitment of large numbers of immature myeloid cells and MDSC to the lungs. These cells fail to mature and die, leading to subsequent necrotic lung damage, loss of pulmonary function, and host death that is partially dependent upon immature Ly6G+ cells. Acceleration of this process may account for the rapid lethality seen with Ft SchuS4. In contrast, during sub-lethal infection with Ft LVS the pulmonary cellular response is characterized by a predominance of mature neutrophils and monocytes required for protection, suggesting a required threshold for lethal bacterial infection. Further, eliciting a mature phagocyte response provides transient, but dramatic, innate protection against Ft SchuS4. This study reveals that the nature of the myeloid cell response may be the primary determinant of host mortality versus survival following Francisella infection. PMID:27015566

  19. An Immature Myeloid/Myeloid-Suppressor Cell Response Associated with Necrotizing Inflammation Mediates Lethal Pulmonary Tularemia.

    Directory of Open Access Journals (Sweden)

    Sivakumar Periasamy

    2016-03-01

    Full Text Available Inhalation of Francisella tularensis (Ft causes acute and fatal pneumonia. The lung cytokine milieu favors exponential Ft replication, but the mechanisms underlying acute pathogenesis and death remain unknown. Evaluation of the sequential and systemic host immune response in pulmonary tularemia reveals that in contrast to overwhelming bacterial burden or cytokine production, an overt innate cellular response to Ft drives tissue pathology and host mortality. Lethal infection with Ft elicits medullary and extra-medullary myelopoiesis supporting recruitment of large numbers of immature myeloid cells and MDSC to the lungs. These cells fail to mature and die, leading to subsequent necrotic lung damage, loss of pulmonary function, and host death that is partially dependent upon immature Ly6G+ cells. Acceleration of this process may account for the rapid lethality seen with Ft SchuS4. In contrast, during sub-lethal infection with Ft LVS the pulmonary cellular response is characterized by a predominance of mature neutrophils and monocytes required for protection, suggesting a required threshold for lethal bacterial infection. Further, eliciting a mature phagocyte response provides transient, but dramatic, innate protection against Ft SchuS4. This study reveals that the nature of the myeloid cell response may be the primary determinant of host mortality versus survival following Francisella infection.

  20. Revascularization of Atherosclerotic Renal Artery Stenosis for Chronic Heart Failure Versus Acute Pulmonary Oedema.

    Science.gov (United States)

    Green, Darren; Ritchie, James P; Chrysochou, Constantina; Kalra, Philip A

    2017-02-27

    To determine whether the apparent benefit of revascularization of renal artery stenosis for "flash" pulmonary oedema extends to heart failure patients without a history of prior acute pulmonary oedema. A prospective study of patients with renal artery stenosis and heart failure at a single centre between 1(st) January 1995 and 31(st) December 2010. Patients were divided into those with and without previous acute pulmonary oedema / decompensation. Survival analysis compared revascularization versus medical therapy in each group using Cox regression adjusted for age, eGFR, blood pressure, and co-morbidities. There were 152 patients: 59% male, 36% diabetic, age 70 ± 9 years, eGFR 29 ± 17 mL/min/1.73 m(2) . 52 had experienced previous acute pulmonary oedema (34%), whereas 100 had no previous acute pulmonary oedema (66%). The revascularization rate was 31% in both groups. For heart failure without previous acute pulmonary oedema, the hazard ratio for death after revascularization compared to medical therapy was 0.76 (0.58-0.99, p = 0.04). In heart failure with previous acute pulmonary enema, the hazard ratio was 0.73 (0.44-1.21, p = 0.22). For those without previous acute pulmonary oedema, the hazard ratio for heart failure hospitalization after revascularization compared to medical therapy was 1.00 (0.17-6.05, p = 1.00). In those with previous acute pulmonary oedema, it was 0.51 (0.08-3.30, p = 0.48). The benefit of revascularization in heart failure may extend beyond the current indication of acute pulmonary oedema. However, findings derive from an observational study. This article is protected by copyright. All rights reserved.

  1. Pharmacological characterisation of anti-inflammatory compounds in acute and chronic mouse models of cigarette smoke-induced inflammation

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    Mok Joanie

    2010-09-01

    Full Text Available Abstract Background Candidate compounds being developed to treat chronic obstructive pulmonary disease are typically assessed using either acute or chronic mouse smoking models; however, in both systems compounds have almost always been administered prophylactically. Our aim was to determine whether the prophylactic effects of reference anti-inflammatory compounds in acute mouse smoking models reflected their therapeutic effects in (more clinically relevant chronic systems. Methods To do this, we started by examining the type of inflammatory cell infiltrate which occurred after acute (3 days or chronic (12 weeks cigarette smoke exposure (CSE using female, C57BL/6 mice (n = 7-10. To compare the effects of anti-inflammatory compounds in these models, mice were exposed to either 3 days of CSE concomitant with compound dosing or 14 weeks of CSE with dosing beginning after week 12. Budesonide (1 mg kg-1; i.n., q.d., roflumilast (3 mg kg-1; p.o., q.d. and fluvastatin (2 mg kg-1; p.o., b.i.d. were dosed 1 h before (and 5 h after for fluvastatin CSE. These dose levels were selected because they have previously been shown to be efficacious in mouse models of lung inflammation. Bronchoalveolar lavage fluid (BALF leukocyte number was the primary endpoint in both models as this is also a primary endpoint in early clinical studies. Results To start, we confirmed that the inflammatory phenotypes were different after acute (3 days versus chronic (12 weeks CSE. The inflammation in the acute systems was predominantly neutrophilic, while in the more chronic CSE systems BALF neutrophils (PMNs, macrophage and lymphocyte numbers were all increased (p Conclusions These results demonstrate that the acute, prophylactic systems can be used to identify compounds with therapeutic potential, but may not predict a compound's efficacy in chronic smoke exposure models.

  2. TLR4 signalling in pulmonary stromal cells is critical for inflammation and immunity in the airways.

    Science.gov (United States)

    Perros, Frederic; Lambrecht, Bart N; Hammad, Hamida

    2011-09-24

    Inflammation of the airways, which is often associated with life-threatening infection by Gram-negative bacteria or presence of endotoxin in the bioaerosol, is still a major cause of severe airway diseases. Moreover, inhaled endotoxin may play an important role in the development and progression of airway inflammation in asthma. Pathologic changes induced by endotoxin inhalation include bronchospasm, airflow obstruction, recruitment of inflammatory cells, injury of the alveolar epithelium, and disruption of pulmonary capillary integrity leading to protein rich fluid leak in the alveolar space. Mammalian Toll-like receptors (TLRs) are important signalling receptors in innate host defense. Among these receptors, TLR4 plays a critical role in the response to endotoxin. Lungs are a complex compartmentalized organ with separate barriers, namely the alveolar-capillary barrier, the microvascular endothelium, and the alveolar epithelium. An emerging theme in the field of lung immunology is that structural cells (SCs) of the airways such as epithelial cells (ECs), endothelial cells, fibroblasts and other stromal cells produce activating cytokines that determine the quantity and quality of the lung immune response. This review focuses on the role of TLR4 in the innate and adaptive immune functions of the pulmonary SCs.

  3. Monoclonal antibody therapy for the treatment of asthma and chronic obstructive pulmonary disease with eosinophilic inflammation.

    Science.gov (United States)

    Nixon, John; Newbold, Paul; Mustelin, Tomas; Anderson, Gary P; Kolbeck, Roland

    2017-01-01

    Eosinophils have been linked with asthma for more than a century, but their role has been unclear. This review discusses the roles of eosinophils in asthma and chronic obstructive pulmonary disease (COPD) and describes therapeutic antibodies that affect eosinophilia. The aims of pharmacologic treatments for pulmonary conditions are to reduce symptoms, slow decline or improve lung function, and reduce the frequency and severity of exacerbations. Inhaled corticosteroids (ICS) are important in managing symptoms and exacerbations in asthma and COPD. However, control with these agents is often suboptimal, especially for patients with severe disease. Recently, new biologics that target eosinophilic inflammation, used as adjunctive therapy to corticosteroids, have proven beneficial and support a pivotal role for eosinophils in the pathology of asthma. Nucala® (mepolizumab; anti-interleukin [IL]-5) and Cinquair® (reslizumab; anti-IL-5), the second and third biologics approved, respectively, for the treatment of asthma, exemplifies these new treatment options. Emerging evidence suggests that eosinophils may contribute to exacerbations and possibly to lung function decline for a subset of patients with COPD. Here we describe the pharmacology of therapeutic antibodies inhibiting IL-5 or targeting the IL-5 receptor, as well as other cytokines contributing to eosinophilic inflammation. We discuss their roles as adjuncts to conventional therapeutic approaches, especially ICS therapy, when disease is suboptimally controlled. These agents have achieved a place in the therapeutic armamentarium for asthma and COPD and will deepen our understanding of the pathogenic role of eosinophils.

  4. TLR4 signalling in pulmonary stromal cells is critical for inflammation and immunity in the airways

    Directory of Open Access Journals (Sweden)

    Lambrecht Bart N

    2011-09-01

    Full Text Available Abstract Inflammation of the airways, which is often associated with life-threatening infection by Gram-negative bacteria or presence of endotoxin in the bioaerosol, is still a major cause of severe airway diseases. Moreover, inhaled endotoxin may play an important role in the development and progression of airway inflammation in asthma. Pathologic changes induced by endotoxin inhalation include bronchospasm, airflow obstruction, recruitment of inflammatory cells, injury of the alveolar epithelium, and disruption of pulmonary capillary integrity leading to protein rich fluid leak in the alveolar space. Mammalian Toll-like receptors (TLRs are important signalling receptors in innate host defense. Among these receptors, TLR4 plays a critical role in the response to endotoxin. Lungs are a complex compartmentalized organ with separate barriers, namely the alveolar-capillary barrier, the microvascular endothelium, and the alveolar epithelium. An emerging theme in the field of lung immunology is that structural cells (SCs of the airways such as epithelial cells (ECs, endothelial cells, fibroblasts and other stromal cells produce activating cytokines that determine the quantity and quality of the lung immune response. This review focuses on the role of TLR4 in the innate and adaptive immune functions of the pulmonary SCs.

  5. Immune modulatory effects of IL-22 on allergen-induced pulmonary inflammation.

    Directory of Open Access Journals (Sweden)

    Ping Fang

    Full Text Available IL-22 is a Th17/Th22 cytokine that is increased in asthma. However, recent animal studies showed controversial findings in the effects of IL-22 in allergic asthma. To determine the role of IL-22 in ovalbumin-induced allergic inflammation we generated inducible lung-specific IL-22 transgenic mice. Transgenic IL-22 expression and signaling activity in the lung were determined. Ovalbumin (OVA-induced pulmonary inflammation, immune responses, and airway hyperresponsiveness (AHR were examined and compared between IL-22 transgenic mice and wild type controls. Following doxycycline (Dox induction, IL-22 protein was readily detected in the large (CC10 promoter and small (SPC promoter airway epithelial cells. IL-22 signaling was evidenced by phosphorylated STAT3. After OVA sensitization and challenge, compared to wild type littermates, IL-22 transgenic mice showed decreased eosinophils in the bronchoalveolar lavage (BAL, and in lung tissue, decreased mucus metaplasia in the airways, and reduced AHR. Among the cytokines and chemokines examined, IL-13 levels were reduced in the BAL fluid as well as in lymphocytes from local draining lymph nodes of IL-22 transgenic mice. No effect was seen on the levels of serum total or OVA-specific IgE or IgG. These findings indicate that IL-22 has immune modulatory effects on pulmonary inflammatory responses in allergen-induced asthma.

  6. Azithromycin reduces inflammation in a rat model of acute conjunctivitis

    Science.gov (United States)

    Fernandez-Robredo, Patricia; Recalde, Sergio; Moreno-Orduña, Maite; García-García, Laura; Zarranz-Ventura, Javier; García-Layana, Alfredo

    2013-01-01

    Purpose Macrolide antibiotics are known to have various anti-inflammatory effects in addition to their antimicrobial activity, but the mechanisms are still unclear. The effect of azithromycin on inflammatory molecules in the lipopolysaccharide-induced rat conjunctivitis model was investigated. Methods Twenty-four Wistar rats were divided into two groups receiving topical ocular azithromycin (15 mg/g) or vehicle. In total, six doses (25 µl) were administered as one dose twice a day for three days before subconjunctival lipopolysaccharide injection (3 mg/ml). Before the rats were euthanized, mucus secretion, conjunctival and palpebral edema and redness were evaluated. Real-time polymerase chain reaction was used to determine gene expression for interleukin-6, cyclooxygenase-2, tumor necrosis factor-α, matrix metalloproteinase (MMP)-2, and MMP-9. Interleukin-6 was determined with enzyme-linked immunosorbent assay, nuclear factor-kappa B with western blot, and MMP-2 activity with gelatin zymogram. Four eyes per group were processed for histology and subsequent periodic acid-Schiff staining and CD68 for immunofluorescence. The Student t test or the Wilcoxon test for independent samples was applied (SPSS v.15.0). Results Azithromycin-treated animals showed a significant reduction in all clinical signs (p<0.05) compared to controls. Interleukin-6 (p<0.05), nuclear factor-kappa B protein expression (p<0.01), and MMP-2 activity (p<0.05) in conjunctival homogenates were significantly reduced compared with the control animals. MMP-2 gene expression showed a tendency to decrease in the azithromycin group (p=0.063). Mucus secretion by goblet cells and the macrophage count in conjunctival tissue were also decreased in the azithromycin group (p<0.05). Conclusions These results suggest that azithromycin administration ameliorates induced inflammation effects in a rat model of acute conjunctivitis. PMID:23378729

  7. Pulmonary inflammation after ethanol exposure and burn injury is attenuated in the absence of IL-6.

    Science.gov (United States)

    Chen, Michael M; Bird, Melanie D; Zahs, Anita; Deburghgraeve, Cory; Posnik, Bartlomiej; Davis, Christopher S; Kovacs, Elizabeth J

    2013-05-01

    Alcohol consumption leads to an exaggerated inflammatory response after burn injury. Elevated levels of interleukin-6 (IL-6) in patients are associated with increased morbidity and mortality after injury, and high systemic and pulmonary levels of IL-6 have been observed after the combined insult of ethanol exposure and burn injury. To further investigate the role of IL-6 in the pulmonary inflammatory response, we examined leukocyte infiltration and cytokine and chemokine production in the lungs of wild-type and IL-6 knockout mice given vehicle or ethanol (1.11 g/kg) and subjected to a sham or 15% total body surface area burn injury. Levels of neutrophil infiltration and neutrophil chemoattractants were increased to a similar extent in wild-type and IL-6 knockout mice 24 h after burn injury. When ethanol exposure preceded the burn injury, however, a further increase of these inflammatory markers was seen only in the wild-type mice. Additionally, signal transducer and activator of transcription-3 (STAT3) phosphorylation did not increase in response to ethanol exposure in the IL-6 knockout mice, in contrast to their wild-type counterparts. Visual and imaging analysis of alveolar wall thickness supported these findings and similar results were obtained by blocking IL-6 with antibody. Taken together, our data suggest a causal relationship between IL-6 and the excessive pulmonary inflammation observed after the combined insult of ethanol and burn injury.

  8. Proteoglycans: key regulators of pulmonary inflammation and the innate immune response to lung infection.

    Science.gov (United States)

    Gill, Sean; Wight, Thomas N; Frevert, Charles W

    2010-06-01

    Exposure to viruses and bacteria results in lung infections and places a significant burden on public health. The innate immune system is an early warning system that recognizes viruses and bacteria, which results in the rapid production of inflammatory mediators such as cytokines and chemokines and the pulmonary recruitment of leukocytes. When leukocytes emigrate from the systemic circulation through the extracellular matrix (ECM) in response to lung infection they encounter proteoglycans, which consist of a core protein and their associated glycosaminoglycans. In this review, we discuss how proteoglycans serve to modify the pulmonary inflammatory response and leukocyte migration through a number of different mechanisms including: (1) The ability of soluble proteoglycans or fragments of glycosaminoglycans to activate Toll-like receptor (TLRs) signaling pathways; (2) The binding and sequestration of cytokines, chemokines, and growth factors by proteoglycans; (3) the ability of proteoglycans and hyaluronan to facilitate leukocyte adhesion and sequestration; and (4) The interactions between proteoglycans and matrix metalloproteinases (MMP) that alter the function of these proteases. In conclusion, proteoglycans fine-tune tissue inflammation through a number of different mechanisms. Clarification of the mechanisms whereby proteoglycans modulate the pulmonary inflammatory response will most likely lead to new therapeutic approaches to inflammatory lung disease and lung infection.

  9. Chronic allergic pulmonary inflammation is aggravated in angiotensin-(1-7) Mas receptor knockout mice.

    Science.gov (United States)

    Magalhães, Giselle S; Rodrigues-Machado, Maria Glória; Motta-Santos, Daisy; Alenina, Natalia; Bader, Michael; Santos, Robson A; Barcelos, Lucíola S; Campagnole-Santos, Maria José

    2016-12-01

    The angiotensin-(1-7) [ANG-(1-7)]/Mas receptor pathway is currently recognized as a counterbalancing mechanism of the renin-angiotensin system in different pathophysiological conditions. We have previously described that treatment with ANG-(1-7) attenuates lung inflammation and remodeling in an experimental model of asthma. In the present study, we investigated whether lack of the Mas receptor could alter the inflammatory response in a model of chronic allergic lung inflammation induced by ovalbumin (OVA). Mas receptor wild-type (MasWT) and knockout (MasKO) mice were subjected to four doses of OVA (20 μg/mice ip) with a 14-day interval. At the 21st day, nebulization with OVA (1%) was started, three times per week until the 46th day. Control groups received saline (0.9% ip) and were nebulized with saline (0.9%). MasWT-OVA developed a modest inflammatory response and minor pulmonary remodeling to OVA challenge. Strikingly, MasKO-OVA presented a significant increase in inflammatory cell infiltrate, increase in extracellular matrix deposition, increase in thickening of the alveolar parenchyma, increase in thickening of the smooth muscle layer of the pulmonary arterioles, increase in proinflammatory cytokine and chemokine levels in the lungs, characteristic of chronic asthma. Additionally, MasKO-OVA presented an increase in ERK1/2 phosphorylation compared with MasWT-OVA. Furthermore, MasKO-OVA showed a worse performance in a test of maximum physical exercise compared with MasWT-OVA. Our study shows that effects triggered by the Mas receptor are important to attenuate the inflammatory and remodeling processes in a model of allergic lung inflammation in mice. Our data indicate that impairment of the ANG-(1-7)/Mas receptor pathway may lead to worsening of the pathophysiological changes of asthma. Copyright © 2016 the American Physiological Society.

  10. Resolvin D1 Dampens Pulmonary Inflammation and Promotes Clearance of Nontypeable Haemophilus influenzae.

    Science.gov (United States)

    Croasdell, Amanda; Lacy, Shannon H; Thatcher, Thomas H; Sime, Patricia J; Phipps, Richard P

    2016-03-15

    Nontypeable Haemophilus influenzae (NTHi) is a Gram-negative, opportunistic pathogen that frequently causes ear infections, bronchitis, pneumonia, and exacerbations in patients with underlying inflammatory diseases, such as chronic obstructive pulmonary disease. In mice, NTHi is rapidly cleared, but a strong inflammatory response persists, underscoring the concept that NTHi induces dysregulation of normal inflammatory responses and causes a failure to resolve. Lipid-derived specialized proresolving mediators (SPMs) play a critical role in the active resolution of inflammation by both suppressing proinflammatory actions and promoting resolution pathways. Importantly, SPMs lack the immunosuppressive properties of classical anti-inflammatory therapies. On the basis of these characteristics, we hypothesized that aspirin-triggered resolvin D1 (AT-RvD1) would dampen NTHi-induced inflammation while still enhancing bacterial clearance. C57BL/6 mice were treated with AT-RvD1 and infected with live NTHi. AT-RvD1-treated mice had lower total cell counts and neutrophils in bronchoalveolar lavage fluid, and had earlier influx of macrophages. In addition, AT-RvD1-treated mice showed changes in temporal regulation of inflammatory cytokines and enzymes, with decreased KC at 6 h and decreased IL-6, TNF-α, and cyclooxygenase-2 expression at 24 h post infection. Despite reduced inflammation, AT-RvD1-treated mice had reduced NTHi bacterial load, mediated by enhanced clearance by macrophages and a skewing toward an M2 phenotype. Finally, AT-RvD1 protected NTHi-infected mice from weight loss, hypothermia, hypoxemia, and respiratory compromise. This research highlights the beneficial role of SPMs in pulmonary bacterial infections and provides the groundwork for further investigation into SPMs as alternatives to immunosuppressive therapies like steroids.

  11. Syncope as a presentation of acute pulmonary embolism

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    Altınsoy B

    2016-06-01

    Full Text Available Bülent Altınsoy, Fatma Erboy, Hakan Tanrıverdi, Fırat Uygur, Tacettin Örnek, Figen Atalay, Meltem Tor Department of Pulmonary Medicine, School of Medicine, Bulent Ecevit University, Kozlu, Zonguldak, Turkey Purpose: Syncope is an atypical presentation for acute pulmonary embolism (APE. There are conflicting data concerning syncope and prognosis of APE. Patients and methods: One hundred and seventy-nine consecutive patients aged 22–96 years (median, 68 years with APE were retrospectively enrolled in the study. Results: Prevalence of syncope was 13% (n=23 at the time of presentation. Compared to patients without syncope, those with syncope had a higher rate of central embolism (83% vs 43%, respectively, P=0.002, right ventricular dysfunction (91% vs 68%, P=0.021, and troponin positivity (80% vs 39%, P=0.001 but not 30-day mortality (13% vs 10%, P=0.716. Multivariate analysis showed that central localization (odds ratio: 9.08 and cardiac troponin positivity (odds ratio: 4.67 were the independent correlates of the presence of syncope in the patients with APE. Frequency of cardiopulmonary disease was lower, and duration from symptom onset to hospital admission was shorter in patients with syncope (P=0.138 and 0.118, respectively, although not significant. Conclusion: Syncope most likely represents an intermediate condition between massive APE and hypotension. In APE patients with syncope, the prognosis seems to depend on the underlying pathology, the patient’s age, comorbidities and duration from symptom onset to hospital admission, and the use of thrombolytic therapy. Keywords: syncope, prognosis, pulmonary embolism, mortality rate, compression sonography, right ventricular dysfunction

  12. Pulmonary Surfactants for Acute and Chronic Lung Diseases (Part II

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    O. A. Rozenberg

    2014-01-01

    Full Text Available Part 2 of the review considers the problem of surfactant therapy for acute respiratory distress syndrome (ARDS in adults and young and old children. It gives information on the results of surfactant therapy and prevention of ARDS in patients with severe concurrent trauma, inhalation injuries, complications due to complex expanded chest surgery, or severe pneumonias, including bilateral pneumonia in the presence of A/H1N1 influenza. There are data on the use of a surfactant in obstetric care and prevention of primary graft dysfunction during lung transplantation. The results of longterm use of surfactant therapy in Russia, suggesting that death rates from ARDS may be substantially reduced (to 20% are discussed. Examples of surfactant therapy for other noncritical lung diseases, such as permanent athelectasis, chronic obstructive pulmonary diseases, and asthma, as well tuberculosis, are also considered.

  13. Functional characterization of recombinant rat macrophage inflammatory protein-1 alpha and mRNA expression in pulmonary inflammation.

    Science.gov (United States)

    Shi, M M; Chong, I W; Long, N C; Love, J A; Godleski, J J; Paulauskis, J D

    1998-02-01

    macrophages and BAL cells in response to inflammatory stimuli suggests a fundamental role in acute pulmonary inflammation.

  14. Acute pulmonary emphysema cum pulmonary edema apparently associated with feeding of Brassica juncea in a dairy buffalo

    OpenAIRE

    Muhammad, Ghulam; Saqib, Muhammad; Naureen, Abeera

    2010-01-01

    This preliminary report describes the occurrence of acute pulmonary emphysema cum pulmonary edema ensuing in extensive subcutaneous emphysematous swellings in a dairy buffalo (Bubalus bubalis) apparently associated with a sudden shift from berseem (Trifolium alexendrinum) to Brassica juncea fodder. Tachypnea, expiratory dyspnea, open-mouth breathing, loud expiratory grunt with abdominal lift, and crackles in ventral aspects of the lungs with normal rectal temperature characterized the conditi...

  15. Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II.

    Science.gov (United States)

    Stein, Paul D; Beemath, Afzal; Matta, Fadi; Weg, John G; Yusen, Roger D; Hales, Charles A; Hull, Russell D; Leeper, Kenneth V; Sostman, H Dirk; Tapson, Victor F; Buckley, John D; Gottschalk, Alexander; Goodman, Lawrence R; Wakefied, Thomas W; Woodard, Pamela K

    2007-10-01

    Selection of patients for diagnostic tests for acute pulmonary embolism requires recognition of the possibility of pulmonary embolism on the basis of the clinical characteristics. Patients in the Prospective Investigation of Pulmonary Embolism Diagnosis II had a broad spectrum of severity, which permits an evaluation of the subtle characteristics of mild pulmonary embolism and the characteristics of severe pulmonary embolism. Data are from the national collaborative study, Prospective Investigation of Pulmonary Embolism Diagnosis II. There may be dyspnea only on exertion. The onset of dyspnea is usually, but not always, rapid. Orthopnea may occur. In patients with pulmonary embolism in the main or lobar pulmonary arteries, dyspnea or tachypnea occurred in 92%, but the largest pulmonary embolism was in the segmental pulmonary arteries in only 65%. In general, signs and symptoms were similar in elderly and younger patients, but dyspnea or tachypnea was less frequent in elderly patients with no previous cardiopulmonary disease. Dyspnea may be absent even in patients with circulatory collapse. Patients with a low-probability objective clinical assessment sometimes had pulmonary embolism, even in proximal vessels. Symptoms may be mild, and generally recognized symptoms may be absent, particularly in patients with pulmonary embolism only in the segmental pulmonary branches, but they may be absent even with severe pulmonary embolism. A high or intermediate-probability objective clinical assessment suggests the need for diagnostic studies, but a low-probability objective clinical assessment does not exclude the diagnosis. Maintenance of a high level of suspicion is critical.

  16. Dioscin relieves endotoxemia induced acute neuro-inflammation and protect neurogenesis via improving 5-HT metabolism

    Science.gov (United States)

    Yang, Rui; Chen, Wei; Lu, Ye; Li, Yingke; Du, Hongli; Gao, Songyan; Dong, Xin; Yuan, Hongbin

    2017-01-01

    Sepsis, in addition to causing fatality, is an independent risk factor for cognitive impairment among sepsis survivors. The pathologic mechanism of endotoxemia induced acute neuro-inflammation still has not been fully understood. For the first time, we found the disruption of neurotransmitters 5-HT, impaired neurogenesis and activation of astrocytes coupled with concomitant neuro-inflammation were the potential pathogenesis of endotoxemia induced acute neuro-inflammation in sepsis survivors. In addition, dioscin a natural steroidal saponin isolated from Chinese medicinal herbs, enhanced the serotonergic system and produced anti-depressant effect by enhancing 5-HT levels in hippocampus. What is more, this finding was verified by metabolic analyses of hippocampus, indicating 5-HT related metabolic pathway was involved in the pathogenesis of endotoxemia induced acute neuro-inflammation. Moreover, neuro-inflammation and neurogenesis within hippocampus were indexed using quantitative immunofluorescence analysis of GFAP DCX and Ki67, as well as real-time RT-PCR analysis of some gene expression levels in hippocampus. Our in vivo and in vitro studies show dioscin protects hippocampus from endotoxemia induced cascade neuro-inflammation through neurotransmitter 5-HT and HMGB-1/TLR4 signaling pathway, which accounts for the dioscin therapeutic effect in behavioral tests. Therefore, the current findings suggest that dioscin could be a potential approach for the therapy of endotoxemia induced acute neuro-inflammation. PMID:28059131

  17. Attenuation of acute nitrogen mustard-induced lung injury, inflammation and fibrogenesis by a nitric oxide synthase inhibitor

    Energy Technology Data Exchange (ETDEWEB)

    Malaviya, Rama; Venosa, Alessandro [Department of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ 08854 (United States); Hall, LeRoy [Drug Safety Sciences, Johnson and Johnson, Raritan, NJ 08869 (United States); Gow, Andrew J. [Department of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ 08854 (United States); Sinko, Patrick J. [Department of Pharmaceutics, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ 08854 (United States); Laskin, Jeffrey D. [Department of Environmental and Occupational Medicine, UMDNJ-Robert Wood Johnson Medical School, Piscataway, NJ 08854 (United States); Laskin, Debra L., E-mail: laskin@eohsi.rutgers.edu [Department of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ 08854 (United States)

    2012-12-15

    Nitrogen mustard (NM) is a toxic vesicant known to cause damage to the respiratory tract. Injury is associated with increased expression of inducible nitric oxide synthase (iNOS). In these studies we analyzed the effects of transient inhibition of iNOS using aminoguanidine (AG) on NM-induced pulmonary toxicity. Rats were treated intratracheally with 0.125 mg/kg NM or control. Bronchoalveolar lavage fluid (BAL) and lung tissue were collected 1 d–28 d later and lung injury, oxidative stress and fibrosis assessed. NM exposure resulted in progressive histopathological changes in the lung including multifocal lesions, perivascular and peribronchial edema, inflammatory cell accumulation, alveolar fibrin deposition, bronchiolization of alveolar septal walls, and fibrosis. This was correlated with trichrome staining and expression of proliferating cell nuclear antigen (PCNA). Expression of heme oxygenase (HO)-1 and manganese superoxide dismutase (Mn-SOD) was also increased in the lung following NM exposure, along with levels of protein and inflammatory cells in BAL, consistent with oxidative stress and alveolar-epithelial injury. Both classically activated proinflammatory (iNOS{sup +} and cyclooxygenase-2{sup +}) and alternatively activated profibrotic (YM-1{sup +} and galectin-3{sup +}) macrophages appeared in the lung following NM administration; this was evident within 1 d, and persisted for 28 d. AG administration (50 mg/kg, 2 ×/day, 1 d–3 d) abrogated NM-induced injury, oxidative stress and inflammation at 1 d and 3 d post exposure, with no effects at 7 d or 28 d. These findings indicate that nitric oxide generated via iNOS contributes to acute NM-induced lung toxicity, however, transient inhibition of iNOS is not sufficient to protect against pulmonary fibrosis. -- Highlights: ► Nitrogen mustard (NM) induces acute lung injury and fibrosis. ► Pulmonary toxicity is associated with increased expression of iNOS. ► Transient inhibition of iNOS attenuates acute

  18. Pathogenic aspects of pulmonary complications in acute pancreatitis patients

    Institute of Scientific and Technical Information of China (English)

    Serge Chooklin

    2009-01-01

    BACKGROUND: Experimental and clinical observations show that proinlfammatory cytokines and oxidative stress are involved in the development of local and particularly systemic complications in acute pancreatitis (AP) patients. There are often pulmonary complications in such patients. The mechanisms through which lung injury is induced in AP are not fully clear. METHODS: In order to assess the role of activated neutrophils, pro- and anti-inlfammatory cytokines and adhesion molecules at the onset and development of respiratory complications and respiratory failure, we measured the serum levels of pro-inlfammatory (IL-1β, IL-6, IL-8, IL-18, TNF-α) and anti-inlfammatory (IL-1ra, IL-10) cytokines in 51 AP patients who had been diagnosed with pancreatitis-associated lung injury with and without the development of organ dysfunction. RESULTS: When admitted to the hospital, severe AP patients had increased concentrations of IL-1β, IL-6, IL-8, IL-18, and TNF-α. The concentration of IL-18 alone was considerably increased in the patients who later developed respiratory failure. The onset of acute respiratory distress syndrome in the AP patients was accompanied by an increase in the level of anti-inlfammatory cytokines, especially IL-10. It was noted that in severe lung injury, myeloperoxidase activity in the blood increased signiifcantly, but still relfected the processes taking place in the lung parenchyma. Increase in the concentrations of adhesion molecules preceded the development of pulmonary inifltration with respiratory failure symptoms, which provoked endothelial dysfunction and determined the capillary surface permeability for neutrophils and monocytes.CONCLUSIONS: In the pathogenesis of respiratory complications in AP cytokines, chemokines and adhesion molecules, in particular IL-1β, IL-6, IL-8, IL-18, TNF-α, ICAM-1, and E-selectin play major roles. At IL-18 concentrations >650 pg/ml, AP patients are likely to develop pulmonary dysfunction (sensitivity

  19. Acute pulmonary embolism | EU Clinical Trials Register [EU Clinical Trials Register

    Lifescience Database Archive (English)

    Full Text Available the Trial E.1 Medical condition or disease under investigation E.1.1Medical condition(s) being investigated Acute... pulmonary embolism Embolismo pulmonar agudo E.1.1.1Medical condition in easily understood language Acute...rial contains a sub-study No E.3Principal inclusion criteria 1) Acute symptomatic PE confirmed by multidetec

  20. Comparison Between the Acute Pulmonary Vascular Effects of Oxygen with Nitric Oxide and Sildenafil

    Directory of Open Access Journals (Sweden)

    Ronald W. Day

    2015-03-01

    Full Text Available Objective. Right heart catheterization is performed in patients with pulmonary arterial hypertension to determine the severity of disease and their pulmonary vascular reactivity. The acute pulmonary vascular effect of inhaled nitric oxide is frequently used to identify patients who will respond favorably to vasodilator therapy. This study sought to determine whether the acute pulmonary vascular effects of oxygen with nitric oxide and intravenous sildenafil are similar. Methods. A retrospective, descriptive study of 13 individuals with pulmonary hypertension who underwent heart catheterization and acute vasodilator testing was performed. The hemodynamic measurements during five phases (21% to 53% oxygen, 100% oxygen, 100% oxygen with 20 ppm nitric oxide, 21% to 51% oxygen, and 21% to 51% oxygen with 0.05 mg/kg to 0.29 mg/kg intravenous sildenafil of the procedures were compared.Results. Mean pulmonary arterial pressure and pulmonary vascular resistance acutely decreased with 100% oxygen with nitric oxide, and 21% to 51% oxygen with sildenafil. Mean pulmonary arterial pressure (mm Hg, mean ± standard error of the mean was 38 ± 4 during 21% to 53% oxygen, 32 ± 3 during 100% oxygen, 29 ± 2 during 100% oxygen with nitric oxide, 37 ± 3 during 21% to 51% oxygen, and 32 ± 2 during 21% to 51% oxygen with sildenafil. There was not a significant correlation between the percent change in pulmonary vascular resistance from baseline with oxygen and nitric oxide, and from baseline with sildenafil (r2 = 0.011, p = 0.738. Conclusions. Oxygen with nitric oxide and sildenafil decreased pulmonary vascular resistance. However, the pulmonary vascular effects of oxygen and nitric oxide cannot be used to predict the acute response to sildenafil. Additional studies are needed to determine whether the acute response to sildenafil can be used to predict the long-term response to treatment with an oral phosphodiesterase V inhibitor.

  1. Effects of vagus nerve stimulation and vagotomy on systemic and pulmonary inflammation in a two-hit model in rats.

    Directory of Open Access Journals (Sweden)

    Matthijs Kox

    Full Text Available Pulmonary inflammation contributes to ventilator-induced lung injury. Sepsis-induced pulmonary inflammation (first hit may be potentiated by mechanical ventilation (MV, second hit. Electrical stimulation of the vagus nerve has been shown to attenuate inflammation in various animal models through the cholinergic anti-inflammatory pathway. We determined the effects of vagotomy (VGX and vagus nerve stimulation (VNS on systemic and pulmonary inflammation in a two-hit model. Male Sprague-Dawley rats were i.v. administered lipopolysaccharide (LPS and subsequently underwent VGX, VNS or a sham operation. 1 hour following LPS, MV with low (8 mL/kg or moderate (15 mL/kg tidal volumes was initiated, or animals were left breathing spontaneously (SP. After 4 hours of MV or SP, rats were sacrificed. Cytokine and blood gas analysis was performed. MV with 15, but not 8 mL/kg, potentiated the LPS-induced pulmonary pro-inflammatory cytokine response (TNF-α, IL-6, KC: p<0.05 compared to LPS-SP, but did not affect systemic inflammation or impair oxygenation. VGX enhanced the LPS-induced pulmonary, but not systemic pro-inflammatory cytokine response in spontaneously breathing, but not in MV animals (TNF-α, IL-6, KC: p<0.05 compared to SHAM, and resulted in decreased pO(2 (p<0.05 compared to sham-operated animals. VNS did not affect any of the studied parameters in both SP and MV animals. In conclusion, MV with moderate tidal volumes potentiates the pulmonary inflammatory response elicited by systemic LPS administration. No beneficial effects of vagus nerve stimulation performed following LPS administration were found. These results questions the clinical applicability of stimulation of the cholinergic anti-inflammatory pathway in systemically inflamed patients admitted to the ICU where MV is initiated.

  2. Resolution of Acute Inflammation and the Role of Resolvins in Immunity, Thrombosis, and Vascular Biology.

    Science.gov (United States)

    Sansbury, Brian E; Spite, Matthew

    2016-06-24

    Acute inflammation is a host-protective response that is mounted in response to tissue injury and infection. Initiated and perpetuated by exogenous and endogenous mediators, acute inflammation must be resolved for tissue repair to proceed and for homeostasis to be restored. Resolution of inflammation is an actively regulated process governed by an array of mediators as diverse as those that initiate inflammation. Among these, resolvins have emerged as a genus of evolutionarily conserved proresolving mediators that act on specific cellular receptors to regulate leukocyte trafficking and blunt production of inflammatory mediators, while also promoting clearance of dead cells and tissue repair. Given that chronic unresolved inflammation is emerging as a central causative factor in the development of cardiovascular diseases, an understanding of the endogenous processes that govern normal resolution of acute inflammation is critical for determining why sterile maladaptive cardiovascular inflammation perpetuates. Here, we provide an overview of the process of resolution with a focus on the enzymatic biosynthesis and receptor-dependent actions of resolvins and related proresolving mediators in immunity, thrombosis, and vascular biology. We discuss how nutritional and current therapeutic approaches modulate resolution and propose that harnessing resolution concepts could potentially lead to the development of new approaches for treating chronic cardiovascular inflammation in a manner that is not host disruptive.

  3. Clinical and morphologic features of acute, subacute and chronic cor pulmonale (pulmonary heart disease).

    Science.gov (United States)

    Roberts, William Clifford; Shafii, Alexis E; Grayburn, Paul A; Ko, Jong Mi; Weissenborn, Matthew R; Rosenblatt, Randall L; Guileyardo, Joseph M

    2015-03-01

    Described are certain clinical and morphologic features of one patient with acute, another with subacute, and one with chronic cor pulmonale. All 3 had evidence of severe pulmonary hypertension. The patient with acute cor pulmonale 4 days after coronary bypass for unstable angina pectoris suddenly developed severe breathlessness with cyanosis and had fatal cardiac arrest and necropsy disclosed massive pulmonary embolism. The patient with subacute cor pulmonale had severe right-sided heart failure for 5 weeks and necropsy disclosed microscopic-sized neoplastic pulmonary emboli from a gastric carcinoma without parenchymal pulmonary metastases. The patient with chronic cor pulmonale had evidence of right-sided heart failure for years, the result of primary or idiopathic pulmonary hypertension almost certainly present from birth because the pattern of elastic fibers in the pulmonary trunk was that seen in newborns where the pressure in the pulmonary trunk and ascending aorta are similar. The patient with chronic cor pulmonale had plexiform pulmonary lesions indicative of irreversible pulmonary hypertension. Neither the acute nor the subacute patient had chronic pulmonary vascular changes. All 3 patients had dilated right ventricular cavities and non-dilated left ventricular cavities and only the patient with chronic cor pulmonale had right ventricular hypertrophy.

  4. Lung inflammation and genotoxicity following pulmonary exposure to nanoparticles in ApoE-/- mice

    Directory of Open Access Journals (Sweden)

    Ladefoged Ole

    2009-01-01

    Full Text Available Abstract Background The toxic and inflammatory potential of 5 different types of nanoparticles were studied in a sensitive model for pulmonary effects in apolipoprotein E knockout mice (ApoE-/-. We studied the effects instillation or inhalation Printex 90 of carbon black (CB and compared CB instillation in ApoE-/- and C57 mice. Three and 24 h after pulmonary exposure, inflammation was assessed by mRNA levels of cytokines in lung tissue, cell composition, genotoxicity, protein and lactate dehydrogenase activity in broncho-alveolar lavage (BAL fluid. Results Firstly, we found that intratracheal instillation of CB caused far more pulmonary toxicity in ApoE-/- mice than in C57 mice. Secondly, we showed that instillation of CB was more toxic than inhalation of a presumed similar dose with respect to inflammation in the lungs of ApoE-/- mice. Thirdly, we compared effects of instillation in ApoE-/- mice of three carbonaceous particles; CB, fullerenes C60 (C60 and single walled carbon nanotubes (SWCNT as well as gold particles and quantum dots (QDs. Characterization of the instillation media revealed that all particles were delivered as agglomerates and aggregates. Significant increases in Il-6, Mip-2 and Mcp-1 mRNA were detected in lung tissue, 3 h and 24 h following instillation of SWCNT, CB and QDs. DNA damage in BAL cells, the fraction of neutrophils in BAL cells and protein in BAL fluid increased statistically significantly. Gold and C60 particles caused much weaker inflammatory responses. Conclusion Our data suggest that ApoE-/- model is sensitive for evaluating particle induced inflammation. Overall QDs had greatest effects followed by CB and SWCNT with C60 and gold being least inflammatory and DNA-damaging. However the gold was used at a much lower mass dose than the other particles. The strong effects of QDs were likely due to Cd release. The surface area of the instilled dose correlated well the inflammatory response for low toxicity particles.

  5. Invariant Natural Killer T (iNKT Cells Prevent Autoimmunity, but Induce Pulmonary Inflammation in Cystic Fibrosis

    Directory of Open Access Journals (Sweden)

    Nanna Siegmann

    2014-06-01

    Full Text Available Background/Aims: Inflammation is a major and critical component of the lung pathology in the hereditary disease cystic fibrosis. The molecular mechanisms of chronic inflammation in cystic fibrosis require definition. Methods: We used several genetic mouse models to test a role of iNKT cells and ceramide in pulmonary inflammation of cystic fibrosis mice. Inflammation was determined by the pulmonary cytokine profil and the abundance of inflammatory cells in the lung. Results: Here we provide a new concept how inflammation in the lung of individuals with cystic fibrosis is initiated. We show that in cystic fibrosis mice the mutation in the Cftr gene provokes a significant up-regulation of iNKT cells in the lung. Accumulation of iNKT cells serves to control autoimmune disease, which is triggered by a ceramide-mediated induction of cell death in CF organs. Autoimmunity becomes in particular overt in cystic fibrosis mice lacking iNKT cells and although suppression of the autoimmune response by iNKT cells is beneficial, IL-17+ iNKT cells attract macrophages and neutrophils to CF lungs resulting in chronic inflammation. Genetic deletion of iNKT cells in cystic fibrosis mice prevents inflammation in CF lungs. Conclusion: Our data demonstrate an important function of iNKT cells in the chronic inflammation affecting cystic fibrosis lungs. iNKT cells suppress the auto-immune response induced by ceramide-mediated death of epithelial cells in CF lungs, but also induce a chronic pulmonary inflammation.

  6. Whole blood viscosity assessment issues IV: Prevalence in acute phase inflammation

    Directory of Open Access Journals (Sweden)

    Ezekiel Uba Nwose

    2010-08-01

    Full Text Available Background: Hyperviscosity syndrome has been suggested as not simply an acute reaction. Yet, erythrocyte sedimentation rate is associated with whole blood viscosity and it is an indirect acute phase inflammation marker. Aims: This work investigates the prevalence of hyperviscosity in acute phase inflammation. Materials and Methods: Archived clinical pathology data for the period of 1999 to 2008 were utilized. 40,632-cases tested for C-reactive protein and/or erythrocyte sedimentation rate from five alternate years, which were concomitantly tested for haematocrit and total proteins, were extracted. The prevalence of abnormal viscosity associated with positive results of C-reactive protein and erythrocyte sedimentation rate were evaluated. Results: Hyperviscosity is infrequently associated with positive C-reactive protein (2.9% and erythrocyte sedimentation rate (2.7% sub-populations, and are not statistically different from their respective negative sub-populations. Normoviscosity is significantly more prevalent in the positive sub-populations (p < 0.01. Further analyses indicate that prevalence of acute phase inflammation is statistically significantly less in hyperviscosity compared to normoviscosity sub-population (p < 0.00001. Actual blood viscosity level increases with level of inflammation though. Conclusion: The study demonstrates that although blood viscosity level may increase with inflammation, hyperviscosity is not frequent in, or sensitive to acute phase inflammation. It portends that whole blood viscosity is not unspecific as acute phase inflammation markers. It calls for clinicians to consider utilizing whole blood viscosity in disease conditions where stasis is implicated, in which it is specific and valuable. It would also benefit to establish whether hyperviscosity is a chronic phase inflammation marker.

  7. Advances in the diagnosis and management of acute pulmonary embolism.

    Science.gov (United States)

    den Exter, Paul L; van der Hulle, Tom; Klok, Frederikus A; Huisman, Menno V

    2014-05-01

    The diagnostic management of acute pulmonary embolism (PE) is complicated by its heterogeneous clinical presentation. Current diagnostic algorithms, combining clinical probability estimation with D-dimer testing and imaging tests, are very safe to exclude PE, although at costs of high numbers of CT-examinations. In view of cost- and time-saving as well as safety issues, several attempts have recently been undertaken to reduce the number of required imaging tests. Especially the age-adjusted D-dimer threshold has greatly improved the potential for non-invasive exclusion of PE. Once the diagnosis of PE is established, immediate initiation of anticoagulant therapy is of vital importance. A new generation of direct oral anticoagulants, which overcomes the main disadvantages of conventional vitamin-K antagonists, has recently emerged. Risk stratification of hemodynamically stable PE patients with use of clinical decision rules, cardiac biomarkers or imaging tests, aids physicians in determining the most appropriate treatment approach for the individual patient. This is essential to differentiate patients at low risk of adverse outcome, who may be safely treated at home, from intermediate-risk patients, who require closer monitoring and for whom recent studies have evaluated the efficacy and safety of systemic thrombolytic therapy. This article reviews recent advances and challenges that remain in the diagnostic work-up and initial management of acute, clinically stable PE. Copyright © 2014 Elsevier Ltd. All rights reserved.

  8. Pharmacological inhibition of GSK-3 in a guinea pig model of LPS-induced pulmonary inflammation : II. Effects on skeletal muscle atrophy

    NARCIS (Netherlands)

    Verhees, Koen J. P.; Pansters, Nicholas A. M.; Baarsma, Hoeke A.; Remels, Alexander H. V.; Haegens, Astrid; de Theije, Chiel C.; Schols, Annemie M. W. J.; Gosens, Reinoud; Langen, Ramon C. J.

    2013-01-01

    Background: Chronic obstructive pulmonary disease (COPD) is accompanied by pulmonary inflammation and associated with extra-pulmonary manifestations, including skeletal muscle atrophy. Glycogen synthase kinase-3 (GSK-3) has been implicated in the regulation of muscle protein-and myonuclear turnover;

  9. Pharmacological inhibition of GSK-3 in a guinea pig model of LPS-induced pulmonary inflammation : II. Effects on skeletal muscle atrophy

    NARCIS (Netherlands)

    Verhees, Koen J. P.; Pansters, Nicholas A. M.; Baarsma, Hoeke A.; Remels, Alexander H. V.; Haegens, Astrid; de Theije, Chiel C.; Schols, Annemie M. W. J.; Gosens, Reinoud; Langen, Ramon C. J.

    2013-01-01

    Background: Chronic obstructive pulmonary disease (COPD) is accompanied by pulmonary inflammation and associated with extra-pulmonary manifestations, including skeletal muscle atrophy. Glycogen synthase kinase-3 (GSK-3) has been implicated in the regulation of muscle protein-and myonuclear turnover;

  10. Inflammation of vertebral bone associated with acute calcific tendinitis of the longus colli muscle

    Energy Technology Data Exchange (ETDEWEB)

    Mihmanli, I.; Kanberoglu, K. [Dept. of Radiology, Istanbul Univ. (Turkey); Karaarslan, E. [Intermed Medical Center, Nisantasi, Istanbul (Turkey)

    2001-12-01

    We present a case of acute retropharyngeal calcific tendinitis with characteristic findings on radiographic, computed tomography, and magnetic resonance imaging (MRI). To our knowledge, this is the first acute retropharyngeal calcific tendinitis report having inflammation of both the vertebra itself and the longus colli muscle diagnosed on MRI. In patients with neck pain, acute retropharyngeal calcific tendinitis should be kept in mind in the differential diagnosis, even if these patients had vertebral pathological signals on MRI. (orig.)

  11. Acute inflammation in horizontal incompletely impacted third molar with radiolucency in the elderly

    Directory of Open Access Journals (Sweden)

    Minoru Yamaoka

    2009-07-01

    Full Text Available Minoru Yamaoka, Yusuke Ono, Masahiro Takahashi, Masahide Ishizuka, Takayuki Uchihashi, Kouichi Yasuda, Takashi Uematsu, Kiyofumi FurusawaMatsumoto Dental University, Oral and Maxillofacial Surgery, Shiojiri, Nagano, JapanAbstract: Although radiolucency has been shown as a risk of infection, the poorly understood effects of aging on radiolucency correlate with acute pericoronitis, which has a high risk of infection extending any complications. We reviewed the records of 346 consecutive patients aged more than 41 years to evaluate whether pericoronal radiolucency below the crown in mandibular horizontal incompletely impacted third molars is related to acute inflammation. The frequency of acute inflammation in teeth with pericoronal radiolucency below the crown was similar to that in teeth without; however, the odds ratio of acute inflammation exhibited in women aged more than 61 years compared to women aged 41–50 years was 9.77 (95% confidence interval [CI]: 1.67–57.29; P <<0.05, and in women aged more than 61 years compared to women aged 51–60 years was 26.25 (95% CI: 2.94–234.38; P < 0.01. The odds ratio of severe acute inflammation exhibited in men aged more than 61 years compared to men aged 41–50 years was 16.67 (95% CI: 1.76–158.27; P < 0.01. These odds ratios indicate an association of acute pericoronitis, including the severe forms of acute inflammation that result from pericoronitis, with pericoronal radiolucency below the crown in the elderly.Keywords: radiolucency, mandible, third molar, acute inflammation, aging

  12. Time course of pulmonary vascular response to an acutely repetitive pulmonary microembolism in dogs--an analysis using pulmonary vascular impedance.

    Science.gov (United States)

    Tobise, K; Tosaka, S; Onodera, S

    1992-05-01

    To understand the mechanism leading to progressive pulmonary hypertension, we investigated the time course of vascular response to an acutely repetitive pulmonary microembolism in dogs by using pulmonary vascular impedance. In a normal state, the mean pulmonary arterial pressure (mPAP) was transiently increased by emboli, and the impedance moduli of 0 Hz (= Rin), 1.5 Hz and 3 Hz were slightly increased. A four-element electrical vascular model showed the transient increase in peripheral pulmonary vascular resistance (R2) and inertia, and reduction in compliance (C). In contrast, in a state of a slight pulmonary hypertension, mPAP was continuously increased by the same amount of emboli, and the impedance moduli of both 0 Hz and 3 Hz were significantly increased. By a four-element model, a severe increase in R2 and reduction in C were observed, and these changes continued. Therefore, although the vascular response to pulmonary microembolism basically depends on the degree of mechanical obstruction, this response is thought to be modulated by the responsiveness of pulmonary vessels at that time, which is involved in the alteration in the local characteristics of pulmonary vessels, and/or the recruitment of a new blood flow.

  13. Cerium Oxide Nanoparticles in Lung Acutely Induce Oxidative Stress, Inflammation, and DNA Damage in Various Organs of Mice

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    Abderrahim Nemmar

    2017-01-01

    Full Text Available CeO2 nanoparticles (CeO2 NPs which are used as a diesel fuel additive are emitted in the particulate phase in the exhaust, posing a health concern. However, limited information exists regarding the in vivo acute toxicity of CeO2 NPs on multiple organs. Presently, we investigated the acute (24 h effects of intratracheally instilled CeO2 NPs in mice (0.5 mg/kg on oxidative stress, inflammation, and DNA damage in major organs including lung, heart, liver, kidneys, spleen, and brain. Lipid peroxidation measured by malondialdehyde production was increased in the lungs only, and reactive oxygen species were increased in the lung, heart, kidney, and brain. Superoxide dismutase activity was decreased in the lung, liver, and kidney, whereas glutathione increased in lung but it decreased in the kidney. Total nitric oxide was increased in the lung and spleen but it decreased in the heart. Tumour necrosis factor-α increased in all organs studied. Interleukin- (IL- 6 increased in the lung, heart, liver, kidney, and spleen. IL-1β augmented in the lung, heart, kidney, and spleen. Moreover, CeO2 NPs induced DNA damage, assessed by COMET assay, in all organs studied. Collectively, these findings indicate that pulmonary exposure to CeO2 NPs causes oxidative stress, inflammation, and DNA damage in multiple organs.

  14. Acute hemodynamic effect of inhaled iloprost in pulmonary artery hypertension evaluated with echocardiography

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    Miranda Rita

    2007-11-01

    Full Text Available Abstract Doppler echocardiography is useful in the initial evaluation and long-term follow-up of patients with pulmonary artery hypertension. Aerosolised iloprost has been shown to reduce pulmonary pressure immediately after inhalation. We report the echocardiographic findings in a patient with severe pulmonary hypertension, before and after the inhalation of aerosolized iloprost. These findings illustrate the acute influence of iloprost in right and left ventricular hemodynamics and morphology. These findings were reproduced in subsequent echocardiographic evaluations.

  15. Referral Patterns and Diagnostic Yield of Lung Scintigraphy in the Diagnosis of Acute Pulmonary Embolism

    National Research Council Canada - National Science Library

    Matthieu Pelletier-Galarneau; Erik Zannier; Lionel S. Zuckier; Gregoire Le Gal

    2017-01-01

    ...) scintigraphy in patients referred for acute pulmonary embolism (PE). Methods. We retrospectively reviewed the charts of all patients who underwent V/Q studies between April 1, 2008, and March 31, 2010...

  16. Cigarette smoke-induced disruption of pulmonary barrier and bacterial translocation drive tumor-associated inflammation and growth.

    Science.gov (United States)

    Jungnickel, C; Wonnenberg, B; Karabiber, O; Wolf, A; Voss, M; Wolf, L; Honecker, A; Kamyschnikow, A; Herr, C; Bals, R; Beisswenger, C

    2015-09-15

    Microorganisms have an important role in tumorgenesis by the induction of inflammation and by a direct impact on tumor cells. Chronic obstructive pulmonary disease (COPD) is associated with an increased risk for lung cancer and microbial colonization. We asked whether bacterial pathogens act as tumor promoters during CS-induced pulmonary inflammation. In a metastatic lung cancer (LC) model, Lewis lung carcinoma (LLC) cells were injected in mice to initiate the growth of tumors in the lung. Exposure to the combination of cigarette smoke (CS) and nontypeable Haemophilus influenzae (NTHi) synergistically increased metastatic growth. Lung levels of albumin and LDH, translocation of bacterial factors into tumor tissue, tumor inflammation, and tumor proliferation were significantly increased in mice exposed to CS in combination with NTHi. Bacterial pathogens increased the proliferation of cultured LLC cells and human cancer cell lines. Metastatic growth induced by the exposure to CS in combination with NTHi was reduced in mice deficient for IL-17. Our data provide evidence that CS-induced loss of pulmonary barrier integrity allows bacterial factors to translocate into tumor tissue and to regulate tumor-associated inflammation and tumor proliferation. Translocation of bacterial factors in tumor tissue links CS-induced inflammation with tumor proliferation.

  17. Systemic Inflammation in Chronic Obstructive Pulmonary Disease: May Adipose Tissue Play a Role? Review of the Literature and Future Perspectives

    Directory of Open Access Journals (Sweden)

    Ruzena Tkacova

    2010-01-01

    Full Text Available Chronic obstructive pulmonary disease (COPD is a major cause of morbidity and mortality worldwide. Low-grade systemic inflammation is considered a hallmark of COPD that potentially links COPD to increased rate of systemic manifestations of the disease. Obesity with/without the metabolic syndrome and cachexia represent two poles of metabolic abnormalities that may relate to systemic inflammation. On one hand systemic inflammatory syndrome likely reflects inflammation in the lungs, i.e. results from lung-to plasma spillover of inflammatory mediators. On the other hand, obesity-related hypoxia results in local inflammatory response within adipose tissue per se, and may contribute to elevations in circulatory mediators by spillover from the adipose tissue to the systemic compartment. The extent to which systemic hypoxia contributes to the adipose tissue inflammation remains unknown. We assume that in patients with COPD and concurrent obesity at least three factors play a role in the systemic inflammatory syndrome: the severity of pulmonary impairment, the degree of obesity-related adipose tissue hypoxia, and the severity of systemic hypoxia due to reduced pulmonary functions. The present review summarizes the epidemiological and clinical evidence linking COPD to obesity, the role of adipose tissue as an endocrine organ, and the role of hypoxia in adipose tissue inflammation.

  18. A Rare Case of Diffuse Alveolar Hemorrhage Secondary to Acute Pulmonary Histoplasmosis

    Directory of Open Access Journals (Sweden)

    Kunal Grover

    2015-01-01

    Full Text Available Diffuse alveolar hemorrhage (DAH is a rare presentation of acute pulmonary histoplasmosis. While histoplasmosis has been reported to cause hemoptysis and alveolar hemorrhage in children, the English language literature lacks any adult case reports documenting this association. We report a case of pulmonary histoplasmosis where the initial presentation was pneumonia with a subsequent diagnosis of DAH.

  19. The Prevalence of Oral Inflammation Among Denture Wearing Patients with Chronic Obstructive Pulmonary Disease.

    Science.gov (United States)

    Przybyłowska, D; Rubinsztajn, R; Chazan, R; Swoboda-Kopeć, E; Kostrzewa-Janicka, J; Mierzwińska-Nastalska, E

    2015-01-01

    Oral inflammation is an important contributor to the etiology of chronic obstructive pulmonary disease, which can impact patient's health status. Previous studies indicate that people with poor oral health are at higher risk for nosocomial pneumonia. Denture wearing is one promoting factor in the development of mucosal infections. Colonization of the denture plaque by Gram-negative bacteria, Candida spp., or other respiratory pathogens, occurring locally, may be aspirated to the lungs. The studies showed that chronic obstructive pulmonary disease (COPD) patients treated with combinations of medicines with corticosteroids more frequently suffer from Candida-associated denture stomatitis. Treatment of oral candidiasis in patients with COPD constitutes a therapeutic problem. Therefore, it is essential to pay attention to the condition of oral mucosal membrane and denture hygiene habits. The guidelines for care and maintenance of dentures for COPD patients are presented in this paper. The majority of patients required improvement of their prosthetic and oral hygiene. Standard oral hygiene procedures in relation to dentures, conducted for prophylaxis of stomatitis complicated by mucosal infection among immunocompromised patients, are essential to maintain healthy oral tissues. The elimination of traumatic denture action in dental office, compliance with oral and denture hygiene, proper use and storage of prosthetic appliances in a dry environment outside the oral cavity can reduce susceptibility to infection. Proper attention to hygiene, including brushing and rinsing the mouth, may also help prevent denture stomatitis in these patients.

  20. Pulmonary inflammation and crystalline silica in respirable coal mine dust: dose-response

    Indian Academy of Sciences (India)

    E D Kuempel; M D Attfield; V Vallyathan; N L Lapp; J M Hale; R J Smith; V Castranova

    2003-02-01

    This study describes the quantitative relationships between early pulmonary responses and the estimated lungburden or cumulative exposure of respirable-quartz or coal mine dust. Data from a previous bronchoalveolar lavage (BAL) study in coal miners ( = 20) and nonminers ( = 16) were used including cell counts of alveolar macrophages (AMs) and polymorphonuclear leukocytes (PMNs), and the antioxidant superoxide dismutase (SOD) levels. Miners’ individual working lifetime particulate exposures were estimated from work histories and mine air sampling data, and quartz lung-burdens were estimated using a lung dosimetry model. Results show that quartz, as either cumulative exposure or estimated lung-burden, was a highly statistically significant predictor of PMN response ( < 0.0001); however cumulative coal dust exposure did not significantly add to the prediction of PMNs ( = 0.2) above that predicted by cumulative quartz exposure ( < 0.0001). Despite the small study size, radiographic category was also significantly related to increasing levels of both PMNs and quartz lung burden (-values < 0.04). SOD in BAL fluid rose linearly with quartz lung burden ( < 0.01), but AM count in BAL fluid did not ( > 0.4). This study demonstrates dose-response relationships between respirable crystalline silica in coal mine dust and pulmonary inflammation, antioxidant production, and radiographic small opacities.

  1. Feasibility of (68)Ga-labeled Siglec-9 peptide for the imaging of acute lung inflammation: a pilot study in a porcine model of acute respiratory distress syndrome.

    Science.gov (United States)

    Retamal, Jaime; Sörensen, Jens; Lubberink, Mark; Suarez-Sipmann, Fernando; Borges, João Batista; Feinstein, Ricardo; Jalkanen, Sirpa; Antoni, Gunnar; Hedenstierna, Göran; Roivainen, Anne; Larsson, Anders; Velikyan, Irina

    2016-01-01

    There is an unmet need for noninvasive, specific and quantitative imaging of inherent inflammatory activity. Vascular adhesion protein-1 (VAP-1) translocates to the luminal surface of endothelial cells upon inflammatory challenge. We hypothesized that in a porcine model of acute respiratory distress syndrome (ARDS), positron emission tomography (PET) with sialic acid-binding immunoglobulin-like lectin 9 (Siglec-9) based imaging agent targeting VAP-1 would allow quantification of regional pulmonary inflammation. ARDS was induced by lung lavages and injurious mechanical ventilation. Hemodynamics, respiratory system compliance (Crs) and blood gases were monitored. Dynamic examination using [(15)O]water PET-CT (10 min) was followed by dynamic (90 min) and whole-body examination using VAP-1 targeting (68)Ga-labeled 1,4,7,10-tetraaza cyclododecane-1,4,7-tris-acetic acid-10-ethylene glycol-conjugated Siglec-9 motif peptide ([(68)Ga]Ga-DOTA-Siglec-9). The animals received an anti-VAP-1 antibody for post-mortem immunohistochemistry assay of VAP-1 receptors. Tissue samples were collected post-mortem for the radioactivity uptake, histology and immunohistochemistry assessment. Marked reduction of oxygenation and Crs, and higher degree of inflammation were observed in ARDS animals. [(68)Ga]Ga-DOTA-Siglec-9 PET showed significant uptake in lungs, kidneys and urinary bladder. Normalization of the net uptake rate (Ki) for the tissue perfusion resulted in 4-fold higher uptake rate of [(68)Ga]Ga-DOTA-Siglec-9 in the ARDS lungs. Immunohistochemistry showed positive VAP-1 signal in the injured lungs. Detection of pulmonary inflammation associated with a porcine model of ARDS was possible with [(68)Ga]Ga-DOTA-Siglec-9 PET when using kinetic modeling and normalization for tissue perfusion.

  2. Modulation of arachidonic and linoleic acid metabolites in myeloperoxidase deficient mice during acute inflammation

    Science.gov (United States)

    Kubala, Lukas; Schmelzer, Kara R.; Klinke, Anna; Kolarova, Hana; Baldus, Stephan; Hammock, Bruce D.; Eiserich, Jason P.

    2010-01-01

    Acute inflammation is a common feature of many life-threatening pathologies, including septic shock. One hallmark of acute inflammation is the peroxidation of polyunsaturated fatty acids forming bioactive products, which regulate inflammation. Myeloperoxidase (MPO) is an abundant phagocyte-derived hemoprotein released during phagocyte activation. Here, we investigated the role of MPO in modulating biologically active arachidonic acid (AA) and linoleic acid (LA) metabolites during acute inflammation. Wild-type and MPO-knockout (KO) mice were exposed to intraperitoneally injected endotoxin for 24 h, and plasma LA and AA oxidation products were comprehensively analyzed using a liquid chromatography-mass spectrometry method. Compared to wild-type mice, MPO-KO mice had significantly lower plasma levels of LA epoxides and corresponding LA- and AA-derived fatty acid diols. AA and LA hydroxy intermediates (hydroxyeicosatetraenoic and hydroxyoctadecadienoic acids) were also significantly lower in MPO-KO mice. Conversely, MPO-deficient mice had significantly higher plasma levels of cysteinyl-leukotrienes with well-known pro-inflammatory properties. In vitro experiments revealed significantly lower amounts of AA and LA epoxides, LA- and AA-derived fatty acid diols, and AA and LA hydroxy intermediates in stimulated polymorphonuclear neutrophils isolated from MPO-KO mice. Our results demonstrate that MPO modulates the balance of pro- and anti-inflammatory lipid mediators during acute inflammation. In this way, may control acute inflammatory diseases. PMID:20156554

  3. Pulmonary vascular responses during acute and sustained respiratory alkalosis or acidosis in intact newborn piglets.

    Science.gov (United States)

    Gordon, J B; Rehorst-Paea, L A; Hoffman, G M; Nelin, L D

    1999-12-01

    Acute alkalosis-induced pulmonary vasodilation and acidosis-induced pulmonary vasoconstriction have been well described, but responses were generally measured within 5-30 min of changing pH. In contrast, several in vitro studies have found that relatively brief periods of sustained alkalosis can enhance, and sustained acidosis can decrease, vascular reactivity. In this study of intact newborn piglets, effects of acute (20 min) and sustained (60-80 min) alkalosis or acidosis on baseline (35% O2) and hypoxic (12% O2) pulmonary vascular resistance (PVR) were compared with control piglets exposed only to eucapnia. Acute alkalosis decreased hypoxic PVR, but sustained alkalosis failed to attenuate either baseline PVR or the subsequent hypoxic response. Acute acidosis did not significantly increase hypoxic PVR, but sustained acidosis markedly increased both baseline PVR and the subsequent hypoxic response. Baseline PVR was similar in all piglets after resumption of eucapnic ventilation, but the final hypoxic response was greater in piglets previously exposed to alkalosis than in controls. Thus, hypoxic pulmonary vasoconstriction was not attenuated during sustained alkalosis, but was accentuated during sustained acidosis and after the resumption of eucapnia in alkalosis-treated piglets. Although extrapolation of data from normal piglets to infants and children with pulmonary hypertension must be done with caution, this study suggests that sustained alkalosis may be of limited efficacy in treating acute hypoxia-induced pulmonary hypertension and the risks of pulmonary hypertension must be considered when using ventilator strategies resulting in permissive hypercapnic acidosis.

  4. Role of acid-sensing ion channel 3 in sub-acute-phase inflammation

    Directory of Open Access Journals (Sweden)

    Chen Chien-Ju

    2009-01-01

    Full Text Available Abstract Background Inflammation-mediated hyperalgesia involves tissue acidosis and sensitization of nociceptors. Many studies have reported increased expression of acid-sensing ion channel 3 (ASIC3 in inflammation and enhanced ASIC3 channel activity with pro-inflammatory mediators. However, the role of ASIC3 in inflammation remains inconclusive because of conflicting results generated from studies of ASIC3 knockout (ASIC3-/- or dominant-negative mutant mice, which have shown normal, decreased or increased hyperalgesia during inflammation. Results Here, we tested whether ASIC3 plays an important role in inflammation of subcutaneous tissue of paw and muscle in ASIC3-/- mice induced by complete Freund's adjuvant (CFA or carrageenan by investigating behavioral and pathological responses, as well as the expression profile of ion channels. Compared with the ASIC3+/+ controls, ASIC3-/- mice showed normal thermal and mechanical hyperalgesia with acute (4-h intraplantar CFA- or carrageenan-induced inflammation, but the hyperalgesic effects in the sub-acute phase (1–2 days were milder in all paradigms except for thermal hyperalgesia with CFA-induced inflammation. Interestingly, carrageenan-induced primary hyperalgesia was accompanied by an ASIC3-dependent Nav1.9 up-regulation and increase of tetrodotoxin (TTX-resistant sodium currents. CFA-inflamed muscle did not evoke hyperalgesia in ASIC3-/- or ASIC3+/+ mice, whereas carrageenan-induced inflammation in muscle abolished mechanical hyperalgesia in ASIC3-/- mice, as previously described. However, ASIC3-/- mice showed attenuated pathological features such as less CFA-induced granulomas and milder carrageenan-evoked vasculitis as compared with ASIC3+/+ mice. Conclusion We provide a novel finding that ASIC3 participates in the maintenance of sub-acute-phase primary hyperalgesia in subcutaneous inflammation and mediates the process of granuloma formation and vasculitis in intramuscular inflammation.

  5. Is airway inflammation in chronic obstructive pulmonary disease (COPD) a risk factor for cardiovascular events?

    Science.gov (United States)

    Calverley, Peter M A; Scott, Stephen

    2006-12-01

    Cardiovascular disease (CVD) is a very common cause of death in patients with chronic obstructive pulmonary disease (COPD). Smoking is a well-described risk factor for both COPD and CVD, but CVD in patients with COPD is likely to be due to other factors in addition to smoking. Inflammation may be an important common etiological link between COPD and CVD, being well described in both diseases. It is hypothesized that in COPD a "spill-over" of local airway inflammation into the systemic circulation could contribute to increased CVD in these patients. Inhaled corticosteroids (ICS) have well-documented anti-inflammatory effects and are commonly used for the treatment of COPD, but their effects on cardiovascular endpoints and all-cause mortality have only just started to be examined. A recent meta-analysis has suggested that ICS may reduce all-cause mortality in COPD by around 25%. A case-controlled study specifically examined the effects of ICS on myocardial infarction and suggested that ICS may decrease the incidence of MI by as much as 32%. A large multicenter prospective randomized trial (Towards a Revolution in COPD Health [TORCH]) is now ongoing and will examine the effect of fluticasone propionate in combination with salmeterol on all-cause mortality.

  6. Mechanisms of particle-induced pulmonary inflammation in a mouse model: exposure to wood dust.

    Science.gov (United States)

    Määttä, Juha; Lehto, Maili; Leino, Marina; Tillander, Sari; Haapakoski, Rita; Majuri, Marja-Leena; Wolff, Henrik; Rautio, Sari; Welling, Irma; Husgafvel-Pursiainen, Kirsti; Savolainen, Kai; Alenius, Harri

    2006-09-01

    Repeated airway exposure to wood dust has long been known to cause adverse respiratory effects such as asthma and chronic bronchitis and impairment of lung function. However, the mechanisms underlying the inflammatory responses of the airways after wood dust exposure are poorly known. We used a mouse model to elucidate the mechanisms of particle-induced inflammatory responses to fine wood dust particles. BALB/c mice were exposed to intranasally administered fine (more than 99% of the particles had a particle size of dusts twice a week for 3 weeks. PBS, LPS, and titanium dioxide were used as controls. Intranasal instillation of birch or oak dusts elicited influx of inflammatory cells to the lungs in mice. Enhancement of lymphocytes and neutrophils was seen after oak dust exposure, whereas eosinophil infiltration was higher after birch dust exposure. Infiltration of inflammatory cells was associated with an increase in the mRNA levels of several cytokines, chemokines, and chemokine receptors in lung tissue. Oak dust appeared to be a more potent inducer of these inflammatory mediators than birch dust. The results from our in vivo mouse model show that repeated airway exposure to wood dust can elicit lung inflammation, which is accompanied by induction of several proinflammatory cytokines and chemokines. Oak and birch dusts exhibited quantitative and qualitative differences in the elicitation of pulmonary inflammation, suggesting that the inflammatory responses induced by the wood species may rise via different cellular mechanisms.

  7. Assessment of heat shock proteins and endothelial dysfunction in acute pulmonary embolism.

    Science.gov (United States)

    İn, Erdal; Deveci, Figen; Kaman, Dilara

    2016-06-01

    We determined the levels of some heat shock proteins (HSP27, HSP70, and HSP90), L-arginine, asymmetric dimethylarginine (ADMA), and symmetric dimethylarginine (SDMA) levels in patients with acute pulmonary embolism. The present case-control study comprised a healthy control group (n = 57) and patients with acute pulmonary embolism (n = 84). HSPs, L-arginine, ADMA, and SDMA levels were measured in all of the cases. The mean age of the control group was 56.72 ± 8.44 years, and the mean age of the patients with acute pulmonary embolism was 60.20 ± 16.56 years (P = 0.104). Compared with controls, patients with acute pulmonary embolism had significantly higher mean serum HSP27, HSP90, and ADMA levels, whereas the mean serum L-arginine and SDMA levels were lower (P In patients with acute pulmonary embolism serum HSP27, HSP70, and ADMA levels were negatively correlated with partial pressures of arterial oxygen levels (r = -0.281, P = 0.01; r = -0.263, P = 0.016; and r = -0.275, P = 0.011, respectively) and arterial oxygen saturation (r = -0.225, P = 0.039; r = -0.400, P in acute pulmonary embolism.

  8. Pharmacologic modulation of acute ocular inflammation with quercetin.

    Science.gov (United States)

    Romero, J; Marak, G E; Rao, N A

    1989-01-01

    Anti-inflammatory potentials of a safe, common dietary component, quercetin, were investigated in suppression of intraocular inflammation induced by retinal S antigen. Lewis rats sensitized to S antigen were treated daily with intraperitoneal injections of quercetin. Control rats with S-antigen-induced uveitis were similarly treated with diluent. When compared with controls the treated group showed marked reduction in uveal and retinal inflammation and in vasculitis and perivasculitis. Morphometric analysis revealed a significant reduction (p less than 0.005) in choroidal thickness when compared with that of control animals. These results clearly show the antiphlogistic effects of quercetin in experimental uveitis.

  9. Macrophage activation in acute exacerbation of idiopathic pulmonary fibrosis.

    Directory of Open Access Journals (Sweden)

    Jonas Christian Schupp

    Full Text Available Acute exacerbation (AE of idiopathic pulmonary fibrosis (IPF is a common cause of disease acceleration in IPF and has a major impact on mortality. The role of macrophage activation in AE of IPF has never been addressed before.We evaluated BAL cell cytokine profiles and BAL differential cell counts in 71 IPF patients w/wo AE and in 20 healthy volunteers. Twelve patients suffered from AE at initial diagnosis while sixteen patients developed AE in the 24 months of follow-up. The levels of IL-1ra, CCL2, CCL17, CCL18, CCL22, TNF-α, IL-1β, CXCL1 and IL-8 spontaneously produced by BAL-cells were analysed by ELISA.In patients with AE, the percentage of BAL neutrophils was significantly increased compared to stable patients. We found an increase in the production rate of the pro-inflammatory cytokines CXCL1 and IL-8 combined with an increase in all tested M2 cytokines by BAL-cells. An increase in CCL18 levels and neutrophil counts during AE was observed in BAL cells from patients from whom serial lavages were obtained. Furthermore, high baseline levels of CCL18 production by BAL cells were significantly predictive for the development of future AE.BAL cell cytokine production levels at acute exacerbation show up-regulation of pro-inflammatory as well as anti-inflammatory/ M2 cytokines. Our data suggest that AE in IPF is not an incidental event but rather driven by cellular mechanisms including M2 macrophage activation.

  10. Oral Administration of Escin Inhibits Acute Inflammation and Reduces Intestinal Mucosal Injury in Animal Models

    Directory of Open Access Journals (Sweden)

    Minmin Li

    2015-01-01

    Full Text Available The present study aimed to investigate the effects of oral administration of escin on acute inflammation and intestinal mucosal injury in animal models. The effects of escin on carrageenan-induced paw edema in a rat model of acute inflammation, cecal ligation and puncture (CLP induced intestinal mucosal injury in a mouse model, were observed. It was shown that oral administration of escin inhibits carrageenan-induced paw edema and decreases the production of prostaglandin E2 (PGE2 and cyclooxygenase- (COX- 2. In CLP model, low dose of escin ameliorates endotoxin induced liver injury and intestinal mucosal injury and increases the expression of tight junction protein claudin-5 in mice. These findings suggest that escin effectively inhibits acute inflammation and reduces intestinal mucosal injury in animal models.

  11. Inhaled iloprost for the control of acute pulmonary hypertension in children: a systematic review.

    Science.gov (United States)

    Mulligan, Claire; Beghetti, Maurice

    2012-07-01

    Inhaled iloprost is attracting growing interest as a potential alternative and/or adjuvant to inhaled nitric oxide in the management of pediatric pulmonary hypertension in the acute and intensive care settings. However, there are currently no formal evidence-based guidelines regarding the use of inhaled iloprost in children with pulmonary hypertension. The aim of this systematic review is to assess the literature concerning the use of inhaled iloprost in children with pulmonary hypertension in the acute setting. Studies were identified from PubMed and Embase. Internal literature databases and recent congress abstracts (2009 onward) were also searched for relevant publications. Studies were included if they examined the use of inhaled iloprost in children with pulmonary hypertension in an acute or intensive care setting. Twenty-eight studies were included in the review. The majority were case studies or case series (n = 17), and in total, the 28 studies represented the treatment of 195 children with iloprost. Iloprost was most frequently studied in children undergoing cardiac surgery (as a bridge to surgery and postoperatively), in children undergoing acute pulmonary vasoreactivity testing, and in neonates with persistent pulmonary hypertension of the newborn. The results of the included studies suggested that inhaled iloprost may have a diverse role in the acute treatment of pediatric pulmonary hypertension and that its acute effects are similar to those of inhaled nitric oxide. However, the iloprost dose was not consistently reported and varied greatly between studies, and several different administration devices were used. Inhaled iloprost may be useful in the acute treatment of children and neonates with pulmonary hypertension, but clinical data are scarce, and the appropriate dosing of iloprost in different scenarios is uncertain. Well-designed prospective clinical trials are needed.

  12. Effects of an acute bout of moderate-intensity exercise on postprandial lipemia and airway inflammation.

    Science.gov (United States)

    Johnson, Ariel M; Kurti, Stephanie P; Smith, Joshua R; Rosenkranz, Sara K; Harms, Craig A

    2016-03-01

    A high-fat meal (HFM) induces an increase in blood lipids (postprandial lipemia; PPL), systemic inflammation, and acute airway inflammation. While acute exercise has been shown to have anti-inflammatory and lipid-lowering effects, it is unknown whether exercise prior to an HFM will translate to reduced airway inflammation post-HFM. Our purpose was to determine the effects of an acute bout of exercise on airway inflammation post-HFM and to identify whether any protective effect of exercise on airway inflammation was associated with a reduction in PPL or systemic inflammation. In a randomized cross-over study, 12 healthy, 18- to 29-year-old men (age, 23.0 ± 3.2 years; height, 178.9 ± 5.5 cm; weight, 78.5 ± 11.7 kg) consumed an HFM (1 g fat/1 kg body weight) 12 h following exercise (EX; 60 min at 60% maximal oxygen uptake) or without exercise (CON). Fractional exhaled nitric oxide (FENO; measure of airway inflammation), triglycerides (TG), and inflammatory markers (high-sensitivity C-reactive protein, tumor-necrosis factor-alpha, and interleukin-6) were measured while fasted at 2 h and 4 h post-HFM. FENO increased over time (2 h: CON, p = 0.001; EX, p = 0.002, but not by condition (p = 0.991). TG significantly increased 2 and 4 h post-HFM (p 0.05). There were no relationships between FENO and TG or systemic inflammatory markers for any time point or condition (p > 0.05). In summary, an acute bout of moderate-intensity exercise performed 12 h prior to an HFM did not change postprandial airway inflammation or lipemia in healthy, 18- to 29-year-old men.

  13. Malnutrition and inflammation in acute kidney injury due to earthquake-related crush syndrome

    OpenAIRE

    2010-01-01

    Abstract Background Malnutrition and inflammation are common and serious complications in patients with acute kidney injury (AKI). However, the profile of these complications in patients with AKI caused by crush syndrome (CS) remains unclear. This study describes the clinical characteristics of malnutrition and inflammation in patients with AKI and CS due to the Wenchuan earthquake. Methods One thousand and twelve victims and eighteen healthy adults were recruited to the study. They were divi...

  14. Management of acute cardiogenic pulmonary edema: a literature review.

    Science.gov (United States)

    Johnson, Jeremy M

    2009-01-01

    Acute cardiogenic pulmonary edema (CPE) is a pathology frequently seen in patients presenting to emergency departments (EDs) and can usually be attributed to preexisting cardiovascular disease. Heart failure alone accounts for more than 1 million hospital admissions annually and has one of the highest ED morbidity and mortality to date (). Historically, CPE has been managed by the treating clinician in a manner that is based largely on anecdotal evidence. Furosemide (Lasix), morphine, and nitroglycerin have historically been the baseline standard for drug therapy in CPE management. A lack of drastic improvement in the patient's condition over the course of the ED visit may reflect a management style that results in higher morbidity and mortality for CPE patients. Several recent articles provide evidence-based outcomes that suggest changing standard therapy along with the adjunctive use of other medications. These articles also describe treatment modalities that result in a marked improvement in the management of patients with CPE along with decreases in adverse outcomes and hospital length of stay. The goal of this article is to present a summary of the evidence regarding the management of CPE and discuss the implications for current practice.

  15. Acute mesenteric ischemia after cardio-pulmonary bypass surgery

    Institute of Scientific and Technical Information of China (English)

    Bassam Abboud; Ronald Daher; Joe Boujaoude

    2008-01-01

    Acute mesenteric ischemia (AMI) is a highly-lethal surgical emergency.Several pathophysiologic events (arterial obstruction,venous thrombosis and diffuse vasospasm) lead to a sudden decrease in mesenteric blood flow.Ischemia/reperfusion syndrome of the intestine is responsible for systemic abnormalities,leading to multi-organ failure and death.Early diagnosis is difficult because the clinical presentation is subtle,and the biological and radiological diagnostic tools lack sensitivity and specificity.Therapeutic options vary from conservative resuscitation,medical treatment,endovascular techniques and surgical resection and revascularization.A high index of suspicion is required for diagnosis,and prompt treatment is the only hope of reducing the mortality rate.Studies are in progress to provide more accurate diagnostic tools for early diagnosis.AMI can complicate the post-operative course of patients following cardio-pulmonary bypass (CPB).Several factors contribute to the systemic hypo-perfusion state,which is the most frequent pathophysiologic event.In this particular setting,the clinical presentation of AMI can be misleading,while the laboratory and radiological diagnostic tests often produce inconclusive results.The management strategies are controversial,but early treatment is critical for saving lives.Based on the experience of our team,we consider prompt exploratory laparotomy,irrespective of the results of the diagnostic tests,is the only way to provide objective assessment and adequate treatment,leading to dramatic reduction in the mortality rate.

  16. Acute kidney injury in patients with pulmonary embolism

    Science.gov (United States)

    Chang, Chih-Hsiang; Fu, Chung-Ming; Fan, Pei-Chun; Chen, Shao-Wei; Chang, Su-Wei; Mao, Chun-Tai; Tian, Ya-Chung; Chen, Yung-Chang; Chu, Pao-Hsien; Chen, Tien-Hsing

    2017-01-01

    Abstract Acute kidney injury (AKI) is overlooked in patients with pulmonary embolism (PE). Risk factors for and long-term outcomes of this complication remain unknown. This study evaluated the predictors and prognosis of AKI in patients with PE. This retrospective cohort study used Taiwan's National Health Insurance Research Database. We enrolled a total of 7588 patients who were admitted to a hospital for PE from January1997 to December 2011 and administered anticoagulation or thrombolytic agents. All demographic data, risk factors, and outcomes were analyzed. AKI was diagnosed in 372 (4.9%) patients. Multivariate logistic regression analysis revealed pre-existing chronic kidney disease, hypertension, diabetes mellitus, massive PE, anemia, and sepsis as independent risk factors for AKI. In the long-term follow-up, the survival rate was similar in the AKI and non-AKI groups. Careful risk factor screening and intensive intervention in patients with AKI might yield outcomes similar to those in patients without AKI. PMID:28248851

  17. Smoking Is Associated with Acute and Chronic Prostatic Inflammation: Results from the REDUCE Study.

    Science.gov (United States)

    Moreira, Daniel M; Nickel, J Curtis; Gerber, Leah; Muller, Roberto L; Andriole, Gerald L; Castro-Santamaria, Ramiro; Freedland, Stephen J

    2015-04-01

    Both anti- and proinflammatory effects of cigarette smoking have been described. As prostate inflammation is common, we hypothesized smoking could contribute to prostate inflammation. Thus, we evaluated the association of smoking status with acute and chronic inflammation within the prostate of men undergoing prostate biopsy. We retrospectively analyzed 8,190 men ages 50 to 75 years with PSA levels between 2.5 and 10 ng/mL enrolled in the Reduction by Dutasteride of Prostate Cancer Events study. Smoking status was self-defined as never, former, or current. Prostate inflammation was assessed by systematic central review blinded to smoking status. The association of smoking with inflammation in the baseline, 2-year, and 4-year biopsies was evaluated with univariable and multivariable logistic regressions. At study enrollment, 1,233 (15%), 3,203 (39%), and 3,754 (46%) men were current, former, and never smokers, respectively. Current smokers were significantly younger and had smaller prostates than former and never smokers (all P chronic prostate inflammations were identified in 1,261 (15%) and 6,352 (78%) baseline biopsies, respectively. In univariable analysis, current smokers were more likely to have acute inflammation than former (OR, 1.35; P, 0.001) and never smokers (OR, 1.36; P, 0.001). The results were unchanged at 2- and 4-year biopsies. In contrast, current smoking was linked with chronic inflammation in the baseline biopsy, but not at 2- and 4-year biopsies. In conclusion, among men undergoing prostate biopsy, current smoking was independently associated with acute and possibly chronic prostate inflammations.

  18. Fundamentals of management of acute postoperative pulmonary hypertension.

    Science.gov (United States)

    Taylor, Mary B; Laussen, Peter C

    2010-03-01

    In the last several years, there have been numerous advancements in the field of pulmonary hypertension as a whole, but there have been few changes in the management of children with pulmonary hypertension after cardiac surgery. Patients at particular risk for postoperative pulmonary hypertension can be identified preoperatively based on their cardiac disease and can be grouped into four broad categories based on the mechanisms responsible for pulmonary hypertension: 1) increased pulmonary vascular resistance; 2) increased pulmonary blood flow with normal pulmonary vascular resistance; 3) a combination of increased pulmonary vascular resistance and increased blood flow; and 4) increased pulmonary venous pressure. In this review of the immediate postoperative management of pulmonary hypertension, various strategies are discussed including medical therapies, monitoring, ventilatory strategies, and weaning from these supports. With early recognition of patients at particular risk for severe pulmonary hypertension, management strategies can be directed at preventing or minimizing hemodynamic instability and thereby prevent the development of ventricular dysfunction and a low output state.

  19. Lack of Correlation Between Pulmonary and Systemic Inflammation Markers in Patients with Chronic Obstructive Pulmonary Disease: A Simultaneous, Two-Compartmental Analysis.

    Science.gov (United States)

    Núñez, Belen; Sauleda, Jaume; Garcia-Aymerich, Judith; Noguera, Aina; Monsó, Eduard; Gómez, Federico; Barreiro, Esther; Marín, Alicia; Antó, Josep Maria; Agusti, Alvar

    2016-07-01

    The origin of systemic inflammation in chronic obstructive pulmonary disease (COPD) patients remains to be defined, but one of the most widely accepted hypothesis is the 'spill over' of inflammatory mediators from the lung to the circulation. To evaluate the relationship between pulmonary and systemic inflammation in COPD quantifying several inflammatory markers in sputum and serum determined simultaneously. Correlations between various inflammatory variables (TNF-α, IL6, IL8) in sputum and serum were evaluated in 133 patients from the PAC-COPD cohort study. A secondary objective was the evaluation of relationships between inflammatory variables and lung function. Inflammatory markers were clearly higher in sputum than in serum. No significant correlation was found (absolute value, r=0.03-0.24) between inflammatory markers in blood and in sputum. There were no significant associations identified between those markers and lung function variables, such as FEV1, DLCO and PaO2 neither. We found no correlation between pulmonary and systemic inflammation in patients with stable COPD, suggesting different pathogenic mechanisms. Copyright © 2016 SEPAR. Published by Elsevier Espana. All rights reserved.

  20. Effects of Flavonoids from French Marigold (Florets of Tagetes patula L. on Acute Inflammation Model

    Directory of Open Access Journals (Sweden)

    Ken Yasukawa

    2013-01-01

    Full Text Available The major components patuletin and patulitrin were isolated from French marigold (florets of Tagetes patula. Patuletin and patulitrin were found to inhibit acute inflammation in mice. Oral administration of patuletin and patulitrin significantly suppressed hind-paw edema induced by carrageenin and histamine, while topical application of patuletin and patulitrin significantly inhibited ear edema induced by 12-O-tetradecanoylphorbol-13-acetate and arachidonic acid. Thus, oral and topical administration of patuletin and patulitrin inhibited acute inflammation in mice. These results suggest the anti-inflammatory efficacy of French marigold.

  1. [A statement the Polish Cardiac Society Working Group on Pulmonary Circulation on screening for CTEPH patients after acute pulmonary embolism].

    Science.gov (United States)

    Ciurzyński, Michał; Kurzyna, Marcin; Kopeć, Grzegorz; Błaszczak, Piotr; Chrzanowski, Łukasz; Kamiński, Karol; Mizia-Stec, Katarzyna; Mularek-Kubzdela, Tatiana; Mroczek, Ewa; Biederman, Andrzej; Pruszczyk, Piotr; Torbicki, Adam

    2017-01-01

    Both pharmacological and invasive treatment of chronic thromboembolic pulmonary hypertension (CTEPH) is now available in Poland and the awareness of the disease among physicians is growing. Thus, the Polish Cardiac Society's Working Group on Pulmonary Circulation in cooperation with independent experts in this field, have launched the statement on algorithm to guide a CTEPH diagnosis in patients with previous acute pulmonary embolism (APE). In Poland, every year this disease affects about 250 patients. CTEPH should be suspected in individuals after APE with dyspnea, despite at least 3 months period of effective anticoagulation, particularly when specified risk factors are present. Echocardiography is a main screening tool. The authors suggest that a diagnostic process of patients with significant clinical suspicion of CTEPH and right ventricle overload in echocardiography should be performed in reference centres. The document contains a list of Polish centres diagnosing patients with suspected CTEPH. Pulmonary scintigraphy is a safe and highly sensitive screening test for CTEPH. Multi-detector computed tomography with precise detection of thromboembolic residues in pulmonary circulation is important for planning of pulmonary endarterectomy. Right heart catheterisation definitely confirms the presence of pulmonary hypertension and direct pulmonary angiography allows for identification of lesions suitable for thromboendarterectomy or pulmonary balloon angioplasty. In this document a diagnostic algorithm in patients with suspected CTEPH is also proposed. With individualised sequential diagnostic strategy each patient can be finally qualified for a particular mode of therapy by dedicated CTEPH Heart Team. Moreover the document contains short information for the primary care physician about the management of patients after APE.

  2. [Effects of erdosteine on inflammation and fibrosis in rats with pulmonary fibrosis induced by bleomycin].

    Science.gov (United States)

    Erden, Ersin Sükrü; Kirkil, Gamze; Deveci, Figen; Ilhan, Nevin; Cobanoğlu, Bengü; Turgut, Teyfik; Muz, Mehmet Hamdi

    2008-01-01

    We aimed to investigate the levels of some chemokines, inflammatory cell counts in bronchoalveolar lavage (BAL) fluid, histopathological changes in lung tissue, to determine the effect of erdosteine on acute inflammatory changes and fibrosis in a rat fibrosis model induced by bleomycine (BLM). Forty-five Wistar male rats were taken into the study. On day 0, intratracheal saline to control group (group 1, n= 15), intratracheal BLM 7.5 U/kg to BLM (group 2, n= 15) and erdosteine group (group 3, n= 15) was administered. In group 3, oral erdosteine (10 mg/kg/day) was applied two days before BLM. On day 0, 14, and 29th five rats in each groups were sacrificed, BAL fluid was performed. Malonyldialdehyde (MDA), macrophage inflammatory protein (MIP)-1alpha, MIP-2 levels in BAL fluid, hydroxyproline levels in lung tissue were measured. Histopathological examination was performed. When BLM group compared to erdosteine group, the levels of MDA, MIP-1alpha, MIP-2, and neutrophil counts, the hydroxyproline (OH-P) level of lung tissue were decreased in erdosteine group on acute inflammatory phase (day 14) (perdosteine group than BLM group on day 29 (p= 0.01). We conclude that erdosteine may prevent the acute lung inflammation and fibrosis by suppressing the accumulation of neutrophils, inhibition of lipid peroxydation, chemokine production, and release.

  3. Acute pulmonary vasodilatory properties of amlodipine in humans with pulmonary hypertension.

    OpenAIRE

    Woodmansey, P. A.; O'Toole, L.; Channer, K S; Morice, A H

    1996-01-01

    OBJECTIVE: Calcium antagonists are the only oral vasodilators shown to influence mortality in primary pulmonary hypertension, but the high doses required are often poorly tolerated. Amlodipine is a novel, relatively well tolerated, calcium antagonist. It has not been previously tested in humans with pulmonary hypertension. DESIGN: Calcium antagonists are claimed to be of benefit in the 20-30% of patients who respond--that is, whose mean pulmonary artery pressure and pulmonary vascular resista...

  4. A case of heart failure due to alcoholic cardiomyopathy combined with acute pulmonary embolism.

    Science.gov (United States)

    Xiao, Feng; Yuan, Wei; Li, Xiaorong; Wang, Gannan; Jiang, Ting; Wang, Weiwei; Zhang, Jinsong; Li, Ping; Qi, Lianwen; Chen, Yan

    2014-09-01

    It has not been reported that cases of alcoholic cardiomyopathy (ACM) combined with acute pulmonary embolism (PE). We hereby present a case of a 48-year-old male with ACM with significant enlargement of the heart and heart failure is described. Then, the patient was seized with acute PE which was confirmed by specific examination and his symptoms.

  5. Acute effect of tetrandrine pulmonary targeting microspheres on hypoxic pulmonary hypertension in rats

    Institute of Scientific and Technical Information of China (English)

    程德云; 陈文彬; 莫晓能

    2002-01-01

    Objective To assess the effect of tetrandrine (Tet) pulmonary targeting microspheres on hypoxic pulmonary hypertension and evaluate its selective action on pulmonary circulation. Methods Twenty rats were exposed to hypoxic conditions for 3 weeks. Ten rats were used as normoxic controls. We administered Tet pulmonary targeting microspheres to 10 hypoxic rats and Tet aqueous solution to 10 hypoxic rats and the 10 control rats. Mean pulmonary arterial pressure (mPAP) was measured by a right cardiac catheterization, and mean systemic blood pressure (mSBP) was measured by left femoral catheterization. Results Rats exposed to hypoxia developed pulmonary hypertension. The decrease in mPAP in rats treated with Tet pulmonary targeting microspheres was significantly greater than that in rats receiving Tet aqueous solution (P<0.05), and the effects were longer with Tet pulmonary targeting microspheres. Moreover, Tet pulmonary targeting microspheres, unlike Tet aqueous solution, did not decrease mSBP. Conclusion Tet pulmonary targeting microspheres were more effective than Tet aqueous solution in treating hypoxic pulmonary hypertension and acted selectively on the pulmonary circulation.

  6. Activation of MTOR in pulmonary epithelium promotes LPS-induced acute lung injury.

    Science.gov (United States)

    Hu, Yue; Lou, Jian; Mao, Yuan-Yuan; Lai, Tian-Wen; Liu, Li-Yao; Zhu, Chen; Zhang, Chao; Liu, Juan; Li, Yu-Yan; Zhang, Fan; Li, Wen; Ying, Song-Min; Chen, Zhi-Hua; Shen, Hua-Hao

    2016-12-01

    MTOR (mechanistic target of rapamycin [serine/threonine kinase]) plays a crucial role in many major cellular processes including metabolism, proliferation and macroautophagy/autophagy induction, and is also implicated in a growing number of proliferative and metabolic diseases. Both MTOR and autophagy have been suggested to be involved in lung disorders, however, little is known about the role of MTOR and autophagy in pulmonary epithelium in the context of acute lung injury (ALI). In the present study, we observed that lipopolysaccharide (LPS) stimulation induced MTOR phosphorylation and decreased the expression of MAP1LC3B/LC3B (microtubule-associated protein 1 light chain 3 β)-II, a hallmark of autophagy, in mouse lung epithelium and in human bronchial epithelial (HBE) cells. The activation of MTOR in HBE cells was mediated by TLR4 (toll-like receptor 4) signaling. Genetic knockdown of MTOR or overexpression of autophagy-related proteins significantly attenuated, whereas inhibition of autophagy further augmented, LPS-induced expression of IL6 (interleukin 6) and IL8, through NFKB signaling in HBE cells. Mice with specific knockdown of Mtor in bronchial or alveolar epithelial cells exhibited significantly attenuated airway inflammation, barrier disruption, and lung edema, and displayed prolonged survival in response to LPS exposure. Taken together, our results demonstrate that activation of MTOR in the epithelium promotes LPS-induced ALI, likely through downregulation of autophagy and the subsequent activation of NFKB. Thus, inhibition of MTOR in pulmonary epithelial cells may represent a novel therapeutic strategy for preventing ALI induced by certain bacteria.

  7. Noninvasive ventilation in patients with acute cardiogenic pulmonary edema

    Directory of Open Access Journals (Sweden)

    Andrea Bellone

    2013-07-01

    Full Text Available The term noninvasive ventilation (NIV encompasses two different modes of delivering positive airway pressure, namely continuous positive airway pressure (CPAP and bilevel positive airway pressure (bilevel-PAP. The two modes are different since CPAP does not actively assist inspiration whereas bilevel-PAP does. Bilevel-PAP is a type of noninvasive ventilation that helps keep the upper airways of the lungs open by providing a flow of air delivered through a face mask. The air is pressurized by a machine, which delivers it to the face mask through long, plastic hosing. With bilevel-PAP, the doctor prescribes specific alternating pressures: a higher pressure is used to breathe in (inspiratory positive airway pressure and a lower pressure is used to breath out (expiratory positive airway pressure. Noninvasive ventilation has been shown to reduce the rate of tracheal intubation. The main indications are exacerbation of chronic obstructive pulmonary disease and acute cardiogenic pulmonary edema (ACPE. This last is a common cause of respiratory failure with high incidence and high mortality rate. Clinical findings of ACPE are related to the increased extra-vascular water in the lungs and the resulting reduced lung compliance, increased airway resistance and elevated inspiratory muscle load which generates a depression in pleural pressure. These large pleural pressure swings are responsible for hemodynamic changes by increasing left ventricular afterload, myocardial transmural pressure, and venous return. These alterations can be detrimental to patients with left ventricular systolic dysfunction. Under these circumstances, NIV, either by CPAP or bilevel-PAP, improves vital signs, gas exchange, respiratory mechanics and hemodynamics by reducing left ventricular afterload and preload. In the first randomized study which compared the effectiveness of CPAP plus medical treatment vs medical treatment alone, the CPAP group showed a significant decrease in its

  8. Acute vasoreactivity test results in severe pulmonary hypertension patients with chronic obstructive pulmonary disease: our experience with 29 cases

    Directory of Open Access Journals (Sweden)

    Asker S

    2015-05-01

    Full Text Available Selvi Asker,1 Muntecep Asker2 ¹Department of Chest Diseases, Van Yuksek Ihtisas Training and Research Hospital, Van, Turkey; 2Department of Cardiology, Van Yuksek Ihtisas Training and Research Hospital, Van, TurkeyAim: The aim of the current study is to evaluate acute vasoreactivity test (AVT results in severe pulmonary hypertension patients with chronic obstructive pulmonary disease and to compare the demographical, clinical, and laboratory variables in positive and negative cases.Methods: This retrospective, clinical study was performed on 29 cases in the departments of cardiology and chest diseases of our tertiary care center. AVT was positive in 12 (41.4% cases and negative in 17 (58.6% cases. Demographical variables, cardiopulmonary indicators, and laboratory findings were compared in these two subgroups.Results: The mean age was 62.3±7.8 years for AVT negative group, while it was 64.8±7.3 years in AVT positive group (P=0.38. Except for the changes in systolic, diastolic, and mean pulmonary arterial pressures before and after iloprost administration, there were no statistically significant differences regarding any of the parameters under investigation in both groups.Conclusion: Despite the high rate of positivity for AVT in severe pulmonary hypertension patients with chronic obstructive pulmonary disease, none of the variables under investigation displayed a noteworthy difference between AVT negative and positive groups. Identification of factors likely to influence AVT results is important for establishment of appropriate treatment protocols especially for AVT negative cases. Keywords: chronic obstructive pulmonary disease, pulmonary hypertension, acute vasoreactivity test

  9. Metabolic reprogramming and inflammation act in concert to control vascular remodeling in hypoxic pulmonary hypertension.

    Science.gov (United States)

    Stenmark, Kurt R; Tuder, Rubin M; El Kasmi, Karim C

    2015-11-15

    Pulmonary hypertension (PH) is a complex, multifactorial syndrome that remains poorly understood despite decades of research. PH is characterized by profound pulmonary artery (PA) remodeling that includes significant fibro-proliferative and inflammatory changes of the PA adventitia. In line with the emerging concept that PH shares key features with cancer, recent work centers on the idea that PH results from a multistep process driven by reprogramming of gene-expression patterns that govern changes in cell metabolism, inflammation, and proliferation. Data demonstrate that in addition to PA endothelial cells and smooth muscle cells, adventitial fibroblasts from animals with experimental hypoxic PH and from humans with PH (hereafter, termed PH-Fibs) exhibit proinflammatory activation, increased proliferation, and apoptosis resistance, all in the context of metabolic reprogramming to aerobic glycolysis. PH-Fibs can also recruit, retain, and activate naïve macrophages (Mϕ) toward a proinflammatory/proremodeling phenotype through secretion of chemokines, cytokines, and glycolytic metabolites, among which IL-6 and lactate play key roles. Furthermore, these fibroblast-activated Mϕ (hereafter, termed FAMϕ) exhibit aerobic glycolysis together with high expression of arginase 1, Vegfa, and I1lb, all of which require hypoxia-inducible factor 1α and STAT3 signaling. Strikingly, in situ, the adventitial Mϕ phenotype in the remodeled PA closely resembles the Mϕ phenotype induced by fibroblasts in vitro (FAMϕ), suggesting that FAMϕ crosstalk involving metabolic and inflammatory signals is a critical, pathogenetic component of vascular remodeling. This review discusses metabolic and inflammatory changes in fibroblasts and Mϕ in PH with the goal of raising ideas about new interventions to abrogate remodeling in hypoxic forms of PH.

  10. IL-6/Stat3-driven pulmonary inflammation, but not emphysema, is dependent on interleukin-17A in mice.

    Science.gov (United States)

    Ruwanpura, Saleela M; McLeod, Louise; Brooks, Gavin D; Bozinovski, Steven; Vlahos, Ross; Longano, Anthony; Bardin, Philip G; Anderson, Gary P; Jenkins, Brendan J

    2014-04-01

    Pulmonary emphysema is linked to T cell-mediated autoimmune inflammation, although the pathogenic role of specific pro-inflammatory cytokines remains unclear. The Th17 type response, characterized by the production of the cytokine interleukin (IL)-17A, is modulated in part by the IL-6/signal transducer and activator of transcription (Stat)3 signalling axis and is associated with numerous autoimmune diseases. We therefore evaluated a causal role for IL-17A in the IL-6-driven gp130(F/F) mouse model for spontaneous pulmonary inflammation and emphysema. The expression of Th17-related factors was quantified in the lungs of gp130(F/F) mice and emphysematous patients, and the degree of pulmonary inflammation and emphysema was measured in gp130(F/F)  : Il17a-/- mice by immunohistochemistry, stereology and respiratory mechanics. In gp130(F/F) mice, lung gene expression of Il17a and other Th17-related factors was augmented compared with gp130+/+ (wild-type), gp130(F/F)  : Il6-/- and gp130(F/F)  : Stat3-/+ mice displaying normalized Stat3 activity and no lung inflammation. Importantly, genetic ablation of Il17a in gp130(F/F)  : Il17a-/- mice prevented lung inflammation; however, emphysema still developed. Additionally, messenger RNA expression of inflammatory genes Cxcl1, Cxcl2, Ccl2 and Tnfα; as well as Il6 and the Stat3-target gene, Socs3, were upregulated in the lungs of gp130(F/F) mice compared with gp130(F/F)  : Il17a-/- and gp130+/+ mice. Consistent with these findings, augmented IL17A expression was observed in emphysema patients presenting with inflammation compared with inflammation-free individuals. Collectively, our data suggest that the integration of IL-17A into the IL-6/Stat3 signalling axis mediates lung inflammation, but not emphysema, and that discrete targeting of IL-17A may alleviate pulmonary inflammatory-related diseases. © 2014 The Authors. Respirology © 2014 Asian Pacific Society of Respirology.

  11. Preferential recruitment of neutrophils by endothelin-1 in acute lung inflammation induced by lipopolysaccharide or cigarette smoke

    Directory of Open Access Journals (Sweden)

    Tapan Bhavsar

    2008-10-01

    Full Text Available Tapan Bhavsar, Xing Jian Liu, Hardik Patel, Ralph Stephani, Jerome O CantorSt John’s University, School of Pharmacy and Allied Health Sciences, New York, USAAbstract: This study examined the role of endothelin-1 (ET-1 in recruiting inflammatory cells to the lung after induction of injury with either lipopolysaccharide (LPS or cigarette smoke. Hamsters injected with either ET-1 or its precursor peptide (Big ET-1 prior to treatment with LPS or cigarette smoke had markedly increased concentrations of neutrophils in bronchoalveolar lavage fluid (BALF despite a reduction in total numbers of BALF leukocytes. Furthermore, the effect of ET-1 on smoke-exposed animals was reversed by addition of an endothelin-A receptor antagonist. These results are consistent with preferential recruitment of neutrophils by ET-1, and suggest that inhibition of this proinfl ammatory mediator may decrease acute pulmonary inflammation associated with cigarette smoke and other pulmonary toxins.Keywords: endothelin, lipopolysaccahride, cigarette smoke, neutrophils, lung

  12. Widening of coronary sinus in CT pulmonary angiography indicates right ventricular dysfunction in patients with acute pulmonary embolism

    Energy Technology Data Exchange (ETDEWEB)

    Staskiewicz, Grzegorz [Medical University of Lublin, 1. Department of Radiology, Lublin (Poland); Medical University of Lublin, Department of Human Anatomy, Lublin (Poland); Czekajska-Chehab, Elzbieta; Trojanowska, Agnieszka; Drop, Andrzej [Medical University of Lublin, 1. Department of Radiology, Lublin (Poland); Przegalinski, Jerzy; Tomaszewski, Andrzej [Medical University of Lublin, Chair and Department of Cardiology, Lublin (Poland); Torres, Kamil; Torres, Anna [Medical University of Lublin, Department of Human Anatomy, Lublin (Poland); Maciejewski, Ryszard [Medical University of Lublin, Department of Human Anatomy, Lublin (Poland); UITM Rzeszow, Medical Emergency Department, Rzeszow (Poland)

    2010-07-15

    Right ventricular dysfunction (RVD) may occur in the course of acute pulmonary embolism (PE). Patients with RVD need more intensive treatment, and the prognosis is more severe. The aim of this study was to evaluate the usefulness of the measurement of the coronary sinus in the assessment of RVD in patients with acute PE and to compare it with other indicators of RVD. Retrospective assessment of 55 CT pulmonary angiography examinations with signs of acute PE was performed. Pulmonary artery systolic pressure (PASP) was echocardiographically assessed in all patients, and RVD was defined as PASP values greater than 30 mmHg. CT measurements included the size of the heart ventricles, mediastinal vessels and the width of the coronary sinus. Median width of the coronary sinus was 16 mm (range 12-24 mm) in patients with increased PASP and 10 mm (range 7-22 mm) in patients with normal PASP (p = 0.001). Best cut-off value was assessed to be 12.5 mm, with sensitivity 94% and specificity 75%. It was characterised by the largest area under ROC curve (0.82) among analysed parameters. Width of the coronary sinus seems to be a promising parameter for identification of RVD in patients with acute PE. A prospective study should be undertaken to further assess its clinical and prognostic applicability. (orig.)

  13. Toward computational identification of multiscale "tipping points" in acute inflammation and multiple organ failure.

    Science.gov (United States)

    An, Gary; Nieman, Gary; Vodovotz, Yoram

    2012-11-01

    Sepsis accounts annually for nearly 10% of total U.S. deaths, costing nearly $17 billion/year. Sepsis is a manifestation of disordered systemic inflammation. Properly regulated inflammation allows for timely recognition and effective reaction to injury or infection, but inadequate or overly robust inflammation can lead to Multiple Organ Dysfunction Syndrome (MODS). There is an incongruity between the systemic nature of disordered inflammation (as the target of inflammation-modulating therapies), and the regional manifestation of organ-specific failure (as the subject of organ support), that presents a therapeutic dilemma: systemic interventions can interfere with an individual organ system's appropriate response, yet organ-specific interventions may not help the overall system reorient itself. Based on a decade of systems and computational approaches to deciphering acute inflammation, along with translationally-motivated experimental studies in both small and large animals, we propose that MODS evolves due to the feed-forward cycle of inflammation → damage → inflammation. We hypothesize that inflammation proceeds at a given, "nested" level or scale until positive feedback exceeds a "tipping point." Below this tipping point, inflammation is contained and manageable; when this threshold is crossed, inflammation becomes disordered, and dysfunction propagates to a higher biological scale (e.g., progressing from cellular, to tissue/organ, to multiple organs, to the organism). Finally, we suggest that a combination of computational biology approaches involving data-driven and mechanistic mathematical modeling, in close association with studies in clinically relevant paradigms of sepsis/MODS, are necessary in order to define scale-specific "tipping points" and to suggest novel therapies for sepsis.

  14. Respiratory viruses in acute exacerbations of chronic obstructive pulmonary disease

    Science.gov (United States)

    Koul, Parvaiz A; Mir, Hyder; Akram, Shabir; Potdar, Varsha; Chadha, Mandeep S

    2017-01-01

    Objective: Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) cause significant morbidity, mortality, and an inexorable decline of lung function. Data from developed countries have shown viruses to be important causes of AECOPD, but data from developing countries like India are scant. We set out to determine the contribution of viruses in the causation of hospitalized patients with AECOPD. Methods: Twin nasopharyngeal/oropharyngeal swabs collected from 233 patients admitted with an acute AECOPD and tested for respiratory viruses including respiratory syncytial virus A and B, parainfluenza were (PIV) 1, 2, 3, and 4, human metapneumovirus (hMPV) A and B, influenza A and B, enterovirus, corona NL65, OC43, and 229E viruses, adenovirus 2 and 4, rhinovirus, and bocavirus, by duplex real time reverse-transcription polymerase chain reaction (qRT-PCR) using CDC approved primers and probes. Samples positive for influenza A were subtyped for A/H1N1pdm09 and A/H3N2 whereas influenza B samples were subtyped into B/Yamagata and B/Victoria subtypes, using primers and probes recommended by CDC, USA. Results: Respiratory viruses were detected in 46 (19.7%) cases, influenza A/H3N2 and rhinoviruses being the most common viruses detected. More than one virus was isolated in four cases consisting of hMPV-B + adeno-2 + Inf-B; rhino + H3N2, PIV-1 + rhino; and PIV-1+ hMPV-B in one case each. Ancillary supportive therapeutic measures included bronchodilators, antibiotics, steroids, and ventilation (noninvasive in 42 and invasive in 4). Antiviral therapy was instituted in influenza-positive patients. Three patients with A/H3N2 infection died during hospitalization. Conclusions: We conclude that respiratory viruses are important contributors to AECOPD in India. Our data calls for prompt investigation during an exacerbation for viruses to obviate inappropriate antibiotic use and institute antiviral therapy in viral disease amenable to antiviral therapy. Appropriate

  15. Radiolucency below the crown of mandibular horizontal incompletely impacted third molars and acute inflammation in men with diabetes

    Directory of Open Access Journals (Sweden)

    Minoru Yamaoka

    2009-05-01

    Full Text Available Minoru Yamaoka, Yusuke Ono, Masahide Ishizuka, Kouichi Yasuda, Takashi Uematsu, Kiyofumi FurusawaOral and Maxillofacial Surgery, Matsumoto Dental University, Shiojiri, Nagano 399-0781, JapanAbstract: Although mandibular third molar has a high risk of infection extending any complications, the influence of diabetes on radiolucency and acute inflammation in pericoronitis remains unclear. The present study was to evaluate whether radiolucency below the crown is related to acute inflammation in mandibular horizontal incompletely impacted third molars and to review the records of 140 men more than 45 years with and without diabetes. The odds ratio of exhibiting acute inflammation was 3.38 (95% CI: 1.13–10.16, p < 0.05 and that of exhibiting severe acute inflammation was 15.38 (95% CI: 3.56–66.49, p < 0.0001, indicating an association of acute pericoronitis in diabetes. The frequency of radiolucency below the crown and below the root in diabetics was similar to that in nondiabetics. However, the odds ratio of exhibiting both radiolucency below the crown and acute inflammation under the diabetic condition was 4.85 (95% CI: 1.60–14.73, p < 0.01, whereas that of diabetics showing both radiolucency below the root and acute inflammation was 0.46 (95% CI: 0.06–3.74, p = 0.74. Radiolucency below the crown and acute inflammation were associated with diabetes, but that below root and acute inflammation were not associated with diabetes, indicating that the region below the crown carries susceptibility to acute pericoronitis, whereas the periodontium shows a protective effect against acute pericoronitis.Keywords: radiolucency, acute inflammation, mandible, third molar, diabetes, periodontium

  16. Two opposite extremes of adiposity similarly reduce inflammatory response of antigen-induced acute joint inflammation

    NARCIS (Netherlands)

    Oliveira, M.C.; Silveira, A.L.; Tavares, L.P.; Rodrigues, D.F.; Loo, F.A.J. van de; Sousa, L.P.; Teixeira, M.M.; Amaral, F.A.; Ferreira, A.V.

    2017-01-01

    OBJECTIVE: Acute inflammation is a normal response of tissue to an injury. During this process, inflammatory mediators are produced and metabolic alterations occur. Adipose tissue is metabolically activated, and upon food consumption, it disrupts the inflammatory response. However, little is known a

  17. The EP1/EP3 receptor agonist 17-pt-PGE2 acts as an EP4 receptor agonist on endothelial barrier function and in a model of LPS-induced pulmonary inflammation.

    Science.gov (United States)

    Theiler, Anna; Konya, Viktoria; Pasterk, Lisa; Maric, Jovana; Bärnthaler, Thomas; Lanz, Ilse; Platzer, Wolfgang; Schuligoi, Rufina; Heinemann, Akos

    2016-12-01

    Endothelial dysfunction is a hallmark of inflammatory conditions. We recently demonstrated that prostaglandin (PG)E2 enhances the resistance of pulmonary endothelium in vitro and counteracts lipopolysaccharide (LPS)-induced pulmonary inflammation in vivo via EP4 receptors. The aim of this study was to investigate the role of the EP1/EP3 receptor agonist 17-phenyl-trinor-(pt)-PGE2 on acute lung inflammation in a mouse model. In LPS-induced pulmonary inflammation in mice, 17-pt-PGE2 reduced neutrophil infiltration and inhibited vascular leakage. These effects were unaltered by an EP1 antagonist, but reversed by EP4 receptor antagonists. 17-pt-PGE2 increased the resistance of pulmonary microvascular endothelial cells and prevented thrombin-induced disruption of endothelial junctions. Again, these effects were not mediated via EP1 or EP3 but through activation of the EP4 receptor, as demonstrated by the lack of effect of more selective EP1 and EP3 receptor agonists, prevention of these effects by EP4 antagonists and EP4 receptor knock-down by siRNA. In contrast, the aggregation enhancing effect of 17-pt-PGE2 in human platelets was mediated via EP3 receptors. Our results demonstrate that 17-pt-PGE2 enhances the endothelial barrier in vitro on pulmonary microvascular endothelial cells, and accordingly ameliorates the recruitment of neutrophils, via EP4 receptors in vivo. This suggests a beneficial effect of 17-pt-PGE2 on pulmonary inflammatory diseases. Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.

  18. Inflammation

    DEFF Research Database (Denmark)

    Holst-Hansen, Thomas

    Inflammation is an intricate response relying on the activation and response of both the innate immune system and the infected tissue to remove a threat. The pro-inflammatory NF-kappaB pathway has been studied extensively, among others because of its key role in regulation of inflammation. However...

  19. Inflammation

    DEFF Research Database (Denmark)

    Holst-Hansen, Thomas

    Inflammation is an intricate response relying on the activation and response of both the innate immune system and the infected tissue to remove a threat. The pro-inflammatory NF-kappaB pathway has been studied extensively, among others because of its key role in regulation of inflammation. However...

  20. Peroxisome proliferator-activated receptor gamma as modulator of inflammation in pulmonary sarcoidosis

    Directory of Open Access Journals (Sweden)

    Pejčić Tatjana

    2013-01-01

    Full Text Available Peroxisome proliferator-activated receptor (PPAR includes the family of ligand-activated transcription factors which belong to the group of nuclear hormone receptors and are connected to retinoid, glucocorticoid and thyroid hormone receptors. There are three subtypes of PPARs: PPARα (also known as NR1C3, PPARγ (known as NR1C1 and PPARδ (known as PPARβ or NR1C2. All of them take part in the metabolism, cell proliferation and immune response. PPARγ and PPARα are identified as important immunomodulators and potentially represent an anti-inflammatory target for respiratory diseases. PPARγ deficiency in the lungs has been observed in the inflammatory diseases such as asthma, pulmonary alveolar proteinosis, fibrosis and sarcoidosis, as well as in the animal models of the lung inflammation. A small number of papers concerned with PPARγ in sarcoidosis point to the lowered activity of this factor in the alveolar macrophages and a lowered gene expression for the PPARγ, while the activity is preserved in healthy individuals. At the same time, an increased activity of the nuclear factor kappa B (NF-kB in the bronchoalveolar lavage has been recorded in patients with sarcoidosis. The reason for the decrease in the production of PPARγ in sarcoidosis remains unknown. Several possible mechanisms are mentioned: genetic defect with lowered production, down-regulation due to the increased values of IFN-γ or an increased decomposition of PPARγ. Further investigation will explain the mechanisms regarding the decreased production of PPARγ in sarcoidosis.

  1. Acrolein induced both pulmonary inflammation and the death of lung epithelial cells.

    Science.gov (United States)

    Sun, Yang; Ito, Sachiko; Nishio, Naomi; Tanaka, Yuriko; Chen, Nana; Isobe, Ken-Ichi

    2014-09-02

    Acrolein, a compound found in cigarette smoke, is a major risk factor for respiratory diseases. Previous research determined that both acrolein and cigarette smoke produced reactive oxygen species (ROS). As many types of pulmonary injuries are associated with inflammation, this study sought to ascertain the extent to which exposure to acrolein advanced inflammatory state in the lungs. Our results showed that intranasal exposure of mice to acrolein increased CD11c(+)F4/80(high) macrophages in the lungs and increased ROS formation via induction of NF-κB signaling. Treatment with acrolein activated macrophages and led to their increased production of ROS and expression of several key pro-inflammatory cytokines. In in vitro studies, acrolein treatment of bone marrow-derived GM-CSF-dependent immature macrophages (GM-IMs), activated the cells and led to their increased production of ROS and expression of several key pro-inflammatory cytokines. Acrolein treatment of macrophages induced apoptosis of lung epithelial cells. Inclusion of an inhibitor of ROS formation markedly decreased acrolein-mediated macrophage activation and reduced the extent of epithelial cell death. These results indicate that acrolein can cause lung damage, in great part by mediating the increased release of pro-inflammatory cytokines/factors by macrophages.

  2. [Pulmonary embolism in an acute manic patient following physical restraint].

    Science.gov (United States)

    Pirsoul, S; De Backer, L; Schrijvers, D

    2014-01-01

    Immobilisation is a risk factor for the development of deep venous thrombosis and pulmonary embolism. We present a case-study in which a patient developed a pulmonary embolism after being immobilised after a short period while subjected to physical restraint. We discuss the risk factors involved and stress the need for research into the prevention of such incidents.

  3. [Inter-society consensus for the management of respiratory infections: acute bronchitis and chronic obstructive pulmonary disease].

    Science.gov (United States)

    Lopardo, Gustavo; Pensotti, Claudia; Scapellato, Pablo; Caberlotto, Oscar; Calmaggi, Aníbal; Clara, Liliana; Klein, Manuel; Levy Hara, Gabriel; López Furst, María J; Mykietiuk, Analía; Pryluka, Daniel; Rial, María J; Vujacich, Claudia; Yahni, Diego

    2013-01-01

    The Argentine Society for Infectious Diseases and other national societies issued updated practical guidelines for the management of acute bronchitis (AB) and reactivations of chronic obstructive pulmonary disease (COPD) with the aim of promoting rational use of diagnostic and therapeutic resources. AB is a condition characterized by inflammation of the bronchial airways which affects adults and children without underlying pulmonary disease. It is usually caused by a virus. The diagnosis is based on clinical findings after community acquired pneumonia has been ruled out. Treatment of AB is mainly symptomatic. Antibiotics should be used in immune-compromised hosts, patients with chronic respiratory or cardiac diseases and in the elderly with co-morbidities. Reactivation of COPD is defined as an acute change in the patient's baseline clinical situation beyond normal day to day variations, with an increase in dyspnea, sputum production and/or sputum purulence, warranting a change in medication. An increase in one symptom is considered a mild exacerbation, two as moderate, and the presence of three symptoms is considered a severe exacerbation. An infectious agent can be isolated in sputum in 50 to 75% of COPD reactivations. Moderate and severe episodes must be treated with antibiotics, amoxicillin/ beta-lactamase inhibitor, macrolides and fluoroquinolones are first choice drugs.

  4. A Plant Proteinase Inhibitor from Enterolobium contortisiliquum Attenuates Pulmonary Mechanics, Inflammation and Remodeling Induced by Elastase in Mice

    Science.gov (United States)

    Theodoro-Júnior, Osmar Aparecido; Righetti, Renato Fraga; Almeida-Reis, Rafael; Martins-Oliveira, Bruno Tadeu; Oliva, Leandro Vilela; Prado, Carla Máximo; Saraiva-Romanholo, Beatriz Mangueira; Leick, Edna Aparecida; Pinheiro, Nathalia Montouro; Lobo, Yara Aparecida; Martins, Mílton de Arruda; Oliva, Maria Luiza Vilela; Tibério, Iolanda de Fátima Lopes Calvo

    2017-01-01

    Proteinase inhibitors have been associated with anti-inflammatory and antioxidant activities and may represent a potential therapeutic treatment for emphysema. Our aim was to evaluate the effects of a plant Kunitz proteinase inhibitor, Enterolobium contortisiliquum trypsin inhibitor (EcTI), on several aspects of experimental elastase-induced pulmonary inflammation in mice. C57/Bl6 mice were intratracheally administered elastase (ELA) or saline (SAL) and were treated intraperitoneally with EcTI (ELA-EcTI, SAL-EcTI) on days 1, 14 and 21. On day 28, pulmonary mechanics, exhaled nitric oxide (ENO) and number leucocytes in the bronchoalveolar lavage fluid (BALF) were evaluated. Subsequently, lung immunohistochemical staining was submitted to morphometry. EcTI treatment reduced responses of the mechanical respiratory system, number of cells in the BALF, and reduced tumor necrosis factor-α (TNF-α), matrix metalloproteinase-9 (MMP-9), matrix metalloproteinase-12 (MMP-12), tissue inhibitor of matrix metalloproteinase (TIMP-1), endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS)-positive cells and volume proportion of isoprostane, collagen and elastic fibers in the airways and alveolar walls compared with the ELA group. EcTI treatment reduced elastase induced pulmonary inflammation, remodeling, oxidative stress and mechanical alterations, suggesting that this inhibitor may be a potential therapeutic tool for chronic obstructive pulmonary disease (COPD) management. PMID:28216579

  5. A Plant Proteinase Inhibitor from Enterolobium contortisiliquum Attenuates Pulmonary Mechanics, Inflammation and Remodeling Induced by Elastase in Mice.

    Science.gov (United States)

    Theodoro-Júnior, Osmar Aparecido; Righetti, Renato Fraga; Almeida-Reis, Rafael; Martins-Oliveira, Bruno Tadeu; Oliva, Leandro Vilela; Prado, Carla Máximo; Saraiva-Romanholo, Beatriz Mangueira; Leick, Edna Aparecida; Pinheiro, Nathalia Montouro; Lobo, Yara Aparecida; Martins, Mílton de Arruda; Oliva, Maria Luiza Vilela; Tibério, Iolanda de Fátima Lopes Calvo

    2017-02-14

    Proteinase inhibitors have been associated with anti-inflammatory and antioxidant activities and may represent a potential therapeutic treatment for emphysema. Our aim was to evaluate the effects of a plant Kunitz proteinase inhibitor, Enterolobium contortisiliquum trypsin inhibitor (EcTI), on several aspects of experimental elastase-induced pulmonary inflammation in mice. C57/Bl6 mice were intratracheally administered elastase (ELA) or saline (SAL) and were treated intraperitoneally with EcTI (ELA-EcTI, SAL-EcTI) on days 1, 14 and 21. On day 28, pulmonary mechanics, exhaled nitric oxide (ENO) and number leucocytes in the bronchoalveolar lavage fluid (BALF) were evaluated. Subsequently, lung immunohistochemical staining was submitted to morphometry. EcTI treatment reduced responses of the mechanical respiratory system, number of cells in the BALF, and reduced tumor necrosis factor-α (TNF-α), matrix metalloproteinase-9 (MMP-9), matrix metalloproteinase-12 (MMP-12), tissue inhibitor of matrix metalloproteinase (TIMP-1), endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS)-positive cells and volume proportion of isoprostane, collagen and elastic fibers in the airways and alveolar walls compared with the ELA group. EcTI treatment reduced elastase induced pulmonary inflammation, remodeling, oxidative stress and mechanical alterations, suggesting that this inhibitor may be a potential therapeutic tool for chronic obstructive pulmonary disease (COPD) management.

  6. Effect of early treatment with transcutaneous electrical diaphragmatic stimulation (TEDS on pulmonary inflammation induced by bleomycin

    Directory of Open Access Journals (Sweden)

    Laisa A. Santos

    2013-12-01

    Full Text Available BACKGROUND : Bleomycin (B is an antineoplastic drug that has pulmonary fibrosis as a side effect. There are few experimental studies about the effects of physical therapy treatment in this case. OBJECTIVE: The objective was to study rat lungs treated with B and precocious intervention by transcutaneous electrical diaphragmatic stimulation (TEDS. METHOD : Wistar rats were divided into 4 groups (n=5: a control group (C; a stimulated group (TEDS; a group treated with a single dose of B (intratracheally, 2.5 mg/kg (B; and a group treated with B and electric stimulation (B + TEDS. After the B instillation, the electrical stimulation was applied for 7 days, for a duration of 20 minutes. Lung fragments were histologically processed with hematoxylin and eosin (HE and 8-isoprostane-PGF2α (8-iso-PGF2α. The density of the alveolar area was determined by planimetry, the inflammatory profile was defined by the number of cells, and the level of oxidative stress in the pulmonary tissue was evaluated by 8-iso-PGF2α. For statistical analysis of the data, the Shapiro-Wilk test was used, followed by a one-way ANOVA with the post-hoc Bonferroni test (p≤0.05. RESULTS : The B group exhibited a significant reduction in the area density, and the acute treatment with B + TEDS prevented this reduction. There were increased numbers of fibroblasts, leukocytes, and macrophages in the B group, as well as increased lipid peroxidation, which was observed only in this group. CONCLUSION : B promoted a reduction in the alveolar density area, thereby inducing the inflammatory process and increasing the production of free radicals. These effects were minimized by the application of TEDS at the initial treatment stage.

  7. Neovestitol, an isoflavonoid isolated from Brazilian red propolis, reduces acute and chronic inflammation: involvement of nitric oxide and IL-6

    OpenAIRE

    Marcelo Franchin; Colón, David F.; da Cunha, Marcos G; Castanheira, Fernanda V. S.; André L. L. Saraiva; Bruno Bueno-Silva; Alencar,Severino M.; Cunha, Thiago M; Rosalen, Pedro L.

    2016-01-01

    Isoflavonoids have been largely studied due to their distinct biological activities identified thus far. Herein, we evaluated the activity of neovestitol, an isoflavonoid isolated from Brazilian red propolis, in acute and chronic inflammation. As for acute inflammation, we found that neovestitol reduced neutrophil migration, leukocyte rolling and adhesion, as well as expression of ICAM-1 in the mesenteric microcirculation during lipopolysaccharide-induced acute peritonitis. No changes were ob...

  8. Acute and Subchronic Airway Inflammation after Intratracheal Instillation of Quartz and Titanium Dioxide Agglomerates in Mice

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    Martin Roursgaard

    2011-01-01

    Full Text Available This study investigated the acute and subchronic inflammatory effects of micrometer-size (micro-size and nanometer-size (nano-size particles after intratracheal (i.t. installation in mice. The role of the type of compound, polymorphism, and size of the particles was investigated. Studied compounds were the two micro-size reference quartzes, SRM1878a and DQ12, a micro- and nano-size rutile titanium dioxide (TiO2, a nano-size anatase, and an amorphous TiO2. Particles were administered by a single i.t. instillation in mice at a fixed dose of 5, 50, and 500 μg, respectively. Inflammation was evaluated from the bronchoalveolar lavage fluid (BALF content of inflammatory cells, the cytokines tumor necrosis factor alpha (TNF-α and interleukin 6 (IL-6, as well as from lung histology. Evaluations were at 24 h (acute effects and 3 months (subchronic effects after instillations. Both types of quartz induced a dose-dependent acute increase of neutrophils, IL-6, and total protein in BALF. Limited subchronic inflammation was observed. All types of TiO2 induced a dose-dependent acute increase of neutrophils in BALF. In the acute phase, micro- and nano-size rutile and nano-size amorphous TiO2 induced elevated levels of IL-6 and total protein in BALF at the highest dose. At the nano-size rutile and amorphous TiO2, subchronic lung inflammation was apparent from a dose-dependent increase in BALF macrophages. Histology showed little inflammation overall. The two types of quartz showed virtually similar inflammatory effects. Nearly similar effects were observed for two sizes of rutile TiO2. Differences were seen between the different polymorphs of nano-size TiO2, with rutile being the most inflammogenic and amorphous being the most potent in regard to acute tissue damage.

  9. Pulmonary Specific Ancillary Treatment for Pediatric Acute Respiratory Distress Syndrome : Proceedings From the Pediatric Acute Lung Injury Consensus Conference

    NARCIS (Netherlands)

    Tamburro, Robert F.; Kneyber, Martin C. J.

    Objective: To provide an overview of the current literature on pulmonary-specific therapeutic approaches to pediatric acute respiratory distress syndrome to determine recommendations for clinical practice and/or future research. Data Sources: PubMed, EMBASE, CINAHL, SCOPUS, and the Cochrane Library

  10. Effects of acute hypercapnia with and without acidosis on lung inflammation and apoptosis in experimental acute lung injury.

    Science.gov (United States)

    Nardelli, L M; Rzezinski, A; Silva, J D; Maron-Gutierrez, T; Ornellas, D S; Henriques, I; Capelozzi, V L; Teodoro, W; Morales, M M; Silva, P L; Pelosi, P; Garcia, C S N B; Rocco, P R M

    2015-01-01

    We investigated the effects of acute hypercapnic acidosis and buffered hypercapnia on lung inflammation and apoptosis in experimental acute lung injury (ALI). Twenty-four hours after paraquat injection, 28 Wistar rats were randomized into four groups (n=7/group): (1) normocapnia (NC, PaCO2=35-45 mmHg), ventilated with 0.03%CO2+21%O2+balancedN2; (2) hypercapnic acidosis (HC, PaCO2=60-70 mmHg), ventilated with 5%CO2+21%O2+balancedN2; and (3) buffered hypercapnic acidosis (BHC), ventilated with 5%CO2+21%O2+balancedN2 and treated with sodium bicarbonate (8.4%). The remaining seven animals were not mechanically ventilated (NV). The mRNA expression of interleukin (IL)-6 (p=0.003), IL-1β (pacidosis, reduced lung inflammation and lung and kidney cell apoptosis.

  11. Severe Acute Pulmonary Toxicity Associated with Brentuximab in a Patient with Refractory Hodgkin’s Lymphoma

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    Yasmin Sabet

    2016-01-01

    Full Text Available Acute pulmonary toxicity associated with brentuximab appears to be a rare but serious adverse effect that can be potentially fatal. We report the case of a twenty-nine-year-old female with Hodgkin’s lymphoma who was treated with brentuximab and later presented with severe acute pulmonary toxicity; she improved after the discontinuation of brentuximab and administration of antibiotics and glucocorticoid therapy. Currently there is very little data in the literature in regard to the clinical manifestations and characteristics of patients taking brentuximab and the potential development of acute severe pulmonary toxicity, as well as the appropriate therapeutic approach, making this particular case of successful treatment and resolution unique.

  12. Subclavian steal syndrome presenting as recurrent pulmonary oedema associated with acute left ventricular diastolic dysfunction.

    Science.gov (United States)

    Mangialavori, Giuseppe; Ballo, Piercarlo; Michelagnoli, Stefano; Ercolini, Leonardo; Barbanti, Enrico; Passuello, Franco; Abbondanti, Alessandro; Consoli, Lorenzo; Chechi, Tania; Fibbi, Veronica; Nannini, Marco; Chiodi, Leandro; Zuppiroli, Alfredo

    2013-01-01

    Subclavian steal syndrome typically presents as angina in patients with internal mammary artery grafts. Atypical clinical presentations have been rarely described. We report an unusual case of subclavian steal syndrome presenting as pulmonary oedema with acute left ventricular diastolic dysfunction and preserved ejection fraction in a patient with internal mammary artery graft and severe stenosis of the proximal left subclavian artery. After successful angioplasty and stenting of subclavian artery, the patient remained asymptomatic for six months, but then experienced acute diastolic dysfunction and recurrent pulmonary oedema associated with critical subclavian in-stent restenosis with stent deformation. This report points out that, in patients with internal mammary-to-LAD grafts, subclavian steal syndrome may present as acute left ventricular diastolic dysfunction and pulmonary oedema even in the presence of normal ejection fraction.

  13. Acute Pulmonary Edema in an Eclamptic Pregnant Patient: A Rare Case of Takotsubo Syndrome

    Science.gov (United States)

    Karamchandani, Kunal; Bortz, Brandon; Vaida, Sonia

    2016-01-01

    Patient: Female, 35 Final Diagnosis: Takotsubo cardiomyopathy Symptoms: Seizures Medication: — Clinical Procedure: Cesarean section Specialty: Critical Care Medicine Objective: Rare co-existance of disease or pathology Background: Acute pulmonary edema in a pregnant patient is associated with significant morbidity and mortality. Takotsubo syndrome, or stress-induced cardiomyopathy, is a rare cause of acute pulmonary edema in a pregnant patient, especially prior to delivery of the fetus. Case Report: We describe a case of a pregnant patient who presented with acute pulmonary edema and eclampsia and was found to have Takotsubo syndrome. To the best of our knowledge, eclampsia as a precipitating factor for Takotsubo syndrome has not been described in literature. Conclusions: Clinicians taking care of pregnant patients should be aware of the potential link between eclampsia and Takotsubo cardiomyopathy. Prompt correction of the precipitating cause along with supportive management as described is the key to a successful outcome. PMID:27658947

  14. Acute Pulmonary Edema in an Eclamptic Pregnant Patient: A Rare Case of Takotsubo Syndrome.

    Science.gov (United States)

    Karamchandani, Kunal; Bortz, Brandon; Vaida, Sonia

    2016-09-23

    BACKGROUND Acute pulmonary edema in a pregnant patient is associated with significant morbidity and mortality. Takotsubo syndrome, or stress-induced cardiomyopathy, is a rare cause of acute pulmonary edema in a pregnant patient, especially prior to delivery of the fetus. CASE REPORT We describe a case of a pregnant patient who presented with acute pulmonary edema and eclampsia and was found to have Takotsubo syndrome. To the best of our knowledge, eclampsia as a precipitating factor for Takotsubo syndrome has not been described in literature. CONCLUSIONS Clinicians taking care of pregnant patients should be aware of the potential link between eclampsia and Takotsubo cardiomyopathy. Prompt correction of the precipitating cause along with supportive management as described is the key to a successful outcome.

  15. Chronic allergic inflammation causes vascular remodeling and pulmonary hypertension in BMPR2 hypomorph and wild-type mice.

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    Elizabeth M Mushaben

    Full Text Available Loss-of-function mutations in the bone morphogenetic protein receptor type 2 (BMPR2 gene have been identified in patients with heritable pulmonary arterial hypertension (PAH; however, disease penetrance is low, suggesting additional factors play a role. Inflammation is associated with PAH and vascular remodeling, but whether allergic inflammation triggers vascular remodeling in individuals with BMPR2 mutations is unknown. Our goal was to determine if chronic allergic inflammation would induce more severe vascular remodeling and PAH in mice with reduced BMPR-II signaling. Groups of Bmpr2 hypomorph and wild-type (WT Balb/c/Byj mice were exposed to house dust mite (HDM allergen, intranasally for 7 or 20 weeks to generate a model of chronic inflammation. HDM exposure induced similar inflammatory cell counts in all groups compared to controls. Muscularization of pulmonary arterioles and arterial wall thickness were increased after 7 weeks HDM, more severe at 20 weeks, but similar in both groups. Right ventricular systolic pressure (RVSP was measured by direct cardiac catheterization to assess PAH. RVSP was similarly increased in both HDM exposed groups after 20 weeks compared to controls, but not after 7 weeks. Airway hyperreactivity (AHR to methacholine was also assessed and interestingly, at 20 weeks, was more severe in HDM exposed Bmpr2 hypomorph mice versus WT. We conclude that chronic allergic inflammation caused PAH and while the severity was mild and similar between WT and Bmpr2 hypomorph mice, AHR was enhanced with reduced BMPR-II signaling. These data suggest that vascular remodeling and PAH resulting from chronic allergic inflammation occurs independently of BMPR-II pathway alterations.

  16. Pulmonary Complications of Azanucleoside Therapy in Patients with Myelodysplastic Syndrome and Acute Myelogenous Leukemia

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    Manuel Molina

    2015-01-01

    Full Text Available Our primary aim was to identify potential risk factors and clinical outcome of azanucleoside induced pulmonary complications in patients with myelodysplastic syndrome (MDS and Acute Myelogenous Leukemia (AML. We present an 89-year-old female with MDS derived AML who developed fatigability, hypoxemia, and bilateral lung infiltrates indicating interstitial lung disease after 11 cycles of azanucleoside. In addition, we describe a cohort of six MDS patients with fever, cough, dyspnea, and pulmonary infiltrates at early time point during azanucleoside treatment. Early and late onset of pulmonary manifestations suggest different pathogenic mechanisms. Brief azanucleoside discontinuation and steroids led to rapid improvement in symptoms.

  17. Epithelial sodium channel is involved in H2S-induced acute pulmonary edema.

    Science.gov (United States)

    Jiang, Lei; Wang, Yixin; Su, Chenglei; Sun, Hao; Zhang, Huazhong; Zhu, Baoli; Zhang, Hengdong; Xiao, Hang; Wang, Jun; Zhang, Jinsong

    2015-01-01

    Acute pulmonary edema is one of the major outcomes of exposure to high levels of hydrogen sulfide (H2S). However, the mechanisms involved in H2S-induced acute pulmonary edema are still poorly understood. Therefore, the present study is designed to evaluate the role of epithelial sodium channel (ENaC) in H2S-induced acute pulmonary edema. The Sprague-Dawley rats were exposed to sublethal concentrations of inhaled H2S, then the pulmonary histological and lung epithelial cell injury were evaluated by hematoxylin-eosin staining and electron microscopy, respectively. In addition to morphological investigation, our results also revealed that H2S exposure significantly decreased the alveolar fluid clearance and increased the lung tissue wet-dry ratio. These changes were demonstrated to be associated with decreased ENaC expression. Furthermore, the extracellular-regulated protein kinases 1/2 pathway was demonstrated to be implicated in H2S-mediated ENaC expression, because PD98059, an ERK1/2 antagonist, significantly mitigated H2S-mediated ENaC down-regulation. Therefore, our results show that ENaC might represent a novel pharmacological target for the treatment of acute pulmonary edema induced by H2S and other hazardous gases.

  18. Oxidative stress, inflammation, and DNA damage in multiple organs of mice acutely exposed to amorphous silica nanoparticles

    Directory of Open Access Journals (Sweden)

    Nemmar A

    2016-03-01

    Full Text Available Abderrahim Nemmar,1 Priya Yuvaraju,1 Sumaya Beegam,1 Javed Yasin,2 Elsadig E Kazzam,2 Badreldin H Ali3 1Department of Physiology, 2Department of Internal Medicine, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain, UAE; 3Department of Pharmacology, College of Medicine and Health Sciences, Sultan Qaboos University, Muscat, Al-Khoudh, Sultanate of Oman Abstract: The use of amorphous silica (SiO2 in biopharmaceutical and industrial fields can lead to human exposure by injection, skin penetration, ingestion, or inhalation. However, the in vivo acute toxicity of amorphous SiO2 nanoparticles (SiNPs on multiple organs and the mechanisms underlying these effects are not well understood. Presently, we investigated the acute (24 hours effects of intraperitoneally administered 50 nm SiNPs (0.25 mg/kg on systemic toxicity, oxidative stress, inflammation, and DNA damage in the lung, heart, liver, kidney, and brain of mice. Lipid peroxidation was significantly increased by SiNPs in the lung, liver, kidney, and brain, but was not changed in the heart. Similarly, superoxide dismutase and catalase activities were significantly affected by SiNPs in all organs studied. While the concentration of tumor necrosis factor α was insignificantly increased in the liver and brain, its increase was statistically significant in the lung, heart, and kidney. SiNPs induced a significant elevation in pulmonary and renal interleukin 6 and interleukin-1 beta in the lung, liver, and brain. Moreover, SiNPs caused a significant increase in DNA damage, assessed by comet assay, in all the organs studied. SiNPs caused leukocytosis and increased the plasma activities of lactate dehydrogenase, creatine kinase, alanine aminotranferase, and aspartate aminotransferase. These results indicate that acute systemic exposure to SiNPs causes oxidative stress, inflammation, and DNA damage in several major organs, and highlight the need for thorough evaluation

  19. Reducing LPS content in cockroach allergens increases pulmonary cytokine production without increasing inflammation: A randomized laboratory study

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    Cruikshank William

    2011-02-01

    Full Text Available Abstract Background Endotoxins are ubiquitously present in the environment and constitute a significant component of ambient air. These substances have been shown to modulate the allergic response, however a consensus has yet to be reached whether they attenuate or exacerbate asthmatic responses. The current investigation examined whether reducing the concentration of lipopolysaccharide (LPS in a house dust extract (HDE containing high concentrations of both cockroach allergens 1 and LPS would attenuate asthma-like pulmonary inflammation. Methods Mice were sensitized with CRA and challenged with the intact HDE, containing 182 ng of LPS, or an LPS-reduced HDE containing 3 ng LPS, but an equivalent amount of CRA. Multiple parameters of asthma-like pulmonary inflammation were measured. Results Compared to HDE challenged mice, the LPS-reduced HDE challenged mice had significantly reduced TNFα levels in the bronchoalveolar lavage fluid. Plasma levels of IgE and IgG1 were significantly reduced, however no change in CRA-specific IgE was detected. In HDE mice, plasma IgG2a levels were similar to naïve mice, while LPS-reduced HDE mice had significantly greater concentrations. Reduced levels of LPS in the HDE did not decrease eosinophil or neutrophil recruitment into the alveolar space. Equivalent inflammatory cell recruitment occurred despite having generally higher pulmonary concentrations of eotaxins and CXC chemokines in the LPS-reduced HDE group. LPS-reduced HDE challenge induced significantly higher concentrations of IFNγ, and IL-5 and IL-13 in the BAL fluid, but did not decrease airways hyperresponsiveness or airway resistance to methacholine challenge. Conclusion: These data show that reduction of LPS levels in the HDE does not significantly protect against the severity of asthma-like pulmonary inflammation.

  20. Pulmonary hydatid cyst in a pregnant patient causing acute respiratory failure

    Directory of Open Access Journals (Sweden)

    Hijazi Mohammed

    2007-01-01

    Full Text Available A 21-year-old primigravida, at 32 weeks of gestation, presented with acute onset of respiratory failure and circulatory shock. Chest imaging showed findings suggestive of ruptured hydatid cyst, which was confirmed by histology post-thoracotomy. Tissue cultures from the removed cyst grew Mycobacterium tuberculosis also. She was successfully managed in the intensive care unit and was then discharged home on antituberculosis medications in addition to albendazole after prolonged hospitalization and a need for chest tube for bronchopleural fistula. Acute respiratory failure and anaphylactic shock secondary to ruptured pulmonary hydatid cyst and superimposed pulmonary tuberculosis in a pregnant lady should be considered in patients living in endemic areas.

  1. How inflammation underlies physical and organ function in acutely admitted older medical patients

    DEFF Research Database (Denmark)

    Klausen, Henrik Hedegaard; Bodilsen, Ann Christine; Petersen, Janne

    2017-01-01

    OBJECTIVES: To investigate whether systemic inflammation in acutely admitted older medical patients (age >65 years) is associated with physical performance and organ dysfunction. Organ dysfunction´s association with physical performance, and whether these associations are mediated by systemic...... inflammation, was also investigated. METHODS: A cross-sectional study in an Emergency Department. Physical performance was assessed by handgrip strength and de Morton Mobility Index (DEMMI), and organ dysfunction by FI-OutRef, the number of standard blood tests outside the reference range. Systemic...... physical performance measures (pphysical performance (all p

  2. Radiolucency below the crown of mandibular horizontal incompletely impacted third molars and acute inflammation in men with diabetes

    Science.gov (United States)

    Yamaoka, Minoru; Ono, Yusuke; Ishizuka, Masahide; Yasuda, Kouichi; Uematsu, Takashi; Furusawa, Kiyofumi

    2009-01-01

    Although mandibular third molar has a high risk of infection extending any complications, the influence of diabetes on radiolucency and acute inflammation in pericoronitis remains unclear. The present study was to evaluate whether radiolucency below the crown is related to acute inflammation in mandibular horizontal incompletely impacted third molars and to review the records of 140 men more than 45 years with and without diabetes. The odds ratio of exhibiting acute inflammation was 3.38 (95% CI: 1.13–10.16, p pericoronitis in diabetes. The frequency of radiolucency below the crown and below the root in diabetics was similar to that in nondiabetics. However, the odds ratio of exhibiting both radiolucency below the crown and acute inflammation under the diabetic condition was 4.85 (95% CI: 1.60–14.73, p pericoronitis, whereas the periodontium shows a protective effect against acute pericoronitis. PMID:23674902

  3. Coronary Artery Calcification Is Often Unreported in CT Pulmonary Angiograms in Patients With Suspected Pulmonary Embolism: An Opportunity to Improve Diagnosis of Acute Coronary Syndrome

    OpenAIRE

    Johnson, Patrick Connor

    2015-01-01

    Objective: In patients with suspected pulmonary thromboembolism (PTE), coronary artery calcification (CAC) can be an incidental finding in CT pulmonary angiograms. We evaluated the frequency of unreported CAC and its association with diagnosis of acute coronary syndrome (ACS). Methods: The data of 469 consecutive patients who were referred to the emergency radiology department for CT pulmonary angiography because of suspicion for PTE were reviewed. Radiology reports were rechecked, and pos...

  4. Use of non-invasive ventilation in acute pulmonary edema and chronic obstructive pulmonary disease exacerbation in emergency medicine: predictors of failure.

    Science.gov (United States)

    Passarini, Juliana Nalin de Souza; Zambon, Lair; Morcillo, André Moreno; Kosour, Carolina; Saad, Ivete Alonso Bredda

    2012-09-01

    This study analyzed acute respiratory failure caused by acute pulmonary edema, as well as chronic obstructive pulmonary disease exacerbation, that was treated with non-invasive mechanical ventilation to identify the factors that are associated with the success or failure non-invasive mechanical ventilation in urgent and emergency service. This study was a prospective, descriptive and analytical study. We included patients of both genders aged >18 years who used non-invasive mechanical ventilation due to acute respiratory failure that was secondary to acute pulmonary edema or chronic obstructive pulmonary disease exacerbation. Patients with acute respiratory failure that was secondary to pathologies other than acute pulmonary edema and chronic obstructive pulmonary disease or who presented with contraindications for the technique were excluded. Expiratory pressures between 5 and 8 cmH2O and inspiratory pressures between 10 and 12 cmH2O were used. Supplemental oxygen maintained peripheral oxygen saturation at >90%. The primary outcome was endotracheal intubation. A total of 152 patients were included. The median non-invasive mechanical ventilation time was 6 hours (range 1 - 32 hours) for chronic obstructive pulmonary disease patients (n=60) and 5 hours (range 2 - 32 hours) for acute pulmonary edema patients (n=92). Most (75.7%) patients progressed successfully. However, reduced APACHE II scores and lower peripheral oxygen saturation were observed. These results were statistically significant in patients who progressed to intubation (pendotracheal intubation 2.3 times (p=0.032). Patients with acute pulmonary edema and elevated GCS scores also increased the probability of success. Respiratory frequency >25 rpm, higher APACHE II scores, BiPAP use and chronic obstructive pulmonary disease diagnosis were associated with endotracheal intubation. Higher GCS and SpO2 values were associated with NIV success. Non-invasive mechanical ventilation can be used in emergency

  5. Anti-inflammatory activity of Justicia prostrata gamble in acute and sub-acute models of inflammation.

    Science.gov (United States)

    Sanmugapriya, E; Shanmugasundaram, P; Venkataraman, S

    2005-01-01

    In this study, the aqueous (AQJP) and alcoholic (ALJP) extracts of the whole plant of Justicia prostrata Gamble (Acanthaceae) were screened for their acute and subacute anti-inflammatory activities using carrageenan-induced acute inflammation and cotton-pellet-induced granuloma (subacute inflammation), respectively, in rats. In the carrageenan-induced rat paw oedema model, both extracts were found to exhibit maximum reduction in paw volume at the first hour in a dose-dependent manner. At the dose of 500 mg/kg p.o., both extracts AQJP and ALJP showed maximum inhibition (51.39% and 62.5%, respectively) in rat paw oedema volume at the first hour of carrageenan-induced acute inflammation. In the cotton pellet granuloma assay, AQJP and ALJP at the dose of 500 mg/kg p.o. suppressed the transudative, exudative and proliferative phases of chronic inflammation. These extracts were able to (i) reduce the lipid peroxide content of exudates and liver and (ii) normalize the increased activity of acid and alkaline phosphatases in serum and liver of cotton pellet granulomatous rats. Preliminary phytochemical screening revealed the presence of lignans, triterpenes and phenolic compounds in ALJP, whereas phenolic compounds and glycosides in AQJP. The anti-inflammatory properties of these extracts may possibly be due to the presence of phenolic compounds. The anti-inflammatory effects produced by the extracts at the dose of 500 mg/kg, p.o. was comparable with the reference drug diclofenac sodium (5 mg/kg p.o.).

  6. Update on the Mechanisms of Pulmonary Inflammation and Oxidative Imbalance Induced by Exercise

    Directory of Open Access Journals (Sweden)

    O. F. Araneda

    2016-01-01

    Full Text Available The mechanisms involved in the generation of oxidative damage and lung inflammation induced by physical exercise are described. Changes in lung function induced by exercise involve cooling of the airways, fluid evaporation of the epithelial surface, increased contact with polluting substances, and activation of the local and systemic inflammatory response. The present work includes evidence obtained from the different types of exercise in terms of duration and intensity, the effect of both acute performance and chronic performance, and the influence of special conditions such as cold weather, high altitude, and polluted environments. Levels of prooxidants, antioxidants, oxidative damage to biomolecules, and cellularity, as well as levels of soluble mediators of the inflammatory response and its effects on tissues, are described in samples of lung origin. These samples include tissue homogenates, induced sputum, bronchoalveolar lavage fluid, biopsies, and exhaled breath condensate obtained in experimental protocols conducted on animal and human models. Finally, the need to simultaneously explore the oxidative/inflammatory parameters to establish the interrelation between them is highlighted.

  7. Critically ill patients with acute cholecystitis are at increased risk for extensive gallbladder inflammation.

    Science.gov (United States)

    Papadakis, Marios; Ambe, Peter C; Zirngibl, Hubert

    2015-01-01

    Acute cholecystitis is a common diagnosis and surgery is the standard of care for young and fit patients. However, due to high risk of postoperative morbidity and mortality, surgical management of critically ill patients remains a controversy. It is not clear, whether the increased risk of perioperative complications associated with the management of critically ill patients with acute cholecystitis is secondary to reduced physiologic reserve per se or to the severity of gallbladder inflammation. A retrospective analysis of prospectively collected data of patients undergoing laparoscopic cholecystectomy for acute cholecystitis in a university hospital over a three-year-period was performed. The ASA scores at the time of presentation were used to categorize patients into two groups. The study group consisted of critically ill patients with ASA 3 and 4, while the control group was made up of fit patients with ASA 1 and 2. Both groups were compared with regard to perioperative data, postoperative outcome and extent of gallbladder inflammation on histopathology. Two hundred and seventeen cases of acute cholecystitis with complete charts were available for analysis. The study group included 67 critically ill patients with ASA 3 and 4, while the control group included 150 fit patients with ASA 1 and 2. Both groups were comparable with regard to perioperative data. Histopathology confirmed severe cholecystitis in a significant number of cases in the study group compared to the control group (37 % vs. 18 %, p = 0.03). Significantly higher rates of morbidity and mortality were recorded in the study group (p < 0.05). Equally, significantly more patients from the study group were managed in the ICU (40 % vs. 8 %, p = 0.001). Critically ill patients presenting with acute cholecystitis are at increased risk for extensive gallbladder inflammation. The increased risk of morbidity and mortality seen in such patients might partly be secondary to severe acute

  8. Quantification of right ventricular function in acute pulmonary embolism: relation to extent of pulmonary perfusion defects

    DEFF Research Database (Denmark)

    Kjaergaard, J.; Schaadt, B.K.; Lund, J.O.;

    2008-01-01

    and regional RV dysfunction in 58 consecutive patients with non-massive PE. Methods and results Patients were compared with 58 age-matched controls that had normal ventilation/perfusion scintigraphies. A 2D, Doppler and Tissue Doppler echocardiography performed on the same day, quantified RV pressure...... and global and regional performance. Intermediate and large pulmonary emboli were associated with a significant impact on RV pressure and function. For small pulmonary emboli obstructing

  9. Pro-Resolving lipid mediators and Mechanisms in the resolution of acute inflammation

    Science.gov (United States)

    Buckley, Christopher D.; Gilroy, Derek W.; Serhan, Charles N.

    2014-01-01

    SUMMARY Inflammatory responses, like all biological cascades, are shaped by a delicate balance between positive and negative feedback loops. It is now clear that in addition to positive and negative checkpoints, the inflammatory cascade rather unexpectedly boasts an additional checkpoint, a family of chemicals that actively promote resolution and tissue repair without compromising host defence. Indeed the resolution phase of inflammation is just as actively orchestrated and carefully choreographed as its induction and inhibition. In this review we explore the immunological consequences of these omega-3-derived specialized pro-resolving mediators (SPMs) and discuss their place within what is currently understood of the role of the arachidonic acid-derived prostaglandins, lipoxins and their natural C15-epimers. We propose that treatment of inflammation should not be restricted to the use of inhibitors of the acute cascade (antagonism) but broadened to take account of the enormous therapeutic potential of inducers (agonists) of the resolution phase of inflammation. PMID:24656045

  10. TRPA1 channels mediate acute neurogenic inflammation and pain produced by bacterial endotoxins

    Science.gov (United States)

    Meseguer, Victor; Alpizar, Yeranddy A.; Luis, Enoch; Tajada, Sendoa; Denlinger, Bristol; Fajardo, Otto; Manenschijn, Jan-Albert; Fernández-Peña, Carlos; Talavera, Arturo; Kichko, Tatiana; Navia, Belén; Sánchez, Alicia; Señarís, Rosa; Reeh, Peter; Pérez-García, María Teresa; López-López, José Ramón; Voets, Thomas; Belmonte, Carlos; Talavera, Karel; Viana, Félix

    2014-01-01

    Gram-negative bacterial infections are accompanied by inflammation and somatic or visceral pain. These symptoms are generally attributed to sensitization of nociceptors by inflammatory mediators released by immune cells. Nociceptor sensitization during inflammation occurs through activation of the Toll-like receptor 4 (TLR4) signalling pathway by lipopolysaccharide (LPS), a toxic by-product of bacterial lysis. Here we show that LPS exerts fast, membrane delimited, excitatory actions via TRPA1, a transient receptor potential cation channel that is critical for transducing environmental irritant stimuli into nociceptor activity. Moreover, we find that pain and acute vascular reactions, including neurogenic inflammation (CGRP release) caused by LPS are primarily dependent on TRPA1 channel activation in nociceptive sensory neurons, and develop independently of TLR4 activation. The identification of TRPA1 as a molecular determinant of direct LPS effects on nociceptors offers new insights into the pathogenesis of pain and neurovascular responses during bacterial infections and opens novel avenues for their treatment.

  11. An interesting cause of pulmonary emboli: Acute carbon monoxide poisoning

    Energy Technology Data Exchange (ETDEWEB)

    Sevinc, A.; Savli, H.; Atmaca, H. [Gaziantep University, Gaziantep (Turkey). School of Medicine

    2005-07-01

    Carbon monoxide poisoning, a public health problem of considerable significance, is a relatively frequent event today, resulting in thousands of hospitalizations annually. A 70-year-old lady was seen in the emergency department with a provisional diagnosis of carbon monoxide poisoning. The previous night, she slept in a tightly closed room heated with coal ember. She was found unconscious in the morning with poor ventilation. She had a rare presentation of popliteal vein thrombosis, pulmonary emboli, and possible tissue necrosis with carbon monoxide poisoning. Oxygen treatment with low-molecular-weight heparin (nadroparine) and warfarin therapy resulted in an improvement in both popliteal and pulmonary circulations. In conclusion, the presence of pulmonary emboli should be sought in patients with carbon monoxide poisoning.

  12. Oxidative stress–induced mitochondrial dysfunction drives inflammation and airway smooth muscle remodeling in patients with chronic obstructive pulmonary disease

    Science.gov (United States)

    Wiegman, Coen H.; Michaeloudes, Charalambos; Haji, Gulammehdi; Narang, Priyanka; Clarke, Colin J.; Russell, Kirsty E.; Bao, Wuping; Pavlidis, Stelios; Barnes, Peter J.; Kanerva, Justin; Bittner, Anton; Rao, Navin; Murphy, Michael P.; Kirkham, Paul A.; Chung, Kian Fan; Adcock, Ian M.; Brightling, Christopher E.; Davies, Donna E.; Finch, Donna K.; Fisher, Andrew J.; Gaw, Alasdair; Knox, Alan J.; Mayer, Ruth J.; Polkey, Michael; Salmon, Michael; Singh, David

    2015-01-01

    Background Inflammation and oxidative stress play critical roles in patients with chronic obstructive pulmonary disease (COPD). Mitochondrial oxidative stress might be involved in driving the oxidative stress–induced pathology. Objective We sought to determine the effects of oxidative stress on mitochondrial function in the pathophysiology of airway inflammation in ozone-exposed mice and human airway smooth muscle (ASM) cells. Methods Mice were exposed to ozone, and lung inflammation, airway hyperresponsiveness (AHR), and mitochondrial function were determined. Human ASM cells were isolated from bronchial biopsy specimens from healthy subjects, smokers, and patients with COPD. Inflammation and mitochondrial function in mice and human ASM cells were measured with and without the presence of the mitochondria-targeted antioxidant MitoQ. Results Mice exposed to ozone, a source of oxidative stress, had lung inflammation and AHR associated with mitochondrial dysfunction and reflected by decreased mitochondrial membrane potential (ΔΨm), increased mitochondrial oxidative stress, and reduced mitochondrial complex I, III, and V expression. Reversal of mitochondrial dysfunction by the mitochondria-targeted antioxidant MitoQ reduced inflammation and AHR. ASM cells from patients with COPD have reduced ΔΨm, adenosine triphosphate content, complex expression, basal and maximum respiration levels, and respiratory reserve capacity compared with those from healthy control subjects, whereas mitochondrial reactive oxygen species (ROS) levels were increased. Healthy smokers were intermediate between healthy nonsmokers and patients with COPD. Hydrogen peroxide induced mitochondrial dysfunction in ASM cells from healthy subjects. MitoQ and Tiron inhibited TGF-β–induced ASM cell proliferation and CXCL8 release. Conclusions Mitochondrial dysfunction in patients with COPD is associated with excessive mitochondrial ROS levels, which contribute to enhanced inflammation and cell

  13. The antioxidant tempol decreases acute pulmonary thromboembolism-induced hemolysis and nitric oxide consumption.

    Science.gov (United States)

    Sousa-Santos, Ozelia; Neto-Neves, Evandro M; Ferraz, Karina C; Sertório, Jonas T; Portella, Rafael L; Tanus-Santos, Jose E

    2013-11-01

    Acute pulmonary thromboembolism (APT) is a critical condition associated with acute pulmonary hypertension. Recent studies suggest that oxidative stress and hemolysis contribute to APT-induced pulmonary hypertension, possibly as a result of increased nitric oxide (NO) consumption. We hypothesized that the antioxidant tempol could attenuate APT-induced hemolysis, and therefore attenuate APT-induced increases in plasma NO consumption. APT was induced in anesthetized sheep with autologous blood clots. The hemodynamic effects of tempol infused at 1.0mg/kg/min 30 min after APT were determined. Hemodynamic measurements were carried out every 15 min. To assess oxidative stress, serum 8-isoprostanes levels were measured by ELISA. Plasma cell-free hemoglobin concentrations and NO consumption by plasma samples were determined. An in vitro oxidative AAPH-induced hemolysis assay was used to further validate the in vivo effects of tempol. APT caused pulmonary hypertension, and increased pulmonary vascular resistance in proportion with the increases in 8-isoprostanes, plasma cell-free hemoglobin concentrations, and NO consumption by plasma (all Phemolysis (Phemolysis and nitric oxide consumption, thus attenuating APT-induced pulmonary hypertension. © 2013.

  14. Clinical effects of clarithromycin on persistent inflammation following Haemophilus influenzae-positive acute otitis media.

    Science.gov (United States)

    Iino, Yukiko; Yoshida, Naohiro; Kato, Toshinori; Kakizaki, Keiko; Miyazawa, Tetsuo; Kakuta, Hiroyuki

    2015-03-01

    Additional treatment with clarithromycin (CAM) reduced persistent middle ear inflammation after acute otitis media (AOM) caused by Haemophilus influenzae in children. CAM is a treatment option for persistent inflammation following AOM and to prevent continuing otitis media with effusion. We conducted a clinical study to evaluate a new method of treatment for persistent inflammation after AOM in children. H. influenzae-infected children with AOM were treated acutely with antimicrobial agents, after which those still demonstrating effusion of the middle ear cavity received additional treatment with carbocysteine (S-CMC) alone or S-CMC combined with clarithromycin (CAM) for 1 week. The two regimens were compared in terms of clinical effects. After the initial acute treatment, many patients still showed abnormal otoscopic findings. At the completion of additional treatment, there were no significant differences between the two treatment groups. However, 1 week after completion of additional treatment, the prevalence of a diminished light reflex was significantly lower in the CAM + S-CMC group than in the S-CMC group (p = 0.017). The prevalence of redness of the tympanic membrane also tended to be lower in the combined treatment group than in those receiving a single drug (p = 0.097).

  15. Guidance Cue Netrin-1 and the Regulation of Inflammation in Acute and Chronic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Punithavathi Ranganathan

    2014-01-01

    Full Text Available Acute kidney injury (AKI is a common problem in the hospital setting and intensive care unit. Despite improved understanding, there are no effective therapies available to treat AKI. A large body of evidence strongly suggests that ischemia reperfusion injury is an inflammatory disease mediated by both adaptive and innate immune systems. Cell migration also plays an important role in embryonic development and inflammation, and this process is highly regulated to ensure tissue homeostasis. One such paradigm exists in the developing nervous system, where neuronal migration is mediated by a balance between chemoattractive and chemorepulsive signals. The ability of the guidance molecule netrin-1 to repulse or abolish attraction of neuronal cells expressing the UNC5B receptor makes it an attractive candidate for the regulation of inflammatory cell migration. Recent identification of netrin-1 as regulators of immune cell migration has led to a large number of studies looking into how netrin-1 controls inflammation and inflammatory cell migration. This review will focus on recent advances in understanding netrin-1 mediated regulation of inflammation during acute and chronic kidney disease and whether netrin-1 and its receptor activation can be used to treat acute and chronic kidney disease.

  16. [Cardiogenic pulmonary edema following β2 agonist infusion for acute, severe asthma].

    Science.gov (United States)

    Bahloul, M; Chaari, A; Dammak, H; Medhioub, F; Abid, L; Chtourou, K; Rekik, N; Chelly, H; Kallel, H; Bouaziz, M

    2015-09-01

    We report the case of a severe acute pulmonary edema secondary to the administration of salbutamol to a patient admitted for severe asthma. The diagnosis of acute pulmonary edema was suspected on the clinical examination, chest radiography, biological (plasmatic Pro-BNP rate) and echocardiographic findings. Rapid improvement under dobutamine and mechanical ventilation argue in favour of cardiogenic pulmonary edema. The young age of our patient, the absence of history of cardiovascular disease and the chronology of this complication onset regarded to salbutamol infusion could suggest β2 agonist involvement in this event. The improvement of cardiac function on echocardiography and the normal results obtained with myocardial perfusion scintigraphy performed 35 days later show the left ventricular reversible dysfunction.

  17. Sporadic multicentric right atrial and right ventricular myxoma presenting as acute pulmonary thromboembolism

    Directory of Open Access Journals (Sweden)

    Satyajit Singh

    2016-01-01

    Full Text Available Multicentric cardiac myxoma is a rare syndrome; usually it is familial. We report a rare case of sporadic right atrium (RA and right ventricle (RV myxoma in a 26-year-old female presenting to our hospital for the evaluation of sudden onset of dyspnea and left precordial pain attributed to the embolization of degenerating tumor fragments to the pulmonary artery (PA. The exact incidence of sporadic multicentric RA and RV myxoma presenting as acute pulmonary embolism is unknown as multicentric RA and RV myxoma are very rare. Myxomas presenting as pulmonary embolism is <10%. Majority of cardiac myxomas present as exertional dyspnea, chest pain, positional syncope, fever, weight loss and other constitutional symptoms. Any young patient presenting with acute onset dyspnea with multiple cardiac masses may have tumor embolization to the PA diagnosis with transthoracic echocardiography and high-resolution computed tomography of thorax, fast-tracks patient transfer for urgent cardiac surgery to prevent further embolization.

  18. Low level of residual thrombotic obstruction following 6 months of anticoagulant treatment for acute pulmonary embolism

    NARCIS (Netherlands)

    Den Exter, P.L.; Van Es, J.; Kroft, L.J.M.; Erkens, P.G.M.; Douma, Renee; Jonkers, G.; Ten Cate, H.; Beenen, L.; Kamphuisen, P.W.; Huisman, M.V.

    2013-01-01

    Background: In patients with acute pulmonary embolism (PE), systematic assessment of residual thrombotic obstruction after long-term anticoagulation has been understudied. This information may be of clinical importance for diagnostic baseline imaging, in case of clinically suspected recurrent PE or

  19. Low level of residual thrombotic obstruction following 6 months of anticoagulant treatment for acute pulmonary embolism

    NARCIS (Netherlands)

    Den Exter, P.L.; Van Es, J.; Kroft, L.J.M.; Erkens, P.G.M.; Douma, Renee; Jonkers, G.; Ten Cate, H.; Beenen, L.; Kamphuisen, P.W.; Huisman, M.V.

    Background: In patients with acute pulmonary embolism (PE), systematic assessment of residual thrombotic obstruction after long-term anticoagulation has been understudied. This information may be of clinical importance for diagnostic baseline imaging, in case of clinically suspected recurrent PE or

  20. Acute exacerbations of chronic obstructive pulmonary disease provide a unique opportunity to take care of patients

    Directory of Open Access Journals (Sweden)

    Bianca Beghé

    2013-04-01

    Full Text Available Exacerbation of chronic obstructive pulmonary disease (ECOPD identifies the acute phase of COPD. The COPD patient is often frail and elderly with concomitant chronic diseases. This requires the physician not only looks at specific symptoms or organs, but to consider the patient in all his or her complexity.

  1. Thickening of the pulmonary artery wall in acute intramural hematoma of the ascending aorta

    Directory of Open Access Journals (Sweden)

    Lardani Héctor

    2007-01-01

    Full Text Available Abstract Background The occurrence of pulmonary artery obstruction in the course of acute aortic dissection is an unusual complication. The mechanism implicated is the rupture of the outer layer of the aorta and the subsequent hemorrhage into the adventitia of the pulmonary artery that causes its wall thickening and, at times, produces extrinsic obstruction of the vessel. There are no reports of this complication in acute intramural hematoma. Case presentation An 87-year-old woman was admitted to the hospital in shock after having had severe chest pain followed by syncope. An urgent transesophageal echocardiogram revealed the presence of acute intramural hematoma, no evidence of aortic dissection, severe pericardial effusion with cardiac tamponade, and periaortic hematoma that involved the pulmonary artery generating circumferential wall thickening of its trunk and right branch with no evidence of flow obstruction. Urgent surgery was performed but the patient died in the operating room. The post mortem examination, in the operating room, confirmed that there was an extensive hematoma around the aorta and beneath the adventitial layer of the pulmonary artery, with no evidence of flow obstruction. Conclusion This is the first time that this rare complication is reported in the scenario of acute intramural hematoma and with the transesophageal echocardiogram as the diagnostic tool.

  2. Bacteriology in acute exacerbation of chronic obstructive pulmonary disease in patients admitted to hospital

    DEFF Research Database (Denmark)

    Larsen, Mette V; Janner, Julie H; Nielsen, Susanne D

    2009-01-01

    We investigated the bacterial flora and antimicrobial sensitivity in sputum from patients admitted to hospital with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) in order to recommend the best empirical treatment for these patients. The survey was a retrospective study of all....... pneumonia, mostly H. influenzae and Moraxella catarrhalis. Patients with low FEV(1)resistant to penicillin. If antibiotics are initiated empirically...

  3. Acute effects of riociguat in borderline or manifest pulmonary hypertension associated with chronic obstructive pulmonary disease.

    Science.gov (United States)

    Ghofrani, Hossein A; Staehler, Gerd; Grünig, Ekkehard; Halank, Michael; Mitrovic, Veselin; Unger, Sigrun; Mueck, Wolfgang; Frey, Reiner; Grimminger, Friedrich; Schermuly, Ralph T; Behr, Juergen

    2015-06-01

    Riociguat is the first oral soluble guanylate cyclase stimulator shown to improve pulmonary hemodynamics in patients with pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension (PH). This pilot study assessed the impact of a single dose of riociguat on hemodynamics, gas exchange, and lung function in patients with PH associated with chronic obstructive pulmonary disease (COPD). Adults with COPD-associated borderline or manifest PH (pulmonary vascular resistance > 270 dyn·s·cm(-5), mean pulmonary artery pressure ≥ 23 mmHg, ratio of forced expiratory volume in 1 second [FEV1] to forced vital capacity 70%, and partial pressure of oxygen and carbon dioxide in arterial blood > 50 and ≤ 55 mmHg, respectively) received riociguat 1 or 2.5 mg during right heart catheterization. Twenty-two patients completed the study (11 men, 11 women, aged 56-82 years; 1-mg group: n = 10 [mean FEV1: 43.1%]; 2.5-mg group: n = 12 [mean FEV1: 41.2%]). Riociguat caused significant improvements (P mmHg [-11.44%]; 2.5 mg: -4.83 mmHg [-14.76%]) and pulmonary vascular resistance (1 mg: -58.32 dyn·s·cm(-5) [-15.35%]; 2.5 mg: -123.8 dyn·s·cm(-5) [-32.96%]). No relevant changes in lung function or gas exchange were observed. Single doses of riociguat were well tolerated and showed promising hemodynamic effects without untoward effects on gas exchange or lung function in patients with COPD-associated PH. Placebo-controlled studies of chronic treatment with riociguat are warranted.

  4. Pulmonary mucormycosis with embolism: two autopsied cases of acute myeloid leukemia.

    Science.gov (United States)

    Kogure, Yasunori; Nakamura, Fumihiko; Shinozaki-Ushiku, Aya; Watanabe, Akira; Kamei, Katsuhiko; Yoshizato, Tetsuichi; Nannya, Yasuhito; Fukayama, Masashi; Kurokawa, Mineo

    2014-01-01

    Mucormycosis is an increasingly important cause of morbidity and mortality for patients with hematological malignancies. The diagnosis of mucormycosis usually requires mycological evidence through tissue biopsy or autopsy because the signs and symptoms are nonspecific and there are currently no biomarkers to identify the disease. We herein present two autopsied cases of acute myeloid leukemia with prolonged neutropenia who developed invasive mucormycosis accompanied by pulmonary artery embolism. Our cases were featured by unexplained fever and rapidly progressive dyspnea. Computed tomography scan detected nodular lesions or nonspecific consolidations in the lungs. Cultures, cytological study, and serum fungal markers consistently gave negative results. Autopsy revealed embolism of the pulmonary artery which consisted of fibrin clots by filamentous fungi. Genomic DNA was extracted from the paraffin-embedded clots and was applied to polymerase chain reaction amplification, leading to the diagnosis of infection by Rhizopus microsporus. We should carefully search for life-threatening pulmonary embolism when patients with hematological malignancies develop pulmonary mucormycosis.

  5. Intravascular lymphoma presenting as a specific pulmonary embolism and acute respiratory failure: a case report

    Directory of Open Access Journals (Sweden)

    Georgin-Lavialle Sophie

    2009-05-01

    Full Text Available Abstract Introduction The occurrence of an intravascular lymphoma with severe pulmonary involvement mimicking pulmonary embolism is described. Case presentation A 38-year-old man was referred to our intensive care unit with acute respiratory failure and long lasting fever. Appropriate investigations failed to demonstrate any bacterial, viral, parasitic or mycobacterial infection. A chest computed tomography scan ruled out any proximal or sub-segmental pulmonary embolism but the ventilation/perfusion lung scan concluded that there was a high probability of pulmonary embolism. The cutaneous biopsy pathology diagnosed intravascular lymphoma. Conclusion Intravascular lymphoma is a rare disease characterized by exclusive or predominant growth of neoplastic cells within the lumina of small blood vessels. Lung involvement seems to be common, but predominant lung presentation of this disease is rare. In our patient, urgent chemotherapy, along with adequate supportive care allowed complete recovery.

  6. Modified PISAPED Criteria in Combination with Ventilation Scintigraphic Finding for Predicting Acute Pulmonary Embolism.

    Science.gov (United States)

    Watanabe, Naoyuki; Fettich, Jure; Küçük, Nurie Özlem; Kraft, Otakar; Mut, Fernando; Choudhury, Partha; Sharma, Surendra K; Endo, Keigo; Dondi, Maurizio

    2015-01-01

    This prospective clinical study aimed at assessing three pulmonary scintigraphic algorithms to detect acute pulmonary embolism (PE): Lung ventilation/perfusion (V/Q) scintigraphy along with modified prospective investigation of pulmonary embolism diagnosis (PIOPED) criteria; lung perfusion scintigraphy along with prospective investigative study of acute pulmonary embolism diagnosis (PISAPED) criteria; and lung perfusion scan in combination with ventilation scan, along with modified PISAPED criteria, which were newly developed. Patients with suspicion of PE were eligible for this study if they had no abnormal chest x-ray. Their diagnostic workup included a clinical assessment, a pulmonary V/Q scintigraphy, and CT pulmonary angiography (CTPA), as well as a clinical outcome assessment over a period of 24 weeks. Referred to the final clinical diagnosis of patients, the sensitivity and specificity of each algorithm were evaluated. The diagnostic performance of each algorithm by the area under the maximum likelihood fitted receiver operating characteristic (ROC) curve was determined. With respect to the PISAPED criteria, the sensitivity was 60.8% and specificity was 87.3%. No patient was classified into nondiagnostic category. The PIOPED criteria showed that the sensitivity was 95.0% and specificity was 88.2%, while 57.4% of the patients were in nondiagnostic category. The areas under the ROC curve constructed from the PISAPED criteria results and the modified PIOPED criteria results were 0.734 and 0.859 (P < 0.01), respectively. The modified PISAPED criteria demonstrated that the sensitivity was 83.8% and specificity was 89.1%. No patient was classified into nondiagnostic category. The area under the ROC curve constructed from modified PISAPED criteria was 0.864 (P < 0.01). Perfusion scans used with ventilation scans and modified PISAPED criteria may increase the diagnostic accuracy of pulmonary scintigraphy for acute PE, compared with the two major algorithms.

  7. H2S Attenuates LPS-Induced Acute Lung Injury by Reducing Oxidative/Nitrative Stress and Inflammation

    Directory of Open Access Journals (Sweden)

    Hong-Xia Zhang

    2016-12-01

    Full Text Available Background: Hydrogen sulfide (H2S, known as the third endogenous gaseous transmitter, has received increasing attention because of its diverse effects, including angiogenesis, vascular relaxation and myocardial protection.We aimed to investigate the role of H2S in oxidative/nitrative stress and inflammation in acute lung injury (ALI induced by endotoxemia. Methods: Male ICR mice were divided in six groups: (1 Control group; (2 GYY4137treatment group; (3 L-NAME treatment group; (4 lipopolysaccharide (LPS treatment group; (5 LPS with GYY4137 treatment group; and (6 LPS with L-NAME treatment group. The lungs were analysed by histology, NO production in the mouse lungs determined by modified Griess (Sigma-Aldrich reaction, cytokine levels utilizing commercialkits, and protein abundance by Western blotting. Results: GYY4137, a slowly-releasing H2S donor, improved the histopathological changes in the lungs of endotoxemic mice. Treatment with NG-nitro-L-arginine methyl ester (L-NAME, a nitric oxide synthase (NOS inhibitor, increased anti-oxidant biomarkers such as thetotal antioxidant capacity (T-AOC and theactivities of catalase (CAT and superoxide dismutase (SOD but decreased a marker of peroxynitrite (ONOO- action and 3-nitrotyrosine (3-NT in endotoxemic lung. L-NAME administration also suppressed inflammation in endotoxemic lung, as evidenced by the decreased pulmonary levels of interleukin (IL-6, IL-8, and myeloperoxidase (MPO and the increased level of anti-inflammatory cytokine IL-10. GYY4137 treatment reversed endotoxin-induced oxidative/nitrative stress, as evidenced by a decrease in malondialdehyde (MDA, hydrogenperoxide (H2O2 and 3-NT and an increase in the antioxidant biomarker ratio of reduced/oxidized glutathione(GSH/GSSG ratio and T-AOC, CAT and SOD activity. GYY4137 also attenuated endotoxin-induced lung inflammation. Moreover, treatment with GYY4137 inhibited inducible NOS (iNOS expression and nitric oxide (NO production in the

  8. Mortality in children with complicated severe acute malnutrition is related to intestinal and systemic inflammation : an observational cohort study

    NARCIS (Netherlands)

    Attia, Suzanna; Versloot, Christian J.; Voskuijl, Wieger; van Vliet, Sara J.; Di Giovanni, Valeria; Zhang, Ling; Richardson, Susan; Bourdon, Celine; Netea, Mihai G.; Berkley, James A.; van Rheenen, Patrick F.; Bandsma, Robert H. J.

    2016-01-01

    Background: Diarrhea affects a large proportion of children with severe acute malnutrition (SAM). However, its etiology and clinical consequences remain unclear. Objective: We investigated diarrhea, enteropathogens, and systemic and intestinal inflammation for their interrelation and their associati

  9. Serum biomarkers and source of inflammation in acute coronary syndromes and percutaneous coronary interventions.

    Science.gov (United States)

    Centurión, Osmar Antonio

    2016-03-01

    There is robust information that confirms the enormous contribution of inflammation to plaque development, progression and vulnerability. The presence of plaques with inflammatory components associates with a greater likelihood of future cardiovascular events. The inflammatory cascade has been implicated during the entire plaque formation, from the early stages of endothelial dysfunction to the development of acute coronary syndromes (ACS). The presence of macrophages, T lymphocytes, dendritic cells, and mast cells in atherosclerotic lesions; the detection of HLA class II antigen expression; and the finding of secretion of several cytokines point to the involvement of immune inflammatory mechanisms in the pathogenesis of atherosclerosis. Serum biomarkers reflecting the activity of biological processes involved in plaque growth or destabilization may provide great help in establishing the appropriate clinical management, and therapeutic interventions. Evidence for a role of inflammation in plaque rupture has been demonstrated by localization of inflammation at plaque rupture sites. However, the focus of inflammation may not precisely reside within the coronary vessel itself but rather in the injured myocardium distal to the disrupted plaque. These observations outline the potential benefits of therapies targeting inflammation in the arterial wall and cardiovascular system. Emerging anti-inflammatory approaches to vascular protection have the potential to benefit patients by marked reductions in serum biomarkers of inflammation and reduce vascular events. With ongoing technical advances, percutaneous coronary interventions (PCI) will continue to play a critical role in the evaluation of novel compounds designed to modulate inflammation. The constant refinements in the different therapeutic strategies, the combination of scientific understanding in the adequate utilization of novel inflammatory markers, the new pharmacologic agents, and the new techniques in PCI will

  10. Differential role of lipocalin-2 during immune-complex mediated acute and chronic inflammation

    Science.gov (United States)

    Shashidharamurthy, Rangaiah; Machiah, Deepa; Aitken, Jesse D; Putty, Kalyani; Srinivasan, Gayathri; Chassaing, Benoit; Parkos, Charles A; Selvaraj, Periasamy; Vijay-Kumar, Matam

    2013-01-01

    Objectives Lipocalin-2 (Lcn2) is an innate immune protein expressed by a variety of cells and is highly upregulated during several pathological conditions including immune-complex (IC) mediated inflammatory/autoimmune disorders. However, the function of Lcn2 during IC-mediated inflammation is largely unknown. Therefore our objective was to investigate the role of Lcn2 in IC-mediated diseases. Methods The upregulation of Lcn2 was determined by ELISA in three different mouse models of IC-mediated autoimmune disease: systemic lupus erythematosus, collagen-induced arthritis and serum-induced arthritis. The in vivo role of Lcn2 during IC-mediated inflammation was investigated using Lcn2 knockout (Lcn2KO) mice and their wild type (WT) littermates. Results Lcn2 levels were significantly elevated in all the three autoimmune disease models. Further, in an acute skin inflammation model, Lcn2KO mice demonstrated a 50% reduction in inflammation with histopathological analysis revealing strikingly reduced immune cell infiltration compared to WT mice. Administration of recombinant Lcn2 to Lcn2KO mice restored inflammation to levels observed in WT mice. Neutralization of Lcn2 using a monoclonal antibody significantly reduced inflammation in WT mice. In contrast, Lcn2KO mice developed more severe serum-induced arthritis compared to WT mice. Histological analysis revealed extensive tissue and bone destruction with significantly reduced neutrophil infiltration but considerably more macrophage migration in Lcn2KO mice when compared to WT. Conclusion These results demonstrate that Lcn2 may regulate immune cell recruitment to the site of inflammation, a process essential for the controlled initiation, perpetuation and resolution of inflammatory processes. Thus, Lcn2 may present a promising target in the treatment of IC-mediated inflammatory/autoimmune diseases. PMID:23280250

  11. Multi-walled carbon nanotube physicochemical properties predict pulmonary inflammation and genotoxicity

    DEFF Research Database (Denmark)

    Poulsen, Sarah S.; Jackson, Petra; Kling, Kirsten

    2016-01-01

    Lung deposition of multi-walled carbon nanotubes (MWCNT) induces pulmonary toxicity. Commercial MWCNT vary greatly in physicochemical properties and consequently in biological effects. To identify determinants of MWCNT-induced toxicity, we analyzed the effects of pulmonary exposure to 10 commerci...

  12. Multi-walled carbon nanotube physicochemical properties predict pulmonary inflammation and genotoxicity

    DEFF Research Database (Denmark)

    Poulsen, Sarah S.; Jackson, Petra; Kling, Kirsten;

    2016-01-01

    Lung deposition of multi-walled carbon nanotubes (MWCNT) induces pulmonary toxicity. Commercial MWCNT vary greatly in physicochemical properties and consequently in biological effects. To identify determinants of MWCNT-induced toxicity, we analyzed the effects of pulmonary exposure to 10 commercial...

  13. [From acute pulmonary embolism to chronic thromboembolic pulmonary hypertension: Pathobiology and pathophysiology].

    Science.gov (United States)

    Beltrán-Gámez, Miguel E; Sandoval-Zárate, Julio; Pulido, Tomás

    Chronic thromboembolic pulmonary hypertension (CTEPH) represents a unique subtype of pulmonary hypertension characterized by the presence of mechanical obstruction of the major pulmonary vessels caused by venous thromboembolism. CTEPH is a progressive and devastating disease if not treated, and is the only subset of PH potentially curable by a surgical procedure known as pulmonary endarterectomy. The clot burden and pulmonary embolism recurrence may contribute to the development of CTEPH however only few thrombophilic factors have been found to be associated. A current hypothesis is that CTEPH results from the incomplete resolution and organization of thrombus modified by inflammatory, immunologic and genetic mechanisms, leading to the development of fibrotic stenosis and adaptive vascular remodeling of resistance vessels. The causes of thrombus non-resolution have yet to be fully clarified. CTEPH patients often display severe PH that cannot be fully explained by the degree of pulmonary vascular obstruction apparent on imaging studies. In such cases, the small vessel disease and distal obstructive thrombotic lesions beyond the sub-segmental level may contribute for out of proportion elevated PVR. The processes implicated in the development of arteriopathy and micro-vascular changes might explain the progressive nature of PH and gradual clinical deterioration with poor prognosis, as well as lack of correlation between measurable hemodynamic parameters and vascular obstruction even in the absence of recurrent venous thromboembolism. This review summarizes the most relevant up-to-date aspects on pathobiology and pathophysiology of CTEPH. Copyright © 2016 Instituto Nacional de Cardiología Ignacio Chávez. Publicado por Masson Doyma México S.A. All rights reserved.

  14. The role of inflammation and interleukin-1 in acute cerebrovascular disease

    Directory of Open Access Journals (Sweden)

    Galea J

    2013-08-01

    Full Text Available James Galea,1 David Brough21Manchester Academic Health Sciences Center, Brain Injury Research Group, Clinical Sciences Building, Salford Royal Foundation Trust, Salford, UK; 2Faculty of Life Sciences, University of Manchester, AV Hill Building, Manchester, UKAbstract: Acute cerebrovascular disease can affect people at all stages of life, from neonates to the elderly, with devastating consequences. It is responsible for up to 10% of deaths worldwide, is a major cause of disability, and represents an area of real unmet clinical need. Acute cerebrovascular disease is multifactorial with many mechanisms contributing to a complex pathophysiology. One of the major processes worsening disease severity and outcome is inflammation. Pro-inflammatory cytokines of the interleukin (IL-1 family are now known to drive damaging inflammatory processes in the brain. The aim of this review is to discuss the recent literature describing the role of IL-1 in acute cerebrovascular disease and to provide an update on our current understanding of the mechanisms of IL-1 production. We also discuss the recent literature where the effects of IL-1 have been targeted in animal models, thus reviewing potential future strategies that may limit the devastating effects of acute cerebrovascular disease.Keywords: cerebral ischemia, stroke, inflammation, microglia, interleukin-1, caspase-1

  15. [Echocardiography in acute pulmonary embolism. Not a routine method but useful in the diagnosis of simultaneous hemodynamic disorders].

    Science.gov (United States)

    Kierkegaard, A

    1998-08-19

    Echocardiographic diagnosis of acute pulmonary embolism as illustrated by three case reports is discussed in the article. Acute pulmonary embolism was diagnosed by demonstration of right heart strain in one case, of long vermiform thrombi floating in the right atrium in another, and in the third case by demonstration of a long thrombus lodged in the foramen ovale, astride the atrial septum, and with its ends floating in either atrium. Thus, as echocardiography enables pulmonary embolism to be diagnosed by demonstration either of right heart strain or of intracardial thrombi, it is a useful diagnostic tool in cases of haemodynamic compromise, though it does not detect minor pulmonary embolism.

  16. A pig model of acute right ventricular afterload increase by hypoxic pulmonary vasoconstriction.

    Science.gov (United States)

    Knai, Kathrine; Skjaervold, Nils Kristian

    2017-01-03

    The aim of this study was to construct a non-invasive model for acute right ventricular afterload increase by hypoxic pulmonary vasoconstriction. Intact animal models are vital to improving our understanding of the pathophysiology of acute right ventricular failure. Acute right ventricular failure is caused by increased afterload of the right ventricle by chronic or acute pulmonary hypertension combined with regionally or globally reduced right ventricular contractile capacity. Previous models are hampered by their invasiveness; this is unfortunate as the pulmonary circulation is a low-pressure system that needs to be studied in closed chest animals. Hypoxic pulmonary vasoconstriction is a mechanism that causes vasoconstriction in alveolar vessels in response to alveolar hypoxia. In this study we explored the use of hypoxic pulmonary vasoconstriction as a means to increase the pressure load on the right ventricle. Pulmonary hypertension was induced by lowering the FiO2 to levels below the physiological range in eight anesthetized and mechanically ventilated pigs. The pigs were monitored with blood pressure measurements and blood gases. The mean pulmonary artery pressures (mPAP) of the animals increased from 18.3 (4.2) to 28.4 (4.6) mmHg and the pulmonary vascular resistance (PVR) from 254 (76) dyns/cm(5) to 504 (191) dyns/cm(5), with a lowering of FiO2 from 0.30 to 0.15 (0.024). The animals' individual baseline mPAPs varied substantially as did their response to hypoxia. The reduced FiO2 level yielded an overall lowering in oxygen offer, but the global oxygen consumption was unaltered. We showed in this study that the mPAP and the PVR could be raised by approximately 100% in the study animals by lowering the FiO2 from 0.30 to 0.15 (0.024). We therefore present a novel method for minimally invasive (closed chest) right ventricular afterload manipulations intended for future studies of acute right ventricular failure. The method should in theory be reversible

  17. Peripheral blood neutrophilia as a biomarker of ozone-induced pulmonary inflammation.

    Directory of Open Access Journals (Sweden)

    Jenny A Bosson

    Full Text Available BACKGROUND: Ozone concentrations are predicted to increase over the next 50 years due to global warming and the increased release of precursor chemicals. It is therefore urgent that good, reliable biomarkers are available to quantify the toxicity of this pollutant gas at the population level. Such a biomarker would need to be easily performed, reproducible, economically viable, and reflective of ongoing pathological processes occurring within the lung. METHODOLOGY: We examined whether blood neutrophilia occurred following a controlled ozone challenge and addressed whether this could serve as a biomarker for ozone-induced airway inflammation. Three separate groups of healthy subjects were exposed to ozone (0.2 ppm, 2h and filtered air (FA on two separate occasions. Peripheral blood samples were collected and bronchoscopy with biopsy sampling and lavages was performed at 1.5h post exposures in group 1 (n=13, at 6h in group 2 (n=15 and at 18h in group 3 (n=15. Total and differential cell counts were assessed in blood, bronchial tissue and airway lavages. RESULTS: In peripheral blood, we observed fewer neutrophils 1.5h after ozone compared with the parallel air exposure (-1.1±1.0x10(9 cells/L, p<0.01, at 6h neutrophil numbers were increased compared to FA (+1.2±1.3x10(9 cells/L, p<0.01, and at 18h this response had fully attenuated. Ozone induced a peak in neutrophil numbers at 6h post exposure in all compartments examined, with a positive correlation between the response in blood and bronchial biopsies. CONCLUSIONS: These data demonstrate a systemic neutrophilia in healthy subjects following an acute ozone exposure, which mirrors the inflammatory response in the lung mucosa and lumen. This relationship suggests that blood neutrophilia could be used as a relatively simple functional biomarker for the effect of ozone on the lung.

  18. Klotho Reduction in Alveolar Macrophages Contributes to Cigarette Smoke Extract-induced Inflammation in Chronic Obstructive Pulmonary Disease.

    Science.gov (United States)

    Li, Lingling; Wang, Yujie; Gao, Wei; Yuan, Cheng; Zhang, Sini; Zhou, Hong; Huang, Mao; Yao, Xin

    2015-11-13

    Abnormal inflammation and accelerated decline in lung function occur in patients with chronic obstructive pulmonary disease (COPD). Klotho, an anti-aging protein, has an anti-inflammatory function. However, the role of Klotho has never been investigated in COPD. The aim of this study is to investigate the possible role of Klotho by alveolar macrophages in airway inflammation in COPD. Klotho levels were assessed in the lung samples and peripheral blood mononuclear cells of non-smokers, smokers, and patients with COPD. The regulation of Klotho expression by cigarette smoke extract (CSE) was studied in vitro, and small interfering RNA (siRNA) and recombinant Klotho were employed to investigate the role of Klotho on CSE-induced inflammation. Klotho expression was reduced in alveolar macrophages in the lungs and peripheral blood mononuclear cells of COPD patients. CSE decreased Klotho expression and release from MH-S cells. Knockdown of endogenous Klotho augmented the expression of the inflammatory mediators, such as MMP-9, IL-6, and TNF-α, by MH-S cells. Exogenous Klotho inhibited the expression of CSE-induced inflammatory mediators. Furthermore, we showed that Klotho interacts with IκBα of the NF-κB pathway. Dexamethasone treatment increased the expression and release level of Klotho in MH-S cells. Our findings suggest that Klotho plays a role in sustained inflammation of the lungs, which in turn may have therapeutic implications in COPD.

  19. Acute Pulmonary Thromboembolism Presenting As Complete Heart Block - A Rare Presentation

    Directory of Open Access Journals (Sweden)

    Vikash Goyal

    2015-08-01

    Full Text Available Acute pulmonary thromboembolism (PTE is a life threatening condition which requires early diagnosis and management. Electrocardiogram (ECG is helpful for suspecting the disease. The various ECG changes are sinus tachycardia, P pulmonale, Right bundle branch block (RBBB -incomplete or complete, axis shift, S1Q3T3, T wave inversion, and ST-segment depression in leads V1-4, aVF, and Lead III, supra ventricular tachycardia, low voltage QRS complex in limb leads. In addition, sinus bradycardia and complete heart block (CHB can be seen. CHB has been reported as an exceptionally rare manifestation of acute PTE. Here, we are reporting a case of 66 year old male presented with CHB with acute pulmonary thromboembolism, who reverted to sinus rhythm after thrombolysis.

  20. Role of interleukin 18 in acute lung inflammation induced by gut ischemia reperfusion

    Institute of Scientific and Technical Information of China (English)

    Yong-Jie Yang; Yun Shen; Song-Hua Chen; Xi-Rui Ge

    2005-01-01

    AIM: To study the changes of endogenous interleukin 18 (IL-18) levels and evaluate the role of IL-18 on lung injury following gut ischemia/reperfusion.METHODS: A superior mesenteric artery occlusion model was selected for this research. The mice were randomly divided into four groups: Sham operation (sham), ischemia (0.5 h) followed by different times of reperfusion (I/R),and I/R pretreated with exogenous IL-18 (I/R+IL-18) or IL-18 neutralizing antibody (I/R+IL-18Ab) 15 min before ischemia. Serum IL-18 levels were detected by Western blot and ELISA, and the levels of IL-18 in lung tissue were evaluated by immunohistochemical staining. For the study of pulmonary inflammation, the lung myeloperoxidase (MPO) contents and morphological changes were evaluated.RESULTS: Gut ischemia/reperfusion induced rapid increase of serum IL-18 levels, peaked at 1 h after reperfusion and then declined. The levels of IL-18 in lung tissue were gradually enhanced as the progress of reperfusion.Compared with I/R group, exogenous administration of IL-18 (I/R+IL-18) further remarkably enhanced the pulmonary MPO activity and inflammatory cell infiltration,and in I/R+IL-18Ab group, the content of MPO were significantly reduced and lung inflammation was also decreased.CONCLUSION: Gut ischemia/reperfusion induces the increase of IL-18 expression, which may make IL-18 act as an important proinflammatory cytokine and contribute to gut ischemia/reperfusion-induced lung inflammation.

  1. Acute Pulmonary Edema in Patients with Cushing’s Syndrome

    OpenAIRE

    Mitra Niafar; Mehrnoush Toufan; Nooshin Milanchian; Farhad Niafar; Kavous Shahsavari Nia

    2015-01-01

    Introduction Dyspnea refers to difficulty in breathing, and short and shallow breaths. This sign is seen in numerous diseases due to pulmonary, cardiac, metabolic and neurological causes. Among cardiac causes, heart failure is considered the main cause of dyspnea. Cardiac failure is a clinical syndrome associated with a set of symptoms (dyspnea, and fatigue) and signs (edema and rales). Common causes of cardiac failure include: myocardial infarction, ischemic heart disease, hypertensi...

  2. [Non-cardiogenic pulmonary edema, acute respiratory distress syndrome].

    Science.gov (United States)

    Skalická, Hana; Bělohlávek, Jan

    2015-01-01

    Non-cardiogenic pulmonary edema is a clinical syndrome manifested by rapidly progressive respiratory distress leading, without therapy, to severe respiratory insufficiency and subsequent multiorgan failure. The pathophysiological causes are: the change in the pressure gradients in the pulmonary capillaries, the impaired membrane permeability of the alveolocapillary in the lungs, and impaired lymphatic drainage. Unlike in cardiogenic pulmonary edema, cardiac disease is not a cause, and there is no increase in wedge pressure (< 18 mm Hg). The aetiological base is diverse and includes more clinical pathological factors. The diagnosis and evaluation are usually very difficult due to the rapidly deteriorating clinical condition of the patients. A decisive, quick and comprehensive approach, using all available invasive and non-invasive methods is necessary. The basic steps of treatment are: the use of different types of ventilatory support in order to achieve adequate oxygenation, dealing with possible hemodynamic instability, and, when needed, other specific procedures. It is always important to keep in mind that this is a very serious condition with a high mortality rate. And there is a need for fast and efficient access to the best specialized clinic.

  3. Sildenafil attenuates pulmonary inflammation and fibrin deposition, mortality and right ventricular hypertrophy in neonatal hyperoxic lung injury

    Directory of Open Access Journals (Sweden)

    Boersma Hester

    2009-04-01

    Full Text Available Abstract Background Phosphodiesterase-5 inhibition with sildenafil has been used to treat severe pulmonary hypertension and bronchopulmonary dysplasia (BPD, a chronic lung disease in very preterm infants who were mechanically ventilated for respiratory distress syndrome. Methods Sildenafil treatment was investigated in 2 models of experimental BPD: a lethal neonatal model, in which rat pups were continuously exposed to hyperoxia and treated daily with sildenafil (50–150 mg/kg body weight/day; injected subcutaneously and a neonatal lung injury-recovery model in which rat pups were exposed to hyperoxia for 9 days, followed by 9 days of recovery in room air and started sildenafil treatment on day 6 of hyperoxia exposure. Parameters investigated include survival, histopathology, fibrin deposition, alveolar vascular leakage, right ventricular hypertrophy, and differential mRNA expression in lung and heart tissue. Results Prophylactic treatment with an optimal dose of sildenafil (2 × 50 mg/kg/day significantly increased lung cGMP levels, prolonged median survival, reduced fibrin deposition, total protein content in bronchoalveolar lavage fluid, inflammation and septum thickness. Treatment with sildenafil partially corrected the differential mRNA expression of amphiregulin, plasminogen activator inhibitor-1, fibroblast growth factor receptor-4 and vascular endothelial growth factor receptor-2 in the lung and of brain and c-type natriuretic peptides and the natriuretic peptide receptors NPR-A, -B, and -C in the right ventricle. In the lethal and injury-recovery model we demonstrated improved alveolarization and angiogenesis by attenuating mean linear intercept and arteriolar wall thickness and increasing pulmonary blood vessel density, and right ventricular hypertrophy (RVH. Conclusion Sildenafil treatment, started simultaneously with exposure to hyperoxia after birth, prolongs survival, increases pulmonary cGMP levels, reduces the pulmonary

  4. Acute Postpartum Pulmonary Edema in a 32-Year-Old Woman Five Days after Cesarean Delivery

    Directory of Open Access Journals (Sweden)

    Masuda Islam Khan

    2013-07-01

    Full Text Available Acute dyspnea after pregnancy is a rare presentation, and a number of important conditions may accompany it. Pulmonary embolism, amniotic fluid embolism, pneumonia, aspiration and pulmonary edema are some of the potential causes that must be considered. The percentage of pregnancies that are complicated by acute pulmonary edema has been estimated 0.08%. The most common contributing factors include the administration of tocolytic agents, underlying cardiac disease, iatrogenic fluid overload and preeclampsia. Here we report a case of 32- year-old woman of 5th postpartum day following lower uterine cesarean section with acute dyspnea from her first pregnancy who was admitted in coronary care unit with history of one episode of raised blood pressure 160/90 mm Hg and cough on 1st postoperative day. Clinical examination and relevant investigations explored that it was a case of bilateral pulmonary edema. Patient was kept in ventilator and was treated with nitroglycerine (GTN, frusemide and ACE inhibitor. After diuresis, considerable improvement was observed in her respiratory status. From the 4th day, the patient became hemodynamically stable and was weaned off the ventilator. After five days, all the biochemical parameters became normal and she had no dyspnea.

  5. Immunological characterization of bronchoalveolar lavage fluid in patients with acute pulmonary coccidioidomycosis.

    Science.gov (United States)

    Nesbit, Lance A; Knox, Kenneth S; Nguyen, Chinh T; Roesch, Justin; Wheat, L Joseph; Johnson, Suzanne M; Pappagianis, Demosthenes; Chavez, Suzette; Ampel, Neil M

    2013-09-01

    The specific cellular immunological characteristics of bronchoalveolar lavage (BAL) fluid in acute pulmonary coccidioidomycosis have not been defined. BAL fluid from patients living in a coccidioidomycosis-endemic region of Arizona who were undergoing bronchoscopy because of pulmonary infiltrates was analyzed. Mononuclear cells from BAL fluid and peripheral blood mononuclear cells (PBMCs) were incubated with the coccidioidal antigen T27K in vitro, and cellular immunological assays were performed. Forty-six patients were studied. Twelve received a diagnosis of acute pulmonary coccidioidomycosis, 17 received other diagnoses, and 17 had no diagnosis established. There was an increased proportion of polyfunctional CD8(+) T cells after antigen stimulation from subjects with coccidioidomycosis as compared to those with another diagnosis (P = .025). In cells collected from BAL fluid and in PBMCs, the concentrations of interferon γ, tumor necrosis factor α, and interleukin 17 (IL-17) were all significantly increased in samples from those with acute pulmonary coccidioidomycosis, compared with the other 2 groups (for all, Pcoccidioidomycosis demonstrated specific cellular immune responses, including expression of IL-17.

  6. Prevalence of acute pulmonary embolism in central and subsegmental pulmonary arteries and relation to probability interpretation of ventilation/perfusion lung scans.

    Science.gov (United States)

    Stein, P D; Henry, J W

    1997-05-01

    The purpose of this investigation is to determine the prevalence of acute pulmonary embolism (PE) limited to subsegmental pulmonary arteries. Contrast-enhanced helical (spiral) and electron-beam CT, in the hands of experienced radiologists who are skillful with this modality, are sensitive for the detection of acute PE in central pulmonary arteries, but have a low sensitivity for the detection of PE limited to subsegmental pulmonary arteries. The potential for CT to diagnose PE, therefore, is partially dependent on the prevalence of PE limited to subsegmental pulmonary arteries. Data are from the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED). The largest pulmonary arteries that showed PE, as interpreted by the PIOPED angiographic readers, were identified in 375 patients in PIOPED with angiographically diagnosed PE. Among all patients with PE, 6% (95% confidence interval [CI], 4 to 9%) had PE limited to subsegmental branches of the pulmonary artery. Patients with high-probability ventilation/ perfusion (V/Q) scans had PE limited to subsegmental branches in only 1% (95% CI, 0 to 4%). Among patients with low-probability V/Q lung scans, 17% (95% CI, 8 to 29%) had PE limited to the subsegmental branches. Patients with low-probability V/Q scans and no prior cardiopulmonary disease had PE limited to the subsegmental pulmonary arteries in 30% (95% CI, 13 to 53%), whereas patients with low-probability V/Q scans who had prior cardiopulmonary disease had PE limited to subsegmental pulmonary arteries in 8% (95% CI, 2 to 22%) (p PIOPED, the prevalence of PE limited to subsegmental pulmonary arteries is low, 6%. PE limited to subsegmental pulmonary arteries was most prevalent among patients with low-probability V/Q scans, particularly if they had no prior cardiopulmonary disease.

  7. A patient with possible TRALI who developed pulmonary hypertensive crisis and acute pulmonary edema during cardiac surgery.

    Science.gov (United States)

    Kojima, Taiki; Nishisako, Ryo; Sato, Hideo

    2012-06-01

    There are very few case reports of transfusion-related acute lung injury (TRALI) under close hemodynamic monitoring. We encountered a case of possible TRALI during on-pump coronary artery bypass grafting (CABG). A 66-year-old man who had undergone on-pump CABG was administered fresh frozen plasma (FFP). One hour after FFP transfusion, pulmonary hypertensive crisis and subsequent hypoxic decompensation occurred. A second cardiopulmonary bypass (CPB) was needed for circulatory and respiratory deterioration. Extracorporeal life support (ECLS), intraaortic balloon pumping (IABP), and nitric oxide therapy were required after the surgery. Despite the severity of the initial state, his recovery was comparatively smooth. ECLS and IABP were removed on postoperative day (POD)1; the patient was extubated and discharged from the ICU on POD7 and POD12, respectively. The diagnosis of TRALI was confirmed by human leukocyte antigen antibody detection in the administered FFP. In addition, lymphocytic immunofluorescence test showed that a cross-match of the plasma from the pooled FFP against the recipient leukocytes was positive. The clinical course of the pulmonary artery hypertension was followed by a decrease in dynamic lung compliance. The mechanism of this phenomenon is unclear. However, it might suggest the possibility of vasoconstriction or obstruction of the peripheral pulmonary artery preceding lung damage, as in the case in animal models reported previously.

  8. Association of air pollution sources and aldehydes with biomarkers of blood coagulation, pulmonary inflammation, and systemic oxidative stress.

    Science.gov (United States)

    Altemose, Brent; Robson, Mark G; Kipen, Howard M; Ohman Strickland, Pamela; Meng, Qingyu; Gong, Jicheng; Huang, Wei; Wang, Guangfa; Rich, David Q; Zhu, Tong; Zhang, Junfeng

    2016-07-20

    Using data collected before, during, and after the 2008 Summer Olympic Games in Beijing, this study examines associations between biomarkers of blood coagulation (vWF, sCD62P and sCD40L), pulmonary inflammation (EBC pH, EBC nitrite, and eNO), and systemic oxidative stress (urinary 8-OHdG) with sources of air pollution identified utilizing principal component analysis and with concentrations of three aldehydes of health concern. Associations between the biomarkers and the air pollution source types and aldehydes were examined using a linear mixed effects model, regressing through seven lag days and controlling for ambient temperature, relative humidity, gender, and day of week for the biomarker measurements. The biomarkers for pulmonary inflammation, particularly EBC pH and eNO, were most consistently associated with vehicle and industrial combustion, oil combustion, and vegetative burning. The biomarkers for blood coagulation, particularly vWF and sCD62p, were most consistently associated with oil combustion. Systemic oxidative stress biomarker (8-OHdG) was most consistently associated with vehicle and industrial combustion. The associations of the biomarkers were generally not significant or consistent with secondary formation of pollutants and with the aldehydes. The findings support policies to control anthropogenic pollution sources rather than natural soil or road dust from a cardio-respiratory health standpoint.Journal of Exposure Science and Environmental Epidemiology advance online publication, 20 July 2016; doi:10.1038/jes.2016.38.

  9. Donor smoking is associated with pulmonary edema, inflammation and epithelial dysfunction in ex vivo human donor lungs

    Science.gov (United States)

    Ware, Lorraine B.; Lee, Jae W.; Wickersham, Nancy; Nguyen, John; Matthay, Michael A.; Calfee, Carolyn S.

    2014-01-01

    Although recipients of donor lungs from smokers have worse clinical outcomes, the underlying mechanisms are unknown. We tested the association between donor smoking and the degree of pulmonary edema (as estimated by lung weight), the rate of alveolar fluid clearance (measured by airspace instillation of 5% albumin) and biomarkers of lung epithelial injury and inflammation (bronchoalveolar lavage surfactant protein-D and IL-8) in ex vivo lungs recovered from 298 organ donors. The extent of pulmonary edema was higher in current smokers (n=127) compared to non-smokers (median 408g, IQR 364-500 vs. 385g, IQR 340 - 460, p=0.009). Oxygenation at study enrollment was worse in current smokers versus non-smokers (median PaO2/FiO2 214 mmHg, IQR 126-323 vs. 266 mmHg, IQR 154-370, p=0.02). Current smokers with the highest exposure (≥20 pack-years) had significantly lower rates of alveolar fluid clearance, suggesting that the effects of cigarette smoke on alveolar epithelial fluid transport function may be dose related. BAL IL-8 was significantly higher in smokers while surfactant protein-D was lower. These findings indicate that chronic exposure to cigarette smoke has important effects on inflammation, gas exchange, lung epithelial function and lung fluid balance in the organ donor that could influence lung function in the lung transplant recipient. PMID:25146497

  10. Algorithm for the diagnosis and follow-up of acute pulmonary embolisms.

    Science.gov (United States)

    Calvillo Batllés, P

    The urgent diagnosis of acute pulmonary thromboembolism benefits from the use of evidence-based clinical guidelines that improve patients' prognoses and reduce the unnecessary use of imaging tests. This article explains the diagnostic algorithms for pulmonary thromboembolism most recently published by the relevant scientific societies both for the general population and for special situations, trying to clear up common doubts and analyzing persistent controversies. It also discusses the need to follow up the thromboembolism after anticoagulation treatment, which is not currently recommended in the guidelines. Copyright © 2016 SERAM. Publicado por Elsevier España, S.L.U. All rights reserved.

  11. Endovascular Management of Acute Pulmonary Embolism Using the Ultrasound-Enhanced EkoSonic System.

    Science.gov (United States)

    Garcia, Mark J

    2015-12-01

    Acute, symptomatic pulmonary embolism (PE) in the massive and submassive categories continues to be a healthcare concern with significant risk for increased morbidity and mortality. Despite increased awareness and venous thromboembolism prophylaxis, endovascular treatment is still an important option for many of these patients. There are a variety of techniques and devices used for treating PE, but none have been evaluated as extensively as the EkoSonic endovascular system that is also currently the only FDA-approved device for the treatment of pulmonary embolism. This article describes the use of the EkoSonic device for this patient population.

  12. Value of the ventilation/perfusion scan in acute pulmonary embolism: Results of the prospective investigation of pulmonary embolism diagnosis (PIOPED)

    Energy Technology Data Exchange (ETDEWEB)

    1990-05-23

    To determine the sensitivities and specificities of ventilation/perfusion lung scans for acute pulmonary embolism, a random sample of 933 of 1,493 patients was studied prospectively. Nine hundred thirty-one underwent scintigraphy and 755 underwent pulmonary angiography; 251 (33%) of 755 demonstrated pulmonary embolism. Almost all patients with pulmonary embolism had abnormal scans of high, intermediate, or low probability, but so did most without pulmonary embolism. Of 116 patients with high-probability scans and definitive angiograms, 102 (88%) had pulmonary embolism, but only a minority with pulmonary embolism had high-probability scans. Of 322 with intermediate-probability scans and definitive angiograms, 105 (33%) had pulmonary embolism. Follow-up and angiography together suggest pulmonary embolism occurred among 12% of patients with low-probability scans. Clinical assessment combined with the ventilation/perfusion scan established the diagnosis or exclusion of pulmonary embolism only for a minority of patients--those with clear and concordant clinical and ventilation/perfusion scan findings.

  13. Value of the ventilation/perfusion scan in acute pulmonary embolism. Results of the prospective investigation of pulmonary embolism diagnosis (PIOPED).

    Science.gov (United States)

    To determine the sensitivities and specificities of ventilation/perfusion lung scans for acute pulmonary embolism, a random sample of 933 of 1493 patients was studied prospectively. Nine hundred thirty-one underwent scintigraphy and 755 underwent pulmonary angiography; 251 (33%) of 755 demonstrated pulmonary embolism. Almost all patients with pulmonary embolism had abnormal scans of high, intermediate, or low probability, but so did most without pulmonary embolism (sensitivity, 98%; specificity, 10%). Of 116 patients with high-probability scans and definitive angiograms, 102 (88%) had pulmonary embolism, but only a minority with pulmonary embolism had high-probability scans (sensitivity, 41%; specificity, 97%). Of 322 with intermediate-probability scans and definitive angiograms, 105 (33%) had pulmonary embolism. Follow-up and angiography together suggest pulmonary embolism occurred among 12% of patients with low-probability scans. Clinical assessment combined with the ventilation/perfusion scan established the diagnosis or exclusion of pulmonary embolism only for a minority of patients--those with clear and concordant clinical and ventilation/perfusion scan findings.

  14. A PAF receptor antagonist inhibits acute airway inflammation and late-phase responses but not chronic airway inflammation and hyperresponsiveness in a primate model of asthma

    Directory of Open Access Journals (Sweden)

    R. H. Gundel

    1992-01-01

    Full Text Available We have examined the effects of a PAF receptor antagonist, WEB 2170, on several indices of acute and chronic airway inflammation and associated changes in lung function in a primate model of allergic asthma. A single oral administration WEB 2170 provided dose related inhibition of the release of leukotriene C4 (LTC4 and prostaglandin D2 (PGD2 recovered and quantified in bronchoalveolar lavage (BAL fluid obtained during the acute phase response to inhaled antigen. In addition, oral WEB 2170 treatment in dual responder primates blocked the acute influx of neutrophils into the airways as well as the associated late-phase airway obstruction occurring 6 h after antigen inhalation. In contrast, a multiple dosing regime with WEB 2170 (once a day for 7 consecutive days failed to reduce the chronic airway inflammation (eosinophilic and associated airway hyperresponsiveness to inhaled methacholine that is characteristic of dual responder monkeys. Thus, we conclude that the generation of PAF following antigen inhalation contributes to the development of lipid mediators, acute airway inflammation and associated late-phase airway obstruction in dual responder primates; however, PAF does not play a significant role in the maintenance of chronic airway inflammation and associated airway hyperresponsiveness in this primate model.

  15. Prevalence of pulmonary edema among the deceased cases with acute Methadone poisoning: A report from Iran

    Science.gov (United States)

    Eizadi-Mood, Nastaran; Naeini, Seyed Amir Hossein Madani; Hedaiaty, Mahrang; Sabzghabaee, Ali Mohammad; Moudi, Maryam

    2016-01-01

    Objective: Methadone poisoning is common in our society, mainly in drug addicts. One of its lethal complications is pulmonary edema. Therefore, we evaluated the prevalence of pulmonary edema in the deceased cases with methadone poisoning and its possible relationship with some medical variables. Methods: In this cross-sectional study which was done in 2014, we have investigated the deceased patients with methadone toxicity who underwent autopsy at Isfahan Forensic Medicine Department (Iran). All variables including age, gender, and autopsy findings were recorded and analyzed. Demographic characteristics and medical complications of the patients were compared between the patients with or without pulmonary edema in the autopsy findings. Findings: There were 64 cases who died with methadone poisoning during the 1-year study period. The average age of cases (±standard deviation) was 32.1 ± 10.29 years, among which 92.2% were male. Based on the autopsy findings, 64.1% were diagnosed with pulmonary edema. There was no statistically significant relationship between pulmonary edema and age, gender, history of addiction, and hepatic or cardiovascular complications. Conclusion: Pulmonary edema is a common finding in deceased methadone poisoning cases and must be considered and ruled out in patients with acute methadone toxicity. PMID:27843967

  16. A role for matrix metalloproteinase-9 in the hemodynamic changes following acute pulmonary embolism.

    Science.gov (United States)

    Fortuna, Geisa M; Figueiredo-Lopes, Lívia; Dias-Junior, Carlos A C; Gerlach, Raquel F; Tanus-Santos, Jose E

    2007-01-02

    Matrix metalloproteinases (MMPs) modulate vascular contractility and may affect acute pulmonary embolism (APE)-induced pulmonary hypertension. We examined the effects of the administration of doxycycline (a MMP inhibitor) following APE in anesthetized dogs. Sham operated dogs (N=5) received only saline. APE was induced by intravenous injections of microspheres in amounts to increase mean pulmonary artery pressure (MPAP) by 20 mm Hg, and embolized dogs received saline (Emb group, N=8), or doxycycline (10 mg/kg, i.v.) 5 or 30 min of APE (Emb+Doxy 5 and Emb+Doxy 30 groups, N=9 and 8, respectively). Hemodynamic evaluation was performed at baseline and 5-120 after APE. Gelatin zymography of MMP-2 and MMP-9 from plasma samples was performed. No significant hemodynamic changes were found in Sham animals. Embolization increased MPAP by 218+/-16% and the pulmonary vascular resistance index (PVRI) by 289+/-42% in Emb group (both PDoxy 30+Emb group. In addition, doxycyline reduced MPAP and PVRI 30 min after APE with maximum effects seen 120 min after APE (25+/-4% decrease in MPAP and 33+/-6% decrease in PVRI; both PDoxy+5 group. Plasma pro-MMP-9 and MMP-9 levels increased only in Emb group and MMP-2 remained unaltered. Our study shows that doxycycline attenuates APE-induced pulmonary hypertension, and indicates that MMP-9 has a role in APE-induced pulmonary hypertension. MMP-9 may be a pharmacological target in APE.

  17. Lipopolysaccharide and Interleukin 1 Augment the Effects of Hypoxia and Inflammation in Human Pulmonary Arterial Tissue

    Science.gov (United States)

    Ziesche, Rolf; Petkov, Venzeslav; Williams, John; Zakeri, Schaker M.; Mosgoller, Wilhelm; Knofler, Martin; Block, Lutz H.

    1996-10-01

    The combined effects of hypoxia and interleukin 1, lipopolysaccharide, or tumor necrosis factor α on the expression of genes encoding endothelial constitutive and inducible nitric oxide synthases, endothelin 1, interleukin 6, and interleukin 8 were investigated in human primary pulmonary endothelial cells and whole pulmonary artery organoid cultures. Hypoxia decreased the expression of constitutive endothelial nitric oxide synthase (NOS-3) mRNA and NOS-3 protein as compared with normoxic conditions. The inhibition of expression of NOS-3 corresponded with a reduced production of NO. A combination of hypoxia with bacterial lipopolysaccharide, interleukin 1β , or tumor necrosis factor α augmented both effects. In contrast, the combination of hypoxia and the inflammatory mediators superinduced the expression of endothelin 1, interleukin 6, and interleukin 8. Here, we have shown that inflammatory mediators aggravate the effect of hypoxia on the down-regulation of NOS-3 and increase the expression of proinflammatory cytokines in human pulmonary endothelial cells and whole pulmonary artery organoid cultures.

  18. Dynamic expression of leukocyte innate immune genes in whole blood from horses with lipopolysaccharide-induced acute systemic inflammation

    DEFF Research Database (Denmark)

    Vinther, Anne Mette L.; Skovgaard, Kerstin; Heegaard, Peter M. H.;

    2015-01-01

    Background: In horses, insights into the innate immune processes in acute systemic inflammation are limited even though these processes may be highly important for future diagnostic and therapeutic advances in high-mortality disease conditions as the systemic inflammatory response syndrome (SIRS......) and sepsis. Therefore, the aim of this study was to investigate the expression of 31 selected blood leukocyte immune genes in an equine model of acute systemic inflammation to identify significantly regulated genes and to describe their expression dynamics during a 24-h experimental period. Systemic...... expressions in blood leukocytes during equine acute LPS-induced systemic inflammation thoroughly characterized a highly regulated and dynamic innate immune response. These results provide new insights into the molecular mechanisms of equine systemic inflammation....

  19. Resveratrol alleviate hypoxic pulmonary hypertension via anti-inflammation and anti-oxidant pathways in rats

    OpenAIRE

    XU, DUNQUAN; Li, Yan; Zhang, Bo; Wang, Yanxia; Liu, Yi; Luo, Ying; Niu, Wen; Dong, Mingqing; Liu, Manling; Dong, Haiying; Zhao, Pengtao; Li, Zhichao

    2016-01-01

    Resveratrol, a plant-derived polyphenolic compound and a phytoestrogen, was shown to possess multiple protective effects including anti-inflammatory response and anti-oxidative stress. Hypoxic pulmonary hypertension (HPH) is a progressive disease characterized by sustained vascular resistance and marked pulmonary vascular remodeling. The exact mechanisms of HPH are still unclear, but inflammatory response and oxidative stress was demonstrated to participate in the progression of HPH. The pres...

  20. Role of bacteria in acute exacerbations of chronic obstructive pulmonary disease

    Directory of Open Access Journals (Sweden)

    Levent Erkan

    2008-10-01

    Full Text Available Levent Erkan, Oguz Uzun, Serhat Findik, Didem Katar, Ahmet Sanic, Atilla G AticiOndokuz Mayis University, Faculty of Medicine, Department of Pulmonary Medicine, Samsun, TurkeyBackground and study objective: Infections are major causes of acute exacerbations of chronic obstructive pulmonary disease (COPD which result in significant mortality and morbidity. The primary aim of the study was to determine the microbiological spectrum including atypical agents in acute exacerbations. The secondary aim was to evaluate resistance patterns in the microorganisms.Methods: The sputum culture of 75 patients admitted to our clinic from January 1, 1999 to December 31, 2002 was evaluated prospectively, for aerobic Gram-positive and Gram-negative bacteria, and serologically for Chlamydophila pneumoniae and Mycoplasma pneumoniae. Sensitivity patterns in potentially pathogenic microorganisms (PPMs were also investigated.Results: An infectious agent was identified in 46 patients, either serologically or with sputum culture. Pathogens most commonly demonstrated were: Haemophilus influenzae (30%, Chlamydophila pneumoniae (17%, and Mycoplasma pneumoniae (9%. Mixed infections were diagnosed in 9 patients. PPMs showed a high resistance rate to commonly used antibiotics.Conclusion: We have shown that microorganisms causing acute exacerbations of COPD are not only typical bacteria (46% but also atypical pathogens (26%, with unpredictable high rates. Typical agents showed a high resistance to commonly used antibiotics.Keywords: chronic obstructive pulmonary disease, acute exacerbation, infection, atypical pathogens, Haemophilus influenzae

  1. Mannose-binding lectin deficiency and acute exacerbations of chronic obstructive pulmonary disease

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    Woodruff PG

    2012-11-01

    Full Text Available Richard K Albert,1 John Connett,2 Jeffrey L Curtis,3,4 Fernando J Martinez,3 MeiLan K Han,3 Stephen C Lazarus,5 Prescott G Woodruff51Medicine Service, Denver Health and Department of Medicine, University of Colorado Denver, Denver, CO, 2Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, MN, 3Pulmonary and Critical Care Medicine, Department of Medicine, University of Michigan, Ann Arbor, MI, 4Pulmonary and Critical Care Medicine, VA Medical Center, Ann Arbor, MI, 5Pulmonary and Critical Care Medicine, Department of Medicine, and Cardiovascular Research Institute, University of California, San Francisco, CA, USABackground: Mannose-binding lectin is a collectin involved in host defense against infection. Whether mannose-binding lectin deficiency is associated with acute exacerbations of chronic obstructive pulmonary disease is debated.Methods: Participants in a study designed to determine if azithromycin taken daily for one year decreased acute exacerbations had serum mannose-binding lectin concentrations measured at the time of enrollment.Results: Samples were obtained from 1037 subjects (91% in the trial. The prevalence of mannose-binding lectin deficiency ranged from 0.5% to 52.2%, depending on how deficiency was defined. No differences in the prevalence of deficiency were observed with respect to any demographic variable assessed, and no differences were observed in time to first exacerbation, rate of exacerbations, or percentage of subjects requiring hospitalization for exacerbations in those with deficiency versus those without, regardless of how deficiency was defined.Conclusion: In a large sample of subjects with chronic obstructive pulmonary disease selected for having an increased risk of experiencing an acute exacerbation of chronic obstructive pulmonary disease, only 1.9% had mannose-binding lectin concentrations below the normal range and we found no association between mannose-binding lectin

  2. Acute hyperammonemia and systemic inflammation is associated with increased extracellular brain adenosine in rats

    DEFF Research Database (Denmark)

    Bjerring, Peter Nissen; Dale, Nicholas; Larsen, Fin Stolze

    2015-01-01

    Acute liver failure (ALF) can lead to brain edema, cerebral hyperperfusion and intracranial hypertension. These complications are thought to be mediated by hyperammonemia and inflammation leading to altered brain metabolism. As increased levels of adenosine degradation products have been found...... in brain tissue of patients with ALF we investigated whether hyperammonemia could induce adenosine release in brain tissue. Since adenosine is a potent vasodilator and modulator of cerebral metabolism we furthermore studied the effect of adenosine receptor ligands on intracranial pressure (ICP......) and cerebral blood flow (CBF). We measured the adenosine concentration with biosensors in rat brain slices exposed to ammonia and in a rat model with hyperammonemia and systemic inflammation. Exposure to ammonia in concentrations from 0.15-10 mM led to increases in the cortical adenosine concentration up to 18...

  3. High mobility group box 1 protein as a late-acting mediator of acute lung inflammation.

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    Lutz, Waldemar; Stetkiewicz, Jan

    2004-01-01

    Acute inflammatory lung injury is often a delayed complication of critical illness and is associated with increased mortality. High mobility group box 1 (HMGB1) protein, in addition to its role as a transcriptional regulator factor, has been identified as a late mediator of endotoxin lethality and might be also involved in the development and progression of acute lung injury. HMGB1 protein itself can cause an acute inflammatory response manifested by increased production of proinflammatory cytokines and neutrophil accumulation. The delayed kinetics of HMGB1 protein release indicate that this protein is a distal mediator of acute inflamatory lung injury. Anti-HMGB1 protein antibodies attenuated endotoxin-induced lung injury, but not the early release of TNF-alpha and IL-1beta, indicating that HMGB1 protein is a late mediator of endotoxin-induced acute lung injury. HMGB1 protein is not released by apoptotic cells but is passively released by necrotic or damaged somatic and immune cells and it functions as a major stimulus of necrosis-induced inflammation. HMGB1 protein is also released by activated monocytes/macrophages and induces delayed and biphasic release of proinflammatory mediators from these cells. HMGB1 protein failed to stimulate cytokines release in lymphocytes, indicating that cellular stimulation is specific. We would like to suggest that HMGB1 protein may be also a primary mediator of the inflammatory responses to lung cells injury caused by toxic environmental chemicals.

  4. Exosomes from Human Dental Pulp Stem Cells Suppress Carrageenan-Induced Acute Inflammation in Mice.

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    Pivoraitė, Ugnė; Jarmalavičiūtė, Akvilė; Tunaitis, Virginijus; Ramanauskaitė, Giedrė; Vaitkuvienė, Aida; Kašėta, Vytautas; Biziulevičienė, Genė; Venalis, Algirdas; Pivoriūnas, Augustas

    2015-10-01

    The primary goal of this study was to examine the effects of human dental pulp stem cell-derived exosomes on the carrageenan-induced acute inflammation in mice. Exosomes were purified by differential ultracentrifugation from the supernatants of stem cells derived from the dental pulp of human exfoliated deciduous teeth (SHEDs) cultivated in serum-free medium. At 1 h post-carrageenan injection, exosomes derived from supernatants of 2 × 10(6) SHEDs were administered by intraplantar injection to BALB/c mice; 30 mg/kg of prednisolone and phosphate-buffered saline (PBS) were used as positive and negative controls, respectively. Edema was measured at 6, 24, and 48 h after carrageenan injection. For the in vivo imaging experiments, AngioSPARK750, Cat B 750 FAST, and MMPSense 750 FAST were administered into the mouse tail vein 2 h post-carrageenan injection. Fluorescence images were acquired at 6, 24, and 48 h after edema induction by IVIS Spectrum in vivo imaging system. Exosomes significantly reduced the carrageenan-induced edema at all the time points studied (by 39.5, 41.6, and 25.6% at 6, 24, and 48 h after injection, respectively), to similar levels seen with the positive control (prednisolone). In vivo imaging experiments revealed that, both exosomes and prednisolone suppress activities of cathepsin B and matrix metalloproteinases (MMPs) at the site of carrageenan-induced acute inflammation, showing more prominent effects of prednisolone at the early stages, while exosomes exerted their suppressive effects gradually and at later time points. Our study demonstrates for the first time that exosomes derived from human dental pulp stem cells suppress carrageenan-induced acute inflammation in mice.

  5. Cardiomyopathy confers susceptibility to particulate matter-induced oxidative stress, vagal dominance, arrhythmia, pulmonary inflammation in heart failure-prone rats

    Science.gov (United States)

    Acute exposure to ambient fine particulate matter (PM2.5) is tied to cardiovascular morbidity and mortality, especially among those with prior cardiac injury. The mechanisms and pathophysiologic events precipitating these outcomes remain poorly understood but may involve inflamm...

  6. Cardiomyopathy confers susceptibility to particulate matter-induced oxidative stress, vagal dominance, arrhythmia, pulmonary inflammation in heart failure-prone rats

    Science.gov (United States)

    Acute exposure to ambient fine particulate matter (PM2.5) is tied to cardiovascular morbidity and mortality, especially among those with prior cardiac injury. The mechanisms and pathophysiologic events precipitating these outcomes remain poorly understood but may involve inflamm...

  7. ROLE OF TOLL-LIKE RECEPTOR 4 IN AIRWAY INFLAMMA-TION OF CHRONIC OBSTRUCTIVE PULMONARY DISEASES

    Institute of Scientific and Technical Information of China (English)

    ZHOU Min; RONG Xia-jun; WAN Huan-ying; HUANG Shao-guang; LI Biao; LI Min

    2008-01-01

    Objective To confirm if pulmonary epithelial cells express Toll-like receptor 4 (TLR4) and investigate the role of TLR4 in airway inflammation of chronic obstructive pulmonary diseases (COPD). Methods The expressions of TLR4, IL-8 mRNA and NF-κB activation stimulated by differen factors [lipopolysacharides (LPS), interleukin-1β, cigarette smoking extract (CSE)] in pulmonary epithelial cells were investigated. Results LPS, CSE and IL-1β induced the production of IL-8 and activation of NF-κB. The levels of IL-8 mRNA and NF-κB protein in ElA+ cell were markedly higher than ElA-cell and A549 cell (P<0.05). The TLR4 mRNA of all the cells increased along with the increase of LPS' stimulated time. There was significant difference among different LPS' doses (12 h: P=0.039; 24 h: P=0.013). The TLR4 mRNA of ElA+ cell was higher than the other two groups (P<0.05). IL-1β induced all the cells expressing TLR4 mRNA. CSE had no effect on the expression of TLR4 mRNA. Conclusion Pulmonary epithelial cells express TLR4. LPS and IL-1β up-regulate IL-8 mediated via the activation of NF-κB induced by TLR4. But CSE up-regulates IL-8 mediated via the activation of NF-κB, which has no relation to TLR4 and may have another signal transduction pathway.

  8. Invasive pulmonary aspergillosis: role of early diagnosis and surgical treatment in patients with acute leukemia

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    Ursavas Ahmet

    2006-07-01

    Full Text Available Abstract Background Aspergillus is a ubiquitous soil-dwelling fungus known to cause significant pulmonary infection in immunocompromised patients. The incidence of aspergillosis has increased during the past two decades and is a frequently lethal complication of acute leukemia patients that occurs following both chemotherapy and bone marrow transplantation. The diagnosis of invasive pulmonary aspergillosis (IPA according to the criteria that are established by European Organization for the Research and Treatment of Cancer and Mycoses Study Group raise difficulties in severely ill patients. Despite established improvements in field of diagnosis (galactomannan antigen, quantitative PCR, real-time PCR for Aspergillus spp., and findings of computed tomography and treatment with new antifungals, it is still a major problem in patients with acute leukemia. However, prompt and effective treatment of IPA is crucial because most patients will need subsequent chemotherapy for underlying hematologic disease as soon as possible. Case presentation We report a 33-year-old male patient with acute promyelocytic leukemia diagnosed in 1993 that developed invasive pulmonary aspergillosis due to A. flavus at relapse in 2003. The patient was successfully treated with liposomal amphotericin B and underwent surgical pulmonary resection. The operative course was uneventful. Conclusion This report emphasizes the clinical picture, applicability of recent advances in diagnostic and therapeutic approaches for IPA. For early identification of a patient infected with IPA, a high index of suspicion and careful clinical and radiological examinations with serial screening for galactomannan should be established. If aspergillosis is suspected, anti-aspergillosis drug should be administered immediately, and if a unique pulmonary lesion remains, surgical resection should be considered to prevent reactivation during consecutive chemotherapy courses and to improve the outcome.

  9. Inflammation Activation Contributes to Adipokine Imbalance in Patients with Acute Coronary Syndrome.

    Science.gov (United States)

    Li, Rong; Chen, Lu-zhu; Zhao, Shui-ping; Huang, Xian-sheng

    2016-01-01

    Inflammation can be activated as a defensive response by the attack of acute coronary syndrome (ACS) for ischemic tissue injury. The aim of the present study was to investigate the impact of ACS-activated inflammation on adipokine imbalance and the effects of statins on the crosstalk between inflammation and adipokine imbalance during ACS. In this study, 586 subjects were categorized into: (1) control group; (2) SA (stable angina) group; and (3) ACS group. Circulating levels of hs-CRP, adiponectin and resistin were measured by ELISA. Furthermore, forty C57BL/6 mice were randomized into: sham, AMI, low-statin (atorvastatin, 2 mg/kg/day) and high-statin (atorvastatin, 20 mg/kg/day) group. After 3 weeks, AMI models were established by surgical coronary artery ligation. Circulating levels and adipose expressions of adiponectin and resistin were assessed in animals. Besides, we investigate the effects of atorvastatin on ox-LDL-induced adipokine imbalance in vitro. As a result, we found that ACS patients had higher hs-CRP and resistin levels and lower adiponectin levels. Our correlation analysis demonstrated hs-CRP concentrations were positively correlated with resistin but negatively with adiponectin levels in humans. Our animal findings indicated higher circulating hs-CRP and resistin levels and lower adiponectin levels in AMI mice. Atorvastatin pre-treatment dose-dependently decreased hs-CRP and resistin levels but increased adiponectin levels in mice. The consistent findings were observed about the adipose expressions of resistin and adiponectin in mice. In study in vitro, ox-LDL increased cellular resistin expressions and otherwise for adiponectin expressions, which dose-dependently reversed by the addition of atorvastatin. Therefore, our study indicates that the ACS attack activates inflammation leading to adipokine imbalance that can be ameliorated by anti-inflammation of atorvastatin.

  10. Inflammation Activation Contributes to Adipokine Imbalance in Patients with Acute Coronary Syndrome.

    Directory of Open Access Journals (Sweden)

    Rong Li

    Full Text Available Inflammation can be activated as a defensive response by the attack of acute coronary syndrome (ACS for ischemic tissue injury. The aim of the present study was to investigate the impact of ACS-activated inflammation on adipokine imbalance and the effects of statins on the crosstalk between inflammation and adipokine imbalance during ACS. In this study, 586 subjects were categorized into: (1 control group; (2 SA (stable angina group; and (3 ACS group. Circulating levels of hs-CRP, adiponectin and resistin were measured by ELISA. Furthermore, forty C57BL/6 mice were randomized into: sham, AMI, low-statin (atorvastatin, 2 mg/kg/day and high-statin (atorvastatin, 20 mg/kg/day group. After 3 weeks, AMI models were established by surgical coronary artery ligation. Circulating levels and adipose expressions of adiponectin and resistin were assessed in animals. Besides, we investigate the effects of atorvastatin on ox-LDL-induced adipokine imbalance in vitro. As a result, we found that ACS patients had higher hs-CRP and resistin levels and lower adiponectin levels. Our correlation analysis demonstrated hs-CRP concentrations were positively correlated with resistin but negatively with adiponectin levels in humans. Our animal findings indicated higher circulating hs-CRP and resistin levels and lower adiponectin levels in AMI mice. Atorvastatin pre-treatment dose-dependently decreased hs-CRP and resistin levels but increased adiponectin levels in mice. The consistent findings were observed about the adipose expressions of resistin and adiponectin in mice. In study in vitro, ox-LDL increased cellular resistin expressions and otherwise for adiponectin expressions, which dose-dependently reversed by the addition of atorvastatin. Therefore, our study indicates that the ACS attack activates inflammation leading to adipokine imbalance that can be ameliorated by anti-inflammation of atorvastatin.

  11. Acute cerebral and pulmonary edema induced by hemodialysis in a dog model

    Institute of Scientific and Technical Information of China (English)

    SHI Zhen-wei; WANG Zhi-gang

    2008-01-01

    Background The dialysis disequilibrium syndrome is characterized by neurologic deterioration and cerebral edema which occurs after hemodialysis. The purpose of this study was to investigate the pathogenesis of acute cerebral and pulmonary edema induced by hemodialysis.Methods We evaluated the effects of hemodialysis on the biochemical and hemodynamic parameters of the plasma and cerebrospinal fluid, including the intracranial pressure, dry/wet ratio, and pulmonary edema index, and we also examined the pathological changes of the brain and lung tissue in dogs suffering from uremia.Results Seventy-two hours after bilateral ureteral ligation, 10 uremic dogs were hemodialyzed for 2 hours, yielding a 73.6% and 60.1% decrease in the plasma urea and creatinine, respectively, a decrease in the plasma osmolality from (359±18) mOsm/kgH2O to (304±6) mOsm/kgH2O (P <0.01 ), a decrease in the dry/wet ratio of the lung and brain tissue,and an increase in the hemodynamic parameters (right atrial pressure, right ventricular pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, and central venous pressure), intracranial pressure, total pulmonary resistance index, and pulmonary edema index. Moreover, the pathological examination revealed lung and brain edema in the dialyzed dogs. This group was compared to 3 control groups: 6 uremic dogs which were sham dialyzed without dialysate so that no fall in the plasma urea occurred, and 12 uremic and 12 nonuremic animals that were not dialyzed.However, the parameters mentioned above were not significantly changed among these 3 control groups.Conclusions The acute brain and lung edema in our model appeared to be primarily due to a large osmotic gradient between the plasma and the brain and lung. This is the "urea reverse effect" which promoted the osmotically-induced lung and brain swelling.

  12. Papillary muscle rupture due to acute myocardial infarction followed by cardiogenic shock, pulmonary edema, and acute renal failure

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    Ilić Radoje

    2005-01-01

    Full Text Available Aim. The case of successful surgical treatment of anterolateral papillary muscle rupture due to acute myocardial infarction with cardiogenic shock, pulmonary edema and acute renal failure. Case report. A 62-year old male from Belgrade with chest pain, hypotension and a new heart murmur refused hospitalization at the Military Medical Academy. On the third day of his illness he was readmitted to MMA as an emergency due to hemoptysis. Examination revealed mitral valve anterolateral papillary muscle rupture. The patient, with signs of cardiogenic shock and acute renal failure, was immediately operated on. The surgery was performed using extracorporeal circulation. An artificial mitral valve was implanted, and myocardial revascularization accomplished with one venous graft of the left anterior descending artery. On the second postoperative day, hemodialysis was carried out due to acute renal failure. On the 28th postoperative day, the patient was discharged from the hospital being hemodynamically stable with normal renal function and balanced anticoagulation. The case is interesting in terms of unrecognized papillary muscle rupture that led to the development of cardiogenic shock, hemoptysis and acute renal failure. Conclusion. Papillary muscle rupture is a fatal complication of acute myocardial infarction. Early recognition and urgent surgical intervention were lifesaving in the case of complete papillary muscle rupture. Surgical treatment, regardless of high risk, is the procedure of choice.

  13. Mechanisms of carbon nanotube-induced toxicity: focus on pulmonary inflammation.

    Science.gov (United States)

    Bhattacharya, Kunal; Andón, Fernando Torres; El-Sayed, Ramy; Fadeel, Bengt

    2013-12-01

    Carbon nanotubes have gained tremendous interest in a wide range of applications due to their unique physical, chemical, and electronic properties. Needless to say, close attention to the potential toxicity of carbon nanotubes is of paramount importance. Numerous studies have linked exposure of carbon nanotubes to the induction of inflammation, a complex protective response to harmful stimuli including pathogens, damaged or dying cells, and other irritants. However, inflammation is a double-edged sword as chronic inflammation can lead to destruction of tissues thus compromising the homeostasis of the organism. Here, we provide an overview of the process of inflammation, the key cells and the soluble mediators involved, and discuss research on carbon nanotubes and inflammation, including recent studies on the activation of the so-called inflammasome complex in macrophages resulting in secretion of pro-inflammatory cytokines. Moreover, recent work has shown that inflammatory cells i.e. neutrophils and eosinophils are capable of enzymatic degradation of carbon nanotubes, with mitigation of the pro-inflammatory and pro-fibrotic effects of nanotubes thus underscoring that inflammation is both good and bad.

  14. Nicardipine-Induced Acute Pulmonary Edema: A Rare but Severe Complication of Tocolysis

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    Claire Serena

    2014-01-01

    Full Text Available We report four cases of acute pulmonary edema that occurred during treatment by intravenous tocolysis using nicardipine in pregnancy patients with no previous heart problems. Clinical severity justified hospitalization in intensive care unit (ICU each time. Acute dyspnea has begun at an average of 63 hours after initiation of treatment. For all patients, the first diagnosis suspected was pulmonary embolism. The patients' condition improved rapidly with appropriate diuretic treatment and by modifying the tocolysis. The use of intravenous nicardipine is widely used for tocolysis in France even if its prescription does not have a marketing authorization. The pathophysiological mechanisms of this complication remain unclear. The main reported risk factors are spontaneous preterm labor, multiple pregnancy, concomitant obstetrical disease, association with beta-agonists, and fetal lung maturation corticotherapy. A better knowledge of this rare but serious adverse event should improve the management of patients. Nifedipine or atosiban, the efficiency of which tocolysis was also studied, could be an alternative.

  15. [Diagnostic imaging in acute pulmonary embolism. The use of spiral computed tomography, lung scintigraphy and echocardiography].

    Science.gov (United States)

    Hess, Søren; Madsen, Poul Henning; Jørgensen, Henrik Boel; Høilund-Carlsen, Poul Flemming

    2005-10-10

    Acute pulmonary embolism is an underdiagnosed and potentially lethal condition. Treatment may be lifesaving but is associated with severe side effects. Thus, reliable diagnostic imaging is essential. We conducted a literature review on the use of spiral computed tomography, lung scintigraphy and echocardiography in acute pulmonary embolism and identified 562 articles, of which 16 original papers met our inclusion criteria. From these, we concluded that none of the modalities is applicable in every situation. Spiral computed tomography can confirm the diagnosis but cannot rule out subsegmental embolism. With lung scintigraphy, perfusion imaging alone is probably sufficient and suited to both confirming and ruling out the diagnosis. Echocardiography should be reserved for patients with an emergent need for treatment and cannot rule out the diagnosis.

  16. Nicardipine-induced acute pulmonary edema: a rare but severe complication of tocolysis.

    Science.gov (United States)

    Serena, Claire; Begot, Emmanuelle; Cros, Jérôme; Hodler, Charles; Fedou, Anne Laure; Nathan-Denizot, Nathalie; Clavel, Marc

    2014-01-01

    We report four cases of acute pulmonary edema that occurred during treatment by intravenous tocolysis using nicardipine in pregnancy patients with no previous heart problems. Clinical severity justified hospitalization in intensive care unit (ICU) each time. Acute dyspnea has begun at an average of 63 hours after initiation of treatment. For all patients, the first diagnosis suspected was pulmonary embolism. The patients' condition improved rapidly with appropriate diuretic treatment and by modifying the tocolysis. The use of intravenous nicardipine is widely used for tocolysis in France even if its prescription does not have a marketing authorization. The pathophysiological mechanisms of this complication remain unclear. The main reported risk factors are spontaneous preterm labor, multiple pregnancy, concomitant obstetrical disease, association with beta-agonists, and fetal lung maturation corticotherapy. A better knowledge of this rare but serious adverse event should improve the management of patients. Nifedipine or atosiban, the efficiency of which tocolysis was also studied, could be an alternative.

  17. Nicardipine-Induced Acute Pulmonary Edema: A Rare but Severe Complication of Tocolysis

    Science.gov (United States)

    Serena, Claire; Begot, Emmanuelle; Cros, Jérôme; Hodler, Charles; Fedou, Anne Laure; Nathan-Denizot, Nathalie; Clavel, Marc

    2014-01-01

    We report four cases of acute pulmonary edema that occurred during treatment by intravenous tocolysis using nicardipine in pregnancy patients with no previous heart problems. Clinical severity justified hospitalization in intensive care unit (ICU) each time. Acute dyspnea has begun at an average of 63 hours after initiation of treatment. For all patients, the first diagnosis suspected was pulmonary embolism. The patients' condition improved rapidly with appropriate diuretic treatment and by modifying the tocolysis. The use of intravenous nicardipine is widely used for tocolysis in France even if its prescription does not have a marketing authorization. The pathophysiological mechanisms of this complication remain unclear. The main reported risk factors are spontaneous preterm labor, multiple pregnancy, concomitant obstetrical disease, association with beta-agonists, and fetal lung maturation corticotherapy. A better knowledge of this rare but serious adverse event should improve the management of patients. Nifedipine or atosiban, the efficiency of which tocolysis was also studied, could be an alternative. PMID:25215245

  18. Acute pulmonary embolism with right ventricular dysfunction and left ventricular collapse. Case report.

    Directory of Open Access Journals (Sweden)

    Jorge Eliécer Rivas-Ibargüen

    2016-06-01

    Full Text Available We present the case of a patient with high risk Pulmonary Embolism (PE due to right ventricular dysfunction and severe hemodynamic dysfunction. The patient required thrombolytic therapy in the context of an initial suspicion of an acute coronary event. PE is a frequent, preventable clinical entity characterized by sudden occlusion of the pulmonary artery. The clinical spectrum is wide, from asymptomatic patients to death by shock and circulatory collapse. The basis of its treatment is anticoagulation. Therapies such as thrombolysis have been shown to have benefits in the mortality of patients in the scenario of shock and hemodynamic instability if there are no contraindications for its use. This entity represents a challenge since the clinical manifestations may be very similar to those of an acute coronary event and other potentially fatal conditions.

  19. Does acute exposure to aldehydes impair pulmonary function and structure?

    Science.gov (United States)

    Abreu, Mariana de; Neto, Alcendino Cândido; Carvalho, Giovanna; Casquillo, Natalia Vasconcelos; Carvalho, Niedja; Okuro, Renata; Ribeiro, Gabriel C Motta; Machado, Mariana; Cardozo, Aléxia; Silva, Aline Santos E; Barboza, Thiago; Vasconcellos, Luiz Ricardo; Rodrigues, Danielle Araujo; Camilo, Luciana; Carneiro, Leticia de A M; Jandre, Frederico; Pino, Alexandre V; Giannella-Neto, Antonio; Zin, Walter A; Corrêa, Leonardo Holanda Travassos; Souza, Marcio Nogueira de; Carvalho, Alysson R

    2016-07-15

    Mixtures of anhydrous ethyl alcohol and gasoline substituted for pure gasoline as a fuel in many Brazilian vehicles. Consequently, the concentrations of volatile organic compounds (VOCs) such as ketones, other organic compounds, and particularly aldehydes increased in many Brazilian cities. The current study aims to investigate whether formaldehyde, acetaldehyde, or mixtures of both impair lung function, morphology, inflammatory and redox responses at environmentally relevant concentrations. For such purpose, C57BL/6 mice were exposed to either medical compressed air or to 4 different mixtures of formaldehyde and acetaldehyde. Eight hours later animals were anesthetized, paralyzed and lung mechanics and morphology, inflammatory cells and IL-1β, KC, TNF-α, IL-6, CCL2, MCP-1 contents, superoxide dismutase and catalalase activities were determined. The extra pulmonary respiratory tract was also analyzed. No differences could be detected between any exposed and control groups. In conclusion, no morpho-functional alterations were detected in exposed mice in relation to the control group.

  20. Erythropoietin augments the cytokine response to acute endotoxin-induced inflammation in humans

    DEFF Research Database (Denmark)

    Hojman, Pernille; Taudorf, Sarah; Lundby, Carsten;

    2009-01-01

    Recent studies have shown that erythropoietin (EPO) offers protection against ischemia, hemorrhagic shock and systemic inflammation in many tissues and it has been suggested that EPO has anti-inflammatory effects. With the aim of investigating the potential acute anti-inflammatory effects of EPO...... receiving either (1) LPS alone, (2) EPO alone (15,000 IE of rHuEPO) or (3) EPO and LPS. Endotoxin administration alone induced a 3-, 12- and 5-fold increase in plasma concentrations of TNF-alpha, IL-6 and IL-10, respectively, 3h after LPS challenge. When EPO was given prior to a bolus injection...... with endotoxin, the levels of TNF-alpha and IL-6 were enhanced by 5- and 40-fold, respectively, whereas the endotoxin-induced increase in IL-10 response was not influenced by EPO. In contrast to our hypothesis, we find that EPO augments the acute inflammatory effect....

  1. [Effect of artificial ventilation on pulmonary capillary pressure in acute respiratory insufficiency].

    Science.gov (United States)

    Labrousse, J; Tenaillon, A; Massabie, P; Simonneau, G; Lissac, J

    1977-05-07

    To determine the influence of intermittent positive pressure breathing (IPPB), the level of pulmonary capillary wedge pressure (PCWP) was compared during IPPB and after a short period off the respirator in 68 occasions on 42 patients with an acute respiratory failure (ARF) of various etiologies. During IPPB, the average PCWP was in the normal range in patients with toxic or neurologic comas and in cases of increased pulmonary capillary permeability edema (IPCPE), PCWP slightly increased within chronic obstructive pulmonary disease (COPD) complicated with ARF and in hemodynamic acute pulmonary edema (HAPE). During the weaning stage, PCWP decreased in the groups of coma, COPD, and IPCPE, but increased in HAPE. The weaning test demonstrates that IPPB influenced PCWP in all patients. Therefore, PCWP cannot be assumed to represent the left ventricle filling pressure. The weaning test allows differentiation of IPCPE from HAPE. In the event of over-infusion or hypovolemia, PCWP measured under IPPB can lead to misinterpretation if not followed up by a second measurement off the respirator.

  2. Management of Acute Exacerbation of Asthma and Chronic Obstructive Pulmonary Disease in the Emergency Department.

    Science.gov (United States)

    Suau, Salvador J; DeBlieux, Peter M C

    2016-02-01

    Acute asthma and chronic obstructive pulmonary disease (COPD) exacerbations are the most common respiratory diseases requiring emergent medical evaluation and treatment. Asthma and COPD are chronic, debilitating disease processes that have been differentiated traditionally by the presence or absence of reversible airflow obstruction. Asthma and COPD exacerbations impose an enormous economic burden on the US health care budget. In daily clinical practice, it is difficult to differentiate these 2 obstructive processes based on their symptoms, and on their nearly identical acute treatment strategies; major differences are important when discussing anatomic sites involved, long-term prognosis, and the nature of inflammatory markers.

  3. A rare case of tricuspid valve thrombus with acute pulmonary embolism

    Institute of Scientific and Technical Information of China (English)

    GUO Chun-yan; TENG Ying-xing; YANG Chuan-rui; SHEN Lu-hua; GU Fu-sheng; LI Hong-wei

    2011-01-01

    The development of thrombus on the tricuspid valve is very rare.This report describes a case of acute pulmonary embolism (PE) with a mass on the tricuspid valve in a normal heart,detected by bedside transthoracic echocardiography (TTE).After successful surgical management,the histopathological examination revealed the mass from the tricuspid valve to be mixed thrombus.The early use of bedside TrE can facilitate the prompt diagnosis and aggressive therapy when PE is suspected.

  4. Effects of budesonide and N-acetylcysteine on acute lung hyperinflation, inflammation and injury in rats.

    Science.gov (United States)

    Jansson, Anne-Helene; Eriksson, Christina; Wang, Xiangdong

    2005-08-01

    Leukocyte activation and production of inflammatory mediators and reactive oxygen species are important in the pathogenesis of lipopolysaccharide (LPS)-induced acute lung injury. The present study investigated acute lung hyperinflation, edema, and lung inflammation 4 h after an intratracheal instillation of LPS (0.5, 2.5, 5, 10, 50, 100, 500, 1000, and 5000 microg/ml/kg). Effects of budesonide, an inhaled anti-inflammatory corticosteroids, and N-acetylcysteine (NAC), an antioxidant, were evaluated in Wistar rats receiving either low (2.5 microg/ml/kg) or high (50 microg/ml/kg) concentrations of LPS. This study demonstrates that LPS in a concentration-dependent pattern induces acute lung hyperinflation measured by excised lung gas volume (25-45% above control), lung injury indicated by increased lung weight (10-60%), and lung inflammation characterized by the infiltration of leukocytes (40-14000%) and neutrophils (80-17000%) and the production of cytokines (up to 2700%) and chemokines (up to 350%) in bronchoalveolar lavage fluid (BALF). Pretreatment with NAC partially prevented tumor necrosis factor alpha (TNFalpha) production induced by the low concentration of LPS, while pretreatment with budesonide totally prevented the increased production of TNFalpha, interleukin (IL)-1beta, IL-6, and monocyte chemoattractive protein (MCP)-1 after LPS challenge at both low and high concentrations. Budesonide failed to prevent BALF levels of macrophage inflammatory protein (MIP)-2 and cytokine-induced neutrophil chemoattractant 1 (GRO/CINC-1) as well as lung hyperinflation induced by both low and high concentrations of LPS. Pretreatment with budesonide totally prevented the formation of lung edema at the low concentration of LPS and had partial effects on acute lung injury and leukocyte influx at the high concentrations. Thus, our data indicate that therapeutic effects of budesonide and NAC are dependent upon the severity of the disease.

  5. Effects of inhaled corticosteroids on airway inflammation in chronic obstructive pulmonary disease: a systematic review and meta-analysis

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    Jen R

    2012-09-01

    Full Text Available Rachel Jen,1 Stephen,1 Rennard,2 Don D Sin1,31Department of Medicine, Respiratory Division, University of British Columbia, Vancouver, BC, Canada; 2Internal Medicine Section of Pulmonary and Critical Care, Nebraska Medical Center, Omaha, NE, USA; 3Institute of Heart and Lung Health and the UBC James Hogg Research Center, St Paul's Hospital, Vancouver, BC, CanadaBackground: Chronic obstructive pulmonary disease (COPD is characterized by chronic inflammation in the small airways. The effect of inhaled corticosteroids (ICS on lung inflammation in COPD remains uncertain. We sought to determine the effects of ICS on inflammatory indices in bronchial biopsies and bronchoalveolar lavage fluid of patients with COPD.Methods: We searched Medline, Embase, Cinahl, and the Cochrane database for randomized, controlled clinical trials that used bronchial biopsies and bronchoalveolar lavage to evaluate the effects of ICS in stable COPD. For each chosen study, we calculated the mean differences in the concentrations of inflammatory cells before and after treatment in both intervention and control groups. These values were then converted into standardized mean differences (SMD to accommodate the differences in patient selection, clinical treatment, and biochemical procedures that were employed across the original studies. If significant heterogeneity was present (P < 0.1, then a random effects model was used to pool the original data; otherwise, a fixed effects model was used.Results: We identified eight original studies that met the inclusion criteria. Four studies used bronchial biopsies (n = 102 participants and showed that ICS were effective in reducing CD4 and CD8 cell counts (SMD, −0.52 units and −0.66 units, 95% confidence interval. The five studies used bronchoalveolar lavage fluid (n = 309, which together showed that ICS reduced neutrophil and lymphocyte counts (SMD, −0.64 units and −0.64 units, 95% confidence interval. ICS on the other hand

  6. Effects of Ischemic Acute Kidney Injury on Lung Water Balance: Nephrogenic Pulmonary Edema?

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    Rajit K. Basu

    2011-01-01

    Full Text Available Pulmonary edema worsens the morbidity and increases the mortality of critically ill patients. Mechanistically, edema formation in the lung is a result of net flow across the alveolar capillary membrane, dependent on the relationship of hydrostatic and oncotic pressures. Traditionally, the contribution of acute kidney injury (AKI to the formation of pulmonary edema has been attributed to bulk fluid accumulation, increasing capillary hydrostatic pressure and the gradient favoring net flow into the alveolar spaces. Recent research has revealed more subtle, and distant, effects of AKI. In this review we discuss the concept of nephrogenic pulmonary edema. Pro-inflammatory gene upregulation, chemokine over-expression, altered biochemical channel function, and apoptotic dysregulation manifest in the lung are now understood as “extra-renal” and pulmonary effects of AKI. AKI should be counted as a disease process that alters the endothelial integrity of the alveolar capillary barrier and has the potential to overpower the ability of the lung to regulate fluid balance. Nephrogenic pulmonary edema, therefore, is the net effect of fluid accumulation in the lung as a result of both the macroscopic and microscopic effects of AKI.

  7. IP-10 is a potential biomarker of cystic fibrosis acute pulmonary exacerbations.

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    George M Solomon

    Full Text Available BACKGROUND: Cystic fibrosis (CF is characterized by acute pulmonary exacerbations (APE. The CF nasal airway exhibits a similar ion transport defect as the lung, and colonization, infection, and inflammation within the nasal passages are common among CF patients. Nasal lavage fluid (NLF is a minimally invasive means to collect upper airway samples. METHODS: We collected NLF at the onset and resolution of CF APE and compared a 27-plex cytokine profile to stable CF outpatients and normal controls. We also tested IP-10 levels in the bronchoalveolar lavage fluid (BALF of CF patients. Well-differentiated murine sinonasal monolayers were exposed to bacterial stimulus, and IP-10 levels were measured to test epithelial secretion. RESULTS: Subjects hospitalized for APE had elevated IP-10 (2582 pg/mL [95% CL of mean: 818,8165], N=13 which significantly decreased (647 pg/mL [357,1174], P<0.05, N =13 following antimicrobial therapy. Stable CF outpatients exhibited intermediately elevated levels (680 pg/mL [281,1644], N=13 that were less than CF inpatients upon admission (P=0.056 but not significantly different than normal controls (342 pg/mL [110,1061]; P=0.3, N=10. IP-10 was significantly increased in CF BALF (2673 pg/mL [1306,5458], N=10 compared to healthy post-lung transplant patients (8.4 pg/mL [0.03,2172], N=5, P<0.001. IP-10 levels from well-differentiated CF murine nasal epithelial monolayers exposed to Pseudomonas PAO-1 bacteria-free prep or LPS (100 nM apically for 24 hours were significantly elevated (1159 ± 147, P<0.001 for PAO-1; 1373 ± 191, P<0.001 for LPS vs. 305 ± 68 for vehicle controls. Human sino-nasal epithelial cells derived from CF patients had a similar response to LPS (34% increase, P<0.05, N=6. CONCLUSIONS: IP-10 is elevated in the nasal lavage of CF patients with APE and responds to antimicrobial therapy. IP-10 is induced by airway epithelia following stimulation with bacterial pathogens in a murine model. Additional research

  8. Eupafolin nanoparticle improves acute renal injury induced by LPS through inhibiting ROS and inflammation.

    Science.gov (United States)

    Zhang, Hao; Chen, Ming-Kun; Li, Ke; Hu, Cheng; Lu, Min-Hua; Situ, Jie

    2017-01-01

    Acute renal injury is a common severe clinical syndrome, occurring in many clinical situations. It is necessary to explore effective drugs to treat it. Eupafolin is a flavonoid compound, derived from Phyla nodiflora, which has been previously reported to possess a variety of pharmacological activities, including anti-inflammatory and antioxidant effects. However, it is known little about how it works in acute renal injury. Also, eupafolin is characterized by skin penetration and poor water solubility, limiting its clinical applications. Thus, we synthesized an eupafolin nanoparticle delivery system. We found that eupafolin nanoparticle could address the physicochemical defects of raw eupafolin and increase water solubility without any toxicity to normal renal cells via reducing particle size. Eupafolin nanoparticle attenuated LPS-induced acute renal injury in mice through inhibiting oxidative stress and inflammation accompanied with up-regulated SOD activity and down-regulated pro-inflammatory cytokines. Additionally, inactivation of NF-κB and MAPKs of p38, ERK1/2 and JNK signaling pathways was a main molecular mechanism by which eupafolin nanoparticle improved renal injury. Together, eupafolin nanoparticle exhibits effective anti-oxidant and anti-inflammatory activities, which could be used as a potential drug to ameliorate acute renal injury clinically.

  9. Sarcoidosis-associated pulmonary hypertension: acute vasoresponsiveness to inhaled nitric oxide and the relation to long-term effect of sildenafil

    DEFF Research Database (Denmark)

    Milman, Nils; Svendsen, Claus Bo; Iversen, Martin

    2009-01-01

    Abstract Background: Severe pulmonary sarcoidosis is often complicated by pulmonary hypertension (PH) caused by different pathophysiological mechanisms. Objectives: To assess the acute vasoresponsiveness in patients with sarcoidosis and PH and the relation to the therapeutic effect of sildenafil...

  10. A review of pulmonary coagulopathy in acute lung injury, acute respiratory distress syndrome and pneumonia

    NARCIS (Netherlands)

    Nieuwenhuizen, Laurens; de Groot, Philip G.; Grutters, Jan C.; Biesma, Douwe H.

    2009-01-01

    Enhanced bronchoalveolar coagulation is a hallmark of many acute inflammatory lung diseases such as acute lung injury, acute respiratory distress syndrome and pneumonia. Intervention with natural anticoagulants in these diseases has therefore become a topic of interest. Recently, new data on the rol

  11. The many faces of airway inflammation - Asthma and chronic obstructive pulmonary disease

    NARCIS (Netherlands)

    O'Byrne, PM; Postma, DS

    1999-01-01

    Airway diseases, predominantly asthma and chronic obstructive pulmonary disease (COPD), are among the world's most prevalent diseases. The prevalence of asthma has been incasing over the past 20 yr in most countries where this has been studied, and it affects up to 10% of the populations of most dev

  12. Changing glucocorticoid action: 11β-hydroxysteroid dehydrogenase type 1 in acute and chronic inflammation.

    Science.gov (United States)

    Chapman, Karen E; Coutinho, Agnes E; Zhang, Zhenguang; Kipari, Tiina; Savill, John S; Seckl, Jonathan R

    2013-09-01

    Since the discovery of cortisone in the 1940s and its early success in treatment of rheumatoid arthritis, glucocorticoids have remained the mainstay of anti-inflammatory therapies. However, cortisone itself is intrinsically inert. To be effective, it requires conversion to cortisol, the active glucocorticoid, by the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). Despite the identification of 11β-HSD in liver in 1953 (which we now know to be 11β-HSD1), its physiological role has been little explored until recently. Over the past decade, however, it has become apparent that 11β-HSD1 plays an important role in shaping endogenous glucocorticoid action. Acute inflammation is more severe with 11β-HSD1-deficiency or inhibition, yet in some inflammatory settings such as obesity or diabetes, 11β-HSD1-deficiency/inhibition is beneficial, reducing inflammation. Current evidence suggests both beneficial and detrimental effects may result from 11β-HSD1 inhibition in chronic inflammatory disease. Here we review recent evidence pertaining to the role of 11β-HSD1 in inflammation. This article is part of a Special Issue entitled 'CSR 2013'.

  13. Effect of Gedunin on Acute Articular Inflammation and Hypernociception in Mice

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    Fernando P. Conte

    2015-02-01

    Full Text Available Gedunin, a natural limonoid from Meliaceae species, has been previously described as an antiinflammatory compound in experimental models of allergic inflammation. Here, we report the antiinflammatory and antinociceptive effects of gedunin in an acute model of articular inflammation induced by zymosan (500 μg/cavity; intra-articular in C57BL/6 mice. Intraperitoneal (i.p. pretreatment with gedunin (0.005–5 mg/kg impaired zymosan-induced edema formation, neutrophil accumulation and hypernociception in mouse knee joints, due to decreased expression of preproET-1 mRNA and production of LTB4, PGE2, TNF-α and IL-6. Mouse post-treatment with gedunin (0.05 mg/kg; i.p. 1 and 6 h after stimulation also impaired articular inflammation, by reverting edema formation, neutrophil accumulation and the production of lipid mediators, cytokines and endothelin. In addition, gedunin directly modulated the functions of neutrophils and macrophages in vitro. The pre-incubation of neutrophil with gedunin (100 µM impaired shape change, adhesion to endothelial cells, chemotaxis and lipid body formation triggered by different stimuli. Macrophage pretreatment with gedunin impaired intracellular calcium mobilization, nitric oxide production, inducible nitric oxide synthase expression and induced the expression of the antiinflammatory chaperone heat shock protein 70. Our results demonstrate that gedunin presents remarkable antiinflammatory and anti-nociceptive effects on zymosan-induced inflamed knee joints, modulating different cell populations.

  14. Inflammation, complement, ischemia and amoebic survival in acute experimental amoebic liver abscesses in hamsters.

    Science.gov (United States)

    Olivos-García, A; Nequiz-Avendaño, M; Tello, E; Martínez, R D; González-Canto, A; López-Vancell, R; García de León, M C; Montfort, I; Pérez-Tamayo, R

    2004-08-01

    We have examined the role of inflammatory cells, ischemia and serum complement on the development of acute experimental amoebic liver abscess in hamsters (AEALAH). In hamsters made leukopenic by whole body radiation (800 rad) and daily intraperitoneal glycogen injections, the absence of inflammatory cells and liver tissue damage surrounding the parasites resulted in their rapid (24 h) disappearance from the liver, which showed no lesions. Focal liver ischemia, always present in control AEALAH with inflammation and tissue destruction, was reproduced in radiated hamsters by injection of amoebae mixed with Superdex microspheres, but again in the absence of inflammation, amoebae caused no liver damage and disappeared in 24 h. In hamsters made hypocomplementemic by injection of purified cobra venom factor (CVF), amoebae caused AEALA indistinguishable from controls, but in leukopenic + hypocomplementemic hamsters, amoebae were unable to produce lesions and disappeared from the liver in 48 h. We conclude that inflammation and tissue damage are required for the survival of amoebae in AEALAH and for the progression of the experimental disease.

  15. MMP-3 Deficiency Alleviates Endotoxin-Induced Acute Inflammation in the Posterior Eye Segment

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    Inge Van Hove

    2016-11-01

    Full Text Available Matrix metalloproteinase-3 (MMP-3 is known to mediate neuroinflammatory processes by activating microglia, disrupting blood–central nervous system barriers and supporting neutrophil influx into the brain. In addition, the posterior part of the eye, more specifically the retina, the retinal pigment epithelium (RPE and the blood–retinal barrier, is affected upon neuroinflammation, but a role for MMP-3 during ocular inflammation remains elusive. We investigated whether MMP-3 contributes to acute inflammation in the eye using the endotoxin-induced uveitis (EIU model. Systemic administration of lipopolysaccharide induced an increase in MMP-3 mRNA and protein expression level in the posterior part of the eye. MMP-3 deficiency or knockdown suppressed retinal leukocyte adhesion and leukocyte infiltration into the vitreous cavity in mice subjected to EIU. Moreover, retinal and RPE mRNA levels of intercellular adhesion molecule 1 (Icam1, interleukin 6 (Il6, cytokine-inducible nitrogen oxide synthase (Nos2 and tumor necrosis factor α (Tnfα, which are key molecules involved in EIU, were clearly reduced in MMP-3 deficient mice. In addition, loss of MMP-3 repressed the upregulation of the chemokines monocyte chemoattractant protein (MCP-1 and (C-X-C motif ligand 1 (CXCL1. These findings suggest a contribution of MMP-3 during EIU, and its potential use as a therapeutic drug target in reducing ocular inflammation.

  16. Changing glucocorticoid action: 11β-Hydroxysteroid dehydrogenase type 1 in acute and chronic inflammation

    Science.gov (United States)

    Chapman, Karen E.; Coutinho, Agnes E.; Zhang, Zhenguang; Kipari, Tiina; Savill, John S.; Seckl, Jonathan R.

    2013-01-01

    Since the discovery of cortisone in the 1940s and its early success in treatment of rheumatoid arthritis, glucocorticoids have remained the mainstay of anti-inflammatory therapies. However, cortisone itself is intrinsically inert. To be effective, it requires conversion to cortisol, the active glucocorticoid, by the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). Despite the identification of 11β-HSD in liver in 1953 (which we now know to be 11β-HSD1), its physiological role has been little explored until recently. Over the past decade, however, it has become apparent that 11β-HSD1 plays an important role in shaping endogenous glucocorticoid action. Acute inflammation is more severe with 11β-HSD1-deficiency or inhibition, yet in some inflammatory settings such as obesity or diabetes, 11β-HSD1-deficiency/inhibition is beneficial, reducing inflammation. Current evidence suggests both beneficial and detrimental effects may result from 11β-HSD1 inhibition in chronic inflammatory disease. Here we review recent evidence pertaining to the role of 11β-HSD1 in inflammation. This article is part of a Special Issue entitled ‘CSR 2013’. PMID:23435016

  17. Corosolic acid ameliorates acute inflammation through inhibition of IRAK-1 phosphorylation in macrophages

    Science.gov (United States)

    Kim, Seung-Jae; Cha, Ji-Young; Kang, Hye Suk; Lee, Jae-Ho; Lee, Ji Yoon; Park, Jae-Hyung; Bae, Jae-Hoon; Song, Dae-Kyu; Im, Seung-Soon

    2016-01-01

    Corosolic acid (CA), a triterpenoid compound isolated from Lagerstroemia speciosa L. (Banaba) leaves, exerts anti-inflammatory effects by regulating phosphorylation of interleukin receptor- associated kinase (IRAK)-2 via the NF-κB cascade. However, the protective effect of CA against endotoxic shock has not been reported. LPS (200 ng/mL, 30 min) induced phosphorylation of IRAK-1 and treatment with CA (10 μM) significantly attenuated this effect. In addition, CA also reduced protein levels of NLRP3 and ASC which are the main components of the inflammasome in BMDMs. LPS-induced inflammasome assembly through activation of IRAK-1 was down-regulated by CA challenge. Treatment with Bay11-7082, an inhibitor of IκB-α, had no effect on CA-mediated inhibition of IRAK-1 activation, indicating that CA-mediated attenuation of IRAK-1 phosphorylation was independent of NF-κB signaling. These results demonstrate that CA ameliorates acute inflammation in mouse BMDMs and CA may be useful as a pharmacological agent to prevent acute inflammation. [BMB Reports 2016; 49(5): 276-281] PMID:26615974

  18. Gender Differences in Acute Cadmium-Induced Systemic Inflammation in Rats

    Institute of Scientific and Technical Information of China (English)

    MILENA KATARANOVSKI; SRDJA JANKOVI(C); DRAGAN KATARANOVSKI; JELENA (S)TOSI(C); DESA BOGOJEVI(C)

    2009-01-01

    Objective To examine the presence of gender differences in pro-inflammatory potential of cadmium in rats by comparing systemic inflammatory response to acute cadmium intoxication in animals of the two sexes. Methods Basic aspects of this response were evaluated, including plasma levels of inflammatory cytokines tumor necrosis factor (TNF) and interleukin-6 (IL-6) and of major rat acute phase protein alpha 2-macroglobulin (alpha2-M), as soluble indicators of inflammation, and the number and activity of peripheral blood leukocytes, as cellular indicators of inflammation. Results Differential increases of IL-6 and alpha 2-M (higher in males than in females) in peripheral blood cell counts and types (leukocytosis and shift in the ratio of granulocytes to lymphocytes more pronounced in males vs females) and in levels of neutrophil priming (higher in males vs females) were noted. Conclusion The data document a more intense inflammatory response to cadmium administration in males. The sex differences in inflammatory effects of cadmium might be taken into consideration in studying the toxicity of this heavy metal.

  19. Effects of Liver × receptor agonist treatment on signal transduction pathways in acute lung inflammation

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    Bramanti Placido

    2010-02-01

    Full Text Available Abstract Background Liver × receptor α (LXRα and β (LXRβ are members of the nuclear receptor super family of ligand-activated transcription factors, a super family which includes the perhaps better known glucocorticoid receptor, estrogen receptor, thyroid receptor, and peroxisome proliferator-activated receptors. There is limited evidence that LXL activation may reduces acute lung inflammation. The aim of this study was to investigate the effects of T0901317, a potent LXR receptor ligand, in a mouse model of carrageenan-induced pleurisy. Methods Injection of carrageenan into the pleural cavity of mice elicited an acute inflammatory response characterized by: accumulation of fluid containing a large number of neutrophils (PMNs in the pleural cavity, infiltration of PMNs in lung tissues and subsequent lipid peroxidation, and increased production of nitrite/nitrate (NOx, tumor necrosis factor-α, (TNF-α and interleukin-1β (IL-1β. Furthermore, carrageenan induced the expression of iNOS, nitrotyrosine and PARP, as well as induced apoptosis (TUNEL staining and Bax and Bcl-2 expression in the lung tissues. Results Administration of T0901317, 30 min after the challenge with carrageenan, caused a significant reduction in a dose dependent manner of all the parameters of inflammation measured. Conclusions Thus, based on these findings we propose that LXR ligand such as T0901317, may be useful in the treatment of various inflammatory diseases.

  20. HELICOBACTER PYLORI-ASSOCIATED INFLAMMATION IN PATIENTS WITH ACUTE CORONARY SYNDROME

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    O. N. Pavlov

    2014-07-01

    Full Text Available The aim – assessment of the prevalence of seropositivity to Helicobacter pylori infection and laboratory comparative study of the peripheralblood in patients depending on the course of coronary heart disease (CHD.Materials and methods. Observation of 100 patients with coronary artery disease and 40 control patients is presented. Investigation indicatorsof clinical blood tests, biochemical blood analysis and determination of immunoglobulin antibody titer against Helicobacter pylori.Results. In patients with coronary artery disease signs of systemic inflammation associated with the development of acute coronary syndrome are marked with increased antibody titers to infection Helicobacter pylori.Conclusion. A history of coronary artery disease in patients with Helicobacter pylori-associated gastroduodenal pathology should be considered as a factor that increases the likelihood of unstable coronary desease course. Detected in patients with coronary artery disease signs of systemic inflammation with an increase in titer of antibodies to Helicobacter pylori infection associated with development of acute coronary syndrome.

  1. The role of phosphoenolpyruvate carboxykinase in neuronal steroidogenesis under acute inflammation.

    Science.gov (United States)

    Sadasivam, Mohanraj; Ramatchandirin, Balamurugan; Balakrishnan, Sivasangari; Selvaraj, Karthikeyan; Prahalathan, Chidambaram

    2014-12-01

    Phosphoenolpyruvate carboxykinase (PEPCK) is a key gluconeogenic enzyme found in many tissues throughout the body including brain. In the present study, we have investigated the effect of bacterial lipopolysaccharide (LPS) on PEPCK and its role in neuronal steroidogenesis. Adult female albino rats were administered LPS (5mg/kg body weight) to induce acute inflammation. LPS administration resulted in a significant increase of PEPCK mRNA expression with concomitant increase in mRNA levels of steroidogenic acute regulatory (StAR) protein and other steroidogenic enzymes including 3β-hydroxysteroid dehydrogenase (3β-HSD), 17β-hydroxysteroid dehydrogenase (17β-HSD) and aromatase in brain tissue. Further, the inhibition of PEPCK expression by glipizide significantly decreased the mRNA expression of steroidogenic proteins and concurrently increased the mRNA levels of proinflammatory cytokines under LPS administration. The results of this study suggest a novel finding that PEPCK may have an important role in neuronal steroidogenesis; which serves as an adaptive response under inflammation.

  2. Administration of reconstituted polyphenol oil bodies efficiently suppresses dendritic cell inflammatory pathways and acute intestinal inflammation.

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    Elisabetta Cavalcanti

    Full Text Available Polyphenols are natural compounds capable of interfering with the inflammatory pathways of several in vitro model systems. In this study, we developed a stable and effective strategy to administer polyphenols to treat in vivo models of acute intestinal inflammation. The in vitro suppressive properties of several polyphenols were first tested and compared for dendritic cells (DCs production of inflammatory cytokines. A combination of the polyphenols, quercetin and piperine, were then encapsulated into reconstituted oil bodies (OBs in order to increase their stability. Our results showed that administration of low dose reconstituted polyphenol OBs inhibited LPS-mediated inflammatory cytokine secretion, including IL-6, IL-23, and IL-12, while increasing IL-10 and IL-1Rα production. Mice treated with the polyphenol-containing reconstituted OBs (ROBs were partially protected from dextran sodium sulfate (DSS-induced colitis and associated weight loss, while mortality and inflammatory scores revealed an overall anti-inflammatory effect that was likely mediated by impaired DC immune responses. Our study indicates that the administration of reconstituted quercetin and piperine-containing OBs may represent an effective and potent anti-inflammatory strategy to treat acute intestinal inflammation.

  3. Acute Pulmonary Edema in Patients with Cushing’s Syndrome

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    Mitra Niafar

    2015-01-01

    Full Text Available IntroductionDyspnea refers to difficulty in breathing, and short and shallow breaths. This sign is seen in numerous diseases due to pulmonary, cardiac, metabolic and neurological causes. Among cardiac causes, heart failure is considered the main cause of dyspnea.Cardiac failure is a clinical syndrome associated with a set of symptoms (dyspnea, and fatigue and signs (edema and rales. Common causes of cardiac failure include: myocardial infarction, ischemic heart disease, hypertension, valvular heart diseases, and cardiomyopathy. Among uncommon causes of heart failure, endocrine disorders such as Cushing’s syndrome can be cited. Cushing’s syndrome can present itself in less common forms such as dyspnea due to heart failure. Cushing’s syndrome’s cardiovascular complications usually occur due to hypertension, end organ damage such as left ventricular heart failure, diastolic and ischemic myocardial heart failure, which are rather seen in chronic cases of the disease and are often irreversible.Transient heart failure in patients with Cushing’s syndrome, due to adrenal adenoma, has been reported in a number of patients. In this case report, a patient is introduced who presented to emergency department with severe dyspnea (FC III, and was ultimately diagnosed with Cushing’s syndrome after work up. Three months after treatment of Cushing’s syndrome, dramatic improvement was observed in this patient’s cardiac function.

  4. Proceedings of the Workshop on Acute Lung Injury and Pulmonary Edema Held in Aberdeen Proving Ground, Maryland on 4-5 May 1989

    Science.gov (United States)

    1989-11-01

    with side effects, including pulmonary edema . The objective of this study was to determine if the pulmonary edema was cardiogenic or noncardio- genic...Proeedings ~FL gof the .1Workshop on Acute Lung Injury and Pulmonary Edema 4-5 May 1989a Aberdeen Proving Ground, Maryland I7 21 Sponsored by the...TITLE (include Security Classification) (U) Proceedings of the" Workshop on Acute Lung Injury and Pulmonary Edema , May 1989 12. PERSONAL AUTHOR(S) David

  5. Activation of Myenteric Glia during Acute Inflammation In Vitro and In Vivo.

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    Corinna Rosenbaum

    susceptible and responsive to acute systemic inflammation of the gut wall and complement knowledge on glial involvement in mucosal inflammation of the intestine.

  6. Malnutrition and inflammation in acute kidney injury due to earthquake-related crush syndrome

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    Zhang Yue

    2010-03-01

    Full Text Available Abstract Background Malnutrition and inflammation are common and serious complications in patients with acute kidney injury (AKI. However, the profile of these complications in patients with AKI caused by crush syndrome (CS remains unclear. This study describes the clinical characteristics of malnutrition and inflammation in patients with AKI and CS due to the Wenchuan earthquake. Methods One thousand and twelve victims and eighteen healthy adults were recruited to the study. They were divided into five groups: Group A was composed of victims without CS and AKI (904 cases; Group B was composed of patients with CS and AKI who haven't received renal replacement therapy (RRT (57 cases; and Group C was composed of patients with CS and AKI receiving RRT (25 cases; Group D was composed of earthquake victims with AKI but without CS (26 cases; and Group E was composed of 18 healthy adult controls. The C-reactive protein (CRP, prealbumin, transferrin, interleukin-6 and TNF-α were measured and compared between Group E and 18 patients from Group C. Results The results indicate that participants in Group C had the highest level of serum creatinine, blood urea nitrogen and uric acid. Approximately 92% of patients with CS who had RRT were suffering from hypoalbuminemia. The interleukin-6 and CRP levels were significantly higher in patients with CS AKI receiving RRT than in the control group. Patients in Group C received the highest dosages of albumin, plasma or red blood cell transfusions. One patient in Group C died during treatment. Conclusions Malnutrition and inflammation was common in patients with earthquake-related CS and had a negative impact on the prognosis of these subjects. The results of this study indicate that the use of RRT, intensive nutritional supplementation and transfusion alleviated the degree of malnutrition and inflammation in hemodialysis patients with crush syndrome.

  7. Inflammation in lung after acute myocardial infarction is induced by dendritic cell-mediated immune response.

    Science.gov (United States)

    Hu, L J; Ren, W Y; Shen, Q J; Ji, H Y; Zhu, L

    2017-01-01

    The present study was performed to describe the changes of lung tissues in mice with acute myocardial infarction (AMI) and also explain the cell mechanism involved in inflammation in lung. AMI was established by left coronary ligation in mice. Then mice were divided into three groups: control group, MW1 group (sampling after surgery for one week) and MW2 group (sampling after surgery for two weeks). Afterwards, measurement of lung weight and lung histology, cell sorting in bronchoalveolar lavage (BAL) fluid and detection of several adhesive molecules, inflammatory molecules as well as enzyme associated with inflammation were performed. Moreover, dendritic cells (DCs) were isolated from bone marrow of C57B/L6 mice. After incubating with necrotic myocardium, the expression of antigen presenting molecules, co-stimulatory molecules and inflammatory molecules were detected by flow cytometry or immunohistochemistry in DCs. We also detected T-cell proliferation after incubating with necrotic myocardium-treated DCs. AMI induced pathological changes of lung tissue and increased inflammatory cell amount in BAL fluid. AMI also increased the expression of several inflammatory factors, adhesive molecules and enzymes associated with inflammation. CD11c and TLR9, which are DC surface markers, showed a significantly increased expression in mice with AMI. Additionally, necrotic myocardium significantly increased the expression of co-stimulatory factors including CD83 and CD80, inflammatory cytokines including TNF-α, IFN-γ and NF-κB in DCs. Furthermore, DCs treated with necrotic myocardium also significantly promoted T-cell proliferation. AMI induced inflammation in lung and these pathological changes were mediated by DC-associated immune response.

  8. Violacein Treatment Modulates Acute and Chronic Inflammation through the Suppression of Cytokine Production and Induction of Regulatory T Cells.

    Science.gov (United States)

    Verinaud, Liana; Lopes, Stefanie Costa Pinto; Prado, Isabel Cristina Naranjo; Zanucoli, Fábio; Alves da Costa, Thiago; Di Gangi, Rosária; Issayama, Luidy Kazuo; Carvalho, Ana Carolina; Bonfanti, Amanda Pires; Niederauer, Guilherme Francio; Duran, Nelson; Costa, Fábio Trindade Maranhão; Oliveira, Alexandre Leite Rodrigues; Höfling, Maria Alice da Cruz; Machado, Dagmar Ruth Stach; Thomé, Rodolfo

    2015-01-01

    Inflammation is a necessary process to control infection. However, exacerbated inflammation, acute or chronic, promotes deleterious effects in the organism. Violacein (viola), a quorum sensing metabolite from the Gram-negative bacterium Chromobacterium violaceum, has been shown to protect mice from malaria and to have beneficial effects on tumors. However, it is not known whether this drug possesses anti-inflammatory activity. In this study, we investigated whether viola administration is able to reduce acute and chronic autoimmune inflammation. For that purpose, C57BL/6 mice were intraperitoneally injected with 1 μg of LPS and were treated with viola (3.5mg/kg) via i.p. at the same time-point. Three hours later, the levels of inflammatory cytokines in the sera and phenotypical characterization of leukocytes were determined. Mice treated with viola presented a significant reduction in the production of inflammatory cytokines compared with untreated mice. Interestingly, although viola is a compound derived from bacteria, it did not induce inflammation upon administration to naïve mice. To test whether viola would protect mice from an autoimmune inflammation, Experimental Autoimmune Encephalomyelitis (EAE)-inflicted mice were given viola i.p. at disease onset, at the 10th day from immunization. Viola-treated mice developed mild EAE disease in contrast with placebo-treated mice. The frequencies of dendritic cells and macrophages were unaltered in EAE mice treated with viola. However, the sole administration of viola augmented the levels of splenic regulatory T cells (CD4+Foxp3+). We also found that adoptive transfer of viola-elicited regulatory T cells significantly reduced EAE. Our study shows, for the first time, that violacein is able to modulate acute and chronic inflammation. Amelioration relied in suppression of cytokine production (in acute inflammation) and stimulation of regulatory T cells (in chronic inflammation). New studies must be conducted in order to

  9. Violacein Treatment Modulates Acute and Chronic Inflammation through the Suppression of Cytokine Production and Induction of Regulatory T Cells.

    Directory of Open Access Journals (Sweden)

    Liana Verinaud

    Full Text Available Inflammation is a necessary process to control infection. However, exacerbated inflammation, acute or chronic, promotes deleterious effects in the organism. Violacein (viola, a quorum sensing metabolite from the Gram-negative bacterium Chromobacterium violaceum, has been shown to protect mice from malaria and to have beneficial effects on tumors. However, it is not known whether this drug possesses anti-inflammatory activity. In this study, we investigated whether viola administration is able to reduce acute and chronic autoimmune inflammation. For that purpose, C57BL/6 mice were intraperitoneally injected with 1 μg of LPS and were treated with viola (3.5mg/kg via i.p. at the same time-point. Three hours later, the levels of inflammatory cytokines in the sera and phenotypical characterization of leukocytes were determined. Mice treated with viola presented a significant reduction in the production of inflammatory cytokines compared with untreated mice. Interestingly, although viola is a compound derived from bacteria, it did not induce inflammation upon administration to naïve mice. To test whether viola would protect mice from an autoimmune inflammation, Experimental Autoimmune Encephalomyelitis (EAE-inflicted mice were given viola i.p. at disease onset, at the 10th day from immunization. Viola-treated mice developed mild EAE disease in contrast with placebo-treated mice. The frequencies of dendritic cells and macrophages were unaltered in EAE mice treated with viola. However, the sole administration of viola augmented the levels of splenic regulatory T cells (CD4+Foxp3+. We also found that adoptive transfer of viola-elicited regulatory T cells significantly reduced EAE. Our study shows, for the first time, that violacein is able to modulate acute and chronic inflammation. Amelioration relied in suppression of cytokine production (in acute inflammation and stimulation of regulatory T cells (in chronic inflammation. New studies must be

  10. Salmon Thrombin as a Treatment to Attenuate Acute Pain and Promote Tissue Healing by Modulating Local Inflammation

    Science.gov (United States)

    2012-12-01

    trauma and in association with the absence of pain . Early cleavage of PAR1 by thrombin may provide its anti- nociceptive properties. We were very...1-1002 TITLE: Salmon Thrombin as a Treatment to Attenuate Acute Pain and Promote Tissue Healing by Modulating Local Inflammation... Pain and 5a. CONTRACT NUMBER Promote Tissue Healing by Modulating Local Inflammation 5b. GRANT NUMBER W81XWH-10-1-1002 5c. PROGRAM ELEMENT

  11. Investigation of Acute Pulmonary Deficits Associated with Biomass Fuel Cookstove Emissions in Rural Bangladesh

    Directory of Open Access Journals (Sweden)

    Danielle N. Medgyesi

    2017-06-01

    Full Text Available The use of solid biomass fuels in cookstoves has been associated with chronic health impacts that disproportionately affect women worldwide. Solid fuel stoves that use wood, plant matter, and cow dung are commonly used for household cooking in rural Bangladesh. This study investigates the immediate effects of acute elevated cookstove emission exposures on pulmonary function. Pulmonary function was measured with spirometry before and during cooking to assess changes in respiratory function during exposure to cookstove emissions for 15 females ages 18–65. Cookstove emissions were characterized using continuous measurements of particulate matter (PM2.5—aerodynamic diameter <2.5 μm concentrations at a 1 s time resolution for each household. Several case studies were observed where women ≥40 years who had been cooking for ≥25 years suffered from severe pulmonary impairment. Forced expiratory volume in one second over forced vital capacity (FEV1/FVC was found to moderately decline (p = 0.06 during cooking versus non-cooking in the study cohort. The study found a significant (α < 0.05 negative association between 3- and 10-min maximum PM2.5 emissions during cooking and lung function measurements of forced vital capacity (FVC, forced expiratory volume in one second (FEV1, and FEV1/FVC obtained during cooking intervals. This study found that exposure to biomass burning emissions from solid fuel stoves- associated with acute elevated PM2.5 concentrations- leads to a decrease in pulmonary function, although further research is needed to ascertain the prolonged (e.g., daily, for multiple years impacts of acute PM2.5 exposure on immediate and sustained respiratory impairment.

  12. Antibiotic and Antiinflammatory Therapy Transiently Reduces Inflammation and Hypercoagulation in Acutely SIV-Infected Pigtailed Macaques.

    Science.gov (United States)

    Pandrea, Ivona; Xu, Cuiling; Stock, Jennifer L; Frank, Daniel N; Ma, Dongzhu; Policicchio, Benjamin B; He, Tianyu; Kristoff, Jan; Cornell, Elaine; Haret-Richter, George S; Trichel, Anita; Ribeiro, Ruy M; Tracy, Russell; Wilson, Cara; Landay, Alan L; Apetrei, Cristian

    2016-01-01

    Increased chronic immune activation and inflammation are hallmarks of HIV/SIV infection and are highly correlated with progression to AIDS and development of non-AIDS comorbidities, such as hypercoagulability and cardiovascular disease. Intestinal dysfunction resulting in microbial translocation has been proposed as a lead cause of systemic immune activation and hypercoagulability in HIV/SIV infection. Our goal was to assess the biological and clinical impact of a therapeutic strategy designed to reduce microbial translocation through reduction of the microbial content of the intestine (Rifaximin-RFX) and of gut inflammation (Sulfasalazine-SFZ). RFX is an intraluminal antibiotic that was successfully used in patients with hepatic encephalopathy. SFZ is an antiinflammatory drug successfully used in patients with mild to moderate inflammatory bowel disease. Both these clinical conditions are associated with increased microbial translocation, similar to HIV-infected patients. Treatment was administered for 90 days to five acutely SIV-infected pigtailed macaques (PTMs) starting at the time of infection; seven untreated SIVsab-infected PTMs were used as controls. RFX+SFZ were also administered for 90 days to three chronically SIVsab-infected PTMs. RFX+SFZ administration during acute SIVsab infection of PTMs resulted in: significantly lower microbial translocation, lower systemic immune activation, lower viral replication, better preservation of mucosal CD4+ T cells and significantly lower levels of hypercoagulation biomarkers. This effect was clear during the first 40 days of treatment and was lost during the last stages of treatment. Administration of RFX+SFZ to chronically SIVsab-infected PTMs had no discernible effect on infection. Our data thus indicate that early RFX+SFZ administration transiently improves the natural history of acute and postacute SIV infection, but has no effect during chronic infection.

  13. Systemic Atherosclerotic Inflammation Following Acute Myocardial Infarction: Myocardial Infarction Begets Myocardial Infarction

    Science.gov (United States)

    Joshi, Nikhil V; Toor, Iqbal; Shah, Anoop S V; Carruthers, Kathryn; Vesey, Alex T; Alam, Shirjel R; Sills, Andrew; Hoo, Teng Y; Melville, Adam J; Langlands, Sarah P; Jenkins, William S A; Uren, Neal G; Mills, Nicholas L; Fletcher, Alison M; van Beek, Edwin J R; Rudd, James H F; Fox, Keith A A; Dweck, Marc R; Newby, David E

    2015-01-01

    Background Preclinical data suggest that an acute inflammatory response following myocardial infarction (MI) accelerates systemic atherosclerosis. Using combined positron emission and computed tomography, we investigated whether this phenomenon occurs in humans. Methods and Results Overall, 40 patients with MI and 40 with stable angina underwent thoracic 18F-fluorodeoxyglucose combined positron emission and computed tomography scan. Radiotracer uptake was measured in aortic atheroma and nonvascular tissue (paraspinal muscle). In 1003 patients enrolled in the Global Registry of Acute Coronary Events, we assessed whether infarct size predicted early (≤30 days) and late (>30 days) recurrent coronary events. Compared with patients with stable angina, patients with MI had higher aortic 18F-fluorodeoxyglucose uptake (tissue-to-background ratio 2.15±0.30 versus 1.84±0.18, P50 000] versus 3800 [1000 to 9200] ng/L, P<0.0001) and greater aortic 18F-fluorodeoxyglucose uptake (2.24±0.32 versus 2.02±0.21, P=0.03) than those with non–ST-segment elevation MI. Peak plasma troponin concentrations correlated with aortic 18F-fluorodeoxyglucose uptake (r=0.43, P=0.01) and, on multivariate analysis, independently predicted early (tertile 3 versus tertile 1: relative risk 4.40 [95% CI 1.90 to 10.19], P=0.001), but not late, recurrent MI. Conclusions The presence and extent of MI is associated with increased aortic atherosclerotic inflammation and early recurrent MI. This finding supports the hypothesis that acute MI exacerbates systemic atherosclerotic inflammation and remote plaque destabilization: MI begets MI. Clinical Trial Registration URL: https://www.clinicaltrials.gov. Unique identifier: NCT01749254. PMID:26316523

  14. Secretoglobin Superfamily Protein SCGB3A2 Deficiency Potentiates Ovalbumin-Induced Allergic Pulmonary Inflammation

    Directory of Open Access Journals (Sweden)

    Taketomo Kido

    2014-01-01

    Full Text Available Secretoglobin (SCGB 3A2, a cytokine-like secretory protein of small molecular weight, which may play a role in lung inflammation, is predominantly expressed in airway epithelial cells. In order to understand the physiological role of SCGB3A2, Scgb3a2−/− mice were generated and characterized. Scgb3a2−/− mice did not exhibit any overt phenotypes. In ovalbumin- (OVA- induced airway allergy inflammation model, Scgb3a2−/− mice in mixed background showed a decreased OVA-induced airway inflammation, while six times C57BL/6NCr backcrossed congenic Scgb3a2−/− mice showed a slight exacerbation of OVA-induced airway inflammation as compared to wild-type littermates. These results indicate that the loss of SCGB3A2 function was influenced by a modifier gene(s in mixed genetic background and suggest that SCGB3A2 has anti-inflammatory property. The results further suggest the possible use of recombinant human SCGB3A2 as an anti-inflammatory agent.

  15. Depletion of Neutrophils Promotes the Resolution of Pulmonary Inflammation and Fibrosis in Mice Infected with Paracoccidioides brasiliensis

    Science.gov (United States)

    Arango, Julián Camilo

    2016-01-01

    Chronic stages of paracoccidioidomycosis (PCM) are characterized by granulomatous lesions which promote the development of pulmonary fibrosis leading to the loss of respiratory function in 50% of patients; in addition, it has been observed that neutrophils predominate during these chronic stages of P. brasiliensis infection. The goal of this study was to evaluate the role of the neutrophil during the chronic stages of experimental pulmonary PCM and during the fibrosis development and tissue repair using a monoclonal specific to this phagocytic cell. Male BALB/c mice were inoculated intranasally with 1.5x106 P. brasiliensis yeast cells. A monoclonal antibody specific to neutrophils was administered at 4 weeks post-inoculation followed by doses every 48h during two weeks. Mice were sacrificed at 8 and 12 weeks post-inoculation to assess cellularity, fungal load, cytokine/chemokine levels, histopathological analysis, collagen and expression of genes related to fibrosis development. Depletion of neutrophils was associated with a significant decrease in the number of eosinophils, dendritic cells, B cells, CD4-T cells, MDSCs and Treg cells, fungal load and levels of most of the pro-inflammatory cytokines/chemokines evaluated, including IL-17, TNF-α and TGF-β1. Recovery of lung architecture was also associated with reduced levels of collagen, high expression of TGF-β3, matrix metalloproteinase (MMP)-12 and -14, and decreased expression of tissue inhibitor metalloproteinase (TIMP)-2, and MMP-8. Depletion of neutrophils might attenuate lung fibrosis and inflammation through down-regulating TGF-β1, TNF-α, IL-17, MMP-8 and TIMP-2. These results suggest that neutrophil could be considered as a therapeutic target in pulmonary fibrosis induced by P. brasiliensis. PMID:27690127

  16. Importance of chronic obstructive pulmonary disease for prognosis and diagnosis of congestive heart failure in patients with acute myocardial infarction

    DEFF Research Database (Denmark)

    Kjøller, Erik; Køber, Lars; Iversen, Kasper

    2004-01-01

    AIMS: To evaluate the importance of chronic obstructive pulmonary disease for prognosis and diagnosis of congestive heart failure in patients with acute myocardial infarction. METHOD AND RESULTS: Prospective registration of 6669 consecutive patients admitted with infarction and screened...... in patients with acute myocardial infarction without congestive heart failure, but is also a confounding factor for the diagnosis of congestive heart failure....

  17. Impacts of acute severe pulmonary regurgitation on right ventricular geometry and contractility assessed by tissue-Doppler echocardiography

    DEFF Research Database (Denmark)

    Kjaergaard, Jesper; Iversen, Kasper K; Vejlstrup, Niels G

    2010-01-01

    Little is known of the impact of acute right ventricular (RV) volume overload on RV function. We assessed the impact of acute severe pulmonary regurgitation (PR) on global and regional RV function by applying novel quantitative echocardiographic markers of myocardial performance in an animal model....

  18. Impacts of acute severe pulmonary regurgitation on right ventricular geometry and contractility assessed by tissue-Doppler echocardiography

    DEFF Research Database (Denmark)

    Kjaergaard, Jesper; Iversen, Kasper K; Vejlstrup, Niels G;

    2010-01-01

    Little is known of the impact of acute right ventricular (RV) volume overload on RV function. We assessed the impact of acute severe pulmonary regurgitation (PR) on global and regional RV function by applying novel quantitative echocardiographic markers of myocardial performance in an animal model....

  19. Interleukin-33 Drives Activation of Alveolar Macrophages and Airway Inflammation in a Mouse Model of Acute Exacerbation of Chronic Asthma

    Directory of Open Access Journals (Sweden)

    Melissa M. Bunting

    2013-01-01

    Full Text Available We investigated the role of interleukin-33 (IL-33 in airway inflammation in an experimental model of an acute exacerbation of chronic asthma, which reproduces many of the features of the human disease. Systemically sensitized female BALB/c mice were challenged with a low mass concentration of aerosolized ovalbumin for 4 weeks to induce chronic asthmatic inflammation and then received a single moderate-level challenge to trigger acute airway inflammation simulating an asthmatic exacerbation. The inflammatory response and expression of cytokines and activation markers by alveolar macrophages (AM were assessed, as was the effect of pretreatment with a neutralizing antibody to IL-33. Compared to chronically challenged mice, AM from an acute exacerbation exhibited significantly enhanced expression of markers of alternative activation, together with enhanced expression of proinflammatory cytokines and of cell surface proteins associated with antigen presentation. In parallel, there was markedly increased expression of both mRNA and immunoreactivity for IL-33 in the airways. Neutralization of IL-33 significantly decreased both airway inflammation and the expression of proinflammatory cytokines by AM. Collectively, these data indicate that in this model of an acute exacerbation of chronic asthma, IL-33 drives activation of AM and has an important role in the pathogenesis of airway inflammation.

  20. Interleukin-33 drives activation of alveolar macrophages and airway inflammation in a mouse model of acute exacerbation of chronic asthma.

    Science.gov (United States)

    Bunting, Melissa M; Shadie, Alexander M; Flesher, Rylie P; Nikiforova, Valentina; Garthwaite, Linda; Tedla, Nicodemus; Herbert, Cristan; Kumar, Rakesh K

    2013-01-01

    We investigated the role of interleukin-33 (IL-33) in airway inflammation in an experimental model of an acute exacerbation of chronic asthma, which reproduces many of the features of the human disease. Systemically sensitized female BALB/c mice were challenged with a low mass concentration of aerosolized ovalbumin for 4 weeks to induce chronic asthmatic inflammation and then received a single moderate-level challenge to trigger acute airway inflammation simulating an asthmatic exacerbation. The inflammatory response and expression of cytokines and activation markers by alveolar macrophages (AM) were assessed, as was the effect of pretreatment with a neutralizing antibody to IL-33. Compared to chronically challenged mice, AM from an acute exacerbation exhibited significantly enhanced expression of markers of alternative activation, together with enhanced expression of proinflammatory cytokines and of cell surface proteins associated with antigen presentation. In parallel, there was markedly increased expression of both mRNA and immunoreactivity for IL-33 in the airways. Neutralization of IL-33 significantly decreased both airway inflammation and the expression of proinflammatory cytokines by AM. Collectively, these data indicate that in this model of an acute exacerbation of chronic asthma, IL-33 drives activation of AM and has an important role in the pathogenesis of airway inflammation.

  1. Evolving role of systemic inflammation in comorbidities of chronic obstructive pulmonary disease

    Institute of Scientific and Technical Information of China (English)

    WANG Zeng-li

    2010-01-01

    @@ The number of individuals affected by chronic obstructive pulmonary disease (COPD) has been increasing in the last decades. As a consequence, COPD is expected to become the third most frequent cause of death worldwide by 2020.1 Exacerbations of COPD is a major cause of morbidity. In particular, they greatly contribute to decline of health-related quality of life,increase in symptoms and breathlessness, Progression of the disease, and increased risk of mortality.2

  2. Pneumocystis colonization, airway inflammation, and pulmonary function decline in acquired immunodeficiency syndrome.

    Science.gov (United States)

    Norris, Karen A; Morris, Alison; Patil, Sangita; Fernandes, Eustace

    2006-01-01

    As a result of improved diagnosis, treatment, and supportive care for HIV-infected patients, AIDS in developed countries has now become a chronic infection with prolonged survival time, but longterm complications are increasing contributors to morbidity and mortality. HIV-infected patients are at increased risk for the development of pulmonary complications, including chronic obstructive pulmonary disease (COPD); however, the mechanisms associated with this increased susceptibility have not been defined. Infectious agents may contribute to the development of COPD by upregulating inflammatory mediators in the lung that act in concert with cigarette smoke to promote lung pathology. Studies in human subjects and non-human primate models of AIDS suggest that the inflammatory response to asymptomatic carriage or colonization by the opportunistic pathogen, Pneumocystis sp. (Pc), is similar to that of COPD, which is characterized by influx of CD8+ T cells, neutrophils, and macrophages into the lungs. We have shown a high frequency of Pc colonization among asymptomatic HIV-infected subjects and in non-HIV infected subjects with COPD. To investigate the role of Pc in the progression of obstructive lung disease in HIV infections, we developed a non-human primate model of Pc colonizatoin and infection in simian immunodeficiency virus (SIV)-infected macaques. These animals develop a prolonged colonization state characterized by a persistent influx of CD8+ T cells and neutrophils, and local increases in IL-8, IFN-gamma, and TNF-alpha. SIV-infected Pc-colonized monkeys show progressive decline in pulmonary function compared to SIV-infected monkeys. We hypothesize that in the context of AIDS-immune dysfunction, Pc colonization induces inflammatory responses leading to changes in pulmonary function and architecture similar to that seen in emphysema. Information gained from these studies will lead to the development of interventions to prevent lung injury associated with Pc

  3. Sesame oil accelerates healing of 2,4,6-trinitrobenzenesulfonic acid-induced acute colitis by attenuating inflammation and fibrosis.

    Science.gov (United States)

    Periasamy, Srinivasan; Hsu, Dur-Zong; Chandrasekaran, Victor Raj Mohan; Liu, Ming-Yie

    2013-09-01

    Sesame oil is a component of traditional health food in Asian countries. Acute colitis is a form of inflammatory bowel disease (IBD) with chronic inflammatory disorder of the bowel. The precise etiology of IBD remains unknown, but it is believed that an abnormal host response to endogenous antigens causes initial tissue injury with amplification of the immune response. We investigated the protective effect of sesame oil against 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced acute colitis in rats. Rats were intracolonically instilled with TNBS (120 mg/kg) using a cannula to induce colitis and then orally gavaged with sesame oil (4 mL/kg for 7 days) to attenuate TNBS-induced acute colitis. The acute colitis activity index (ACAI) was assessed using the colon weight/length ratio (mg/cm), thickness, extension of lesion, diarrhea, and macroscopic and microscopic damage scores. In addition, the degree of inflammation, mucins, and fibrosis was assessed by measuring mast cells, CD68(+) cells, neutral mucin, acidic mucin, collagen, and laminin on day 8 after inducing acute colitis. All tested parameters except neutral mucins were significantly higher in TNBS-induced acute colitis. Sesame oil significantly decreased the degree of inflammation, fibrosis, and acidic mucin and increased neutral mucin. We conclude that sesame oil accelerates the healing of an inflamed colon by inhibiting inflammation, acidic mucin, and fibrosis in TNBS-induced acute colitis in rats.

  4. Biodiesel versus diesel exposure: Enhanced pulmonary inflammation, oxidative stress, and differential morphological changes in the mouse lung

    Energy Technology Data Exchange (ETDEWEB)

    Yanamala, Naveena, E-mail: wqu1@cdc.gov [Pathology and Physiology Research Branch/NIOSH/CDC, Morgantown, WV 26505 (United States); Hatfield, Meghan K., E-mail: wla4@cdc.gov [Pathology and Physiology Research Branch/NIOSH/CDC, Morgantown, WV 26505 (United States); Farcas, Mariana T., E-mail: woe7@cdc.gov [Pathology and Physiology Research Branch/NIOSH/CDC, Morgantown, WV 26505 (United States); Schwegler-Berry, Diane [Pathology and Physiology Research Branch/NIOSH/CDC, Morgantown, WV 26505 (United States); Hummer, Jon A., E-mail: qzh3@cdc.gov [Office of Mine Safety and Health Research/NIOSH/CDC, Pittsburgh, PA 15236 (United States); Shurin, Michael R., E-mail: shurinmr@upmc.edu [Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, PA (United States); Birch, M. Eileen, E-mail: mib2@cdc.gov [NIOSH/CDC, 4676 Columbia Parkway, Cincinnati, OH 45226 (United States); Gutkin, Dmitriy W., E-mail: dwgutkin@hotmail.com [Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, PA (United States); Kisin, Elena, E-mail: edk8@cdc.gov [Pathology and Physiology Research Branch/NIOSH/CDC, Morgantown, WV 26505 (United States); Kagan, Valerian E., E-mail: kagan@pitt.edu [Department of Environmental and Occupational Health, University of Pittsburgh, PA (United States); Bugarski, Aleksandar D., E-mail: zjl1@cdc.gov [Office of Mine Safety and Health Research/NIOSH/CDC, Pittsburgh, PA 15236 (United States); Shvedova, Anna A., E-mail: ats1@cdc.gov [Pathology and Physiology Research Branch/NIOSH/CDC, Morgantown, WV 26505 (United States); Department Physiology and Pharmacology, WVU, Morgantown, WV 26505 (United States)

    2013-10-15

    The use of biodiesel (BD) or its blends with petroleum diesel (D) is considered to be a viable approach to reduce occupational and environmental exposures to particulate matter (PM). Due to its lower particulate mass emissions compared to D, use of BD is thought to alleviate adverse health effects. Considering BD fuel is mainly composed of unsaturated fatty acids, we hypothesize that BD exhaust particles could induce pronounced adverse outcomes, due to their ability to readily oxidize. The main objective of this study was to compare the effects of particles generated by engine fueled with neat BD and neat petroleum-based D. Biomarkers of tissue damage and inflammation were significantly elevated in lungs of mice exposed to BD particulates. Additionally, BD particulates caused a significant accumulation of oxidatively modified proteins and an increase in 4-hydroxynonenal. The up-regulation of inflammatory cytokines/chemokines/growth factors was higher in lungs upon BD particulate exposure. Histological evaluation of lung sections indicated presence of lymphocytic infiltrate and impaired clearance with prolonged retention of BD particulate in pigment laden macrophages. Taken together, these results clearly indicate that BD exhaust particles could exert more toxic effects compared to D. - Highlights: • Exposure of mice to BDPM caused higher pulmonary toxicity compared to DPM. • Oxidative stress and inflammation were higher in BD vs to D exposed mice. • Inflammatory lymphocyte infiltrates were seen only in lungs of mice exposed to BD. • Ineffective clearance, prolonged PM retention was present only after BD exposure.

  5. Autocrine regulation of pulmonary inflammation by effector T-cell derived IL-10 during infection with respiratory syncytial virus.

    Directory of Open Access Journals (Sweden)

    Jie Sun

    2011-08-01

    Full Text Available Respiratory syncytial virus (RSV infection is the leading viral cause of severe lower respiratory tract illness in young infants. Clinical studies have documented that certain polymorphisms in the gene encoding the regulatory cytokine IL-10 are associated with the development of severe bronchiolitis in RSV infected infants. Here, we examined the role of IL-10 in a murine model of primary RSV infection and found that high levels of IL-10 are produced in the respiratory tract by anti-viral effector T cells at the onset of the adaptive immune response. We demonstrated that the function of the effector T cell -derived IL-10 in vivo is to limit the excess pulmonary inflammation and thereby to maintain critical lung function. We further identify a novel mechanism by which effector T cell-derived IL-10 controls excess inflammation by feedback inhibition through engagement of the IL-10 receptor on the antiviral effector T cells. Our findings suggest a potentially critical role of effector T cell-derived IL-10 in controlling disease severity in clinical RSV infection.

  6. Prevalence of acute pulmonary embolism among patients in a general hospital and at autopsy.

    Science.gov (United States)

    Stein, P D; Henry, J W

    1995-10-01

    The purpose of this investigation is to estimate the prevalence of acute pulmonary embolism (PE) in a general hospital, its frequency among patients who died, and the ability of physicians to diagnose PE antemortem. The prevalence of acute PE among 51,645 patients hospitalized over a 21-month period was assessed in 1 of the 6 clinical centers (Henry Ford Hospital) that participated in the collaborative study, prospective investigation of pulmonary embolism diagnosis (PIOPED). The diagnosis of PE was made by pulmonary angiography, or in those who did not undergo pulmonary angiography because they declined or were ineligible for randomization to angiography in PIOPED, the diagnosis was based on the ventilation/perfusion (V/Q) lung scan. Based on data in PIOPED, PE was considered to be present in 87% of patients with high probability V/Q scam interpretations, 30% with intermediate probability interpretations, 14% with low probability interpretations, and 4% with nearly normal V/Q scans. The estimated prevalence of acute PE in hospitalized patients was 526 of 51,645 (1.0%; 95% confidence interval [CI], 0.9 to 1.1%). Based on extrapolated data from autopsy, PE was estimated to have caused or contributed to death in 122 of 51,645 (0.2%; 95% CI, 0.19 to 0.29%). Pulmonary embolism was observed at autopsy in 59 of 404 (14.6%; 95% CI, 11.3 to 18.4%). Among patients with PE at autopsy, the PE caused or contributed to death in 22 of 59 (37.3%; 95% CI, 25.0 to 50.9%) and PE was incidental in 37 of 59 (62.7%; 95% CI, 49.1 to 75.0%). Among patients at autopsy who died from PE, the diagnosis was unsuspected in 14 of 20 (70.0%; 95% CI, 45.7 to 88.1%). Most of these patients had advanced associated disease. In these patients, death from PE occurred within 2.5 h in 13 of 14 (92.9%; 95% CI, 66.1 to 99.8%). Pulmonary embolism is common in a general hospital. The prevalence of PE at autopsy has not changed over 3 decades. The frequency of unsuspected PE in patients at autopsy has not

  7. Early Hemodynamic Disorders and Their Association with the Development of Acute Pulmonary Lesion in Severe Concomitant Injury

    Directory of Open Access Journals (Sweden)

    V. V. Moroz

    2005-01-01

    Full Text Available Early changes in the parameters of central hemodynamics and pulmonary extravascular fluid were studied in patients who had sustained a severe concomitant injury in combination with acute massive blood loss. Early postoperative monitoring of these parameters by a «Pulsion Picco Plus» invasive monitoring apparatus was ascertained to verify the early stages on non-cardiogenic pulmonary edema, to assess a risk for acute lung lesion and acute respiratory distress syndrome in the phase of reperfusion lesions, and to perform an adequate correction of therapy.

  8. Dual energy CT pulmonary blood volume assessment in acute pulmonary embolism - correlation with D-dimer level, right heart strain and clinical outcome

    Energy Technology Data Exchange (ETDEWEB)

    Bauer, Ralf W.; Frellesen, Claudia; Schell, Boris; Lehnert, Thomas; Jacobi, Volkmar; Vogl, Thomas J.; Kerl, J.M. [Clinic of the Goethe University, Department of Diagnostic and Interventional Radiology, Frankfurt (Germany); Renker, Matthias [Clinic of the Goethe University, Department of Diagnostic and Interventional Radiology, Frankfurt (Germany); Medical University of South Carolina, Heart and Vascular Center, Ashley River Tower, Charleston, SC (United States); Ackermann, Hanns [Clinic of the Goethe University, Department of Biostatistics and Mathematical Modelling, Frankfurt (Germany); Schoepf, U.J. [Medical University of South Carolina, Heart and Vascular Center, Ashley River Tower, Charleston, SC (United States)

    2011-09-15

    To investigate the role of perfusion defect (PD) size on dual energy CT pulmonary blood volume assessment as predictor of right heart strain and patient outcome and its correlation with d-dimer levels in acute pulmonary embolism (PE). 53 patients with acute PE who underwent DECT pulmonary angiography were retrospectively analyzed. Pulmonary PD size caused by PE was measured on DE iodine maps and quantified absolutely (VolPD) and relatively to the total lung volume (RelPD). Signs of right heart strain (RHS) on CT were determined. Information on d-dimer levels and readmission for recurrent onset of PE and death was collected. D-dimer level was mildly (r = 0.43-0.47) correlated with PD size. Patients with RHS had significantly higher VolPD (215 vs. 73 ml) and RelPD (9.9 vs. 2.9%) than patients without RHS (p < 0.003). There were 2 deaths and 1 readmission due of PE in 18 patients with >5% RelPD, while no such events were found for patients with <5% RelPD. Pulmonary blood volume on DECT in acute PE correlates with RHS and appears to be a predictor of patient outcome in this pilot study. (orig.)

  9. Long-term outcome of patients with persistent vascular obstruction on computed tomography pulmonary angiography 6 months after acute pulmonary embolism

    Energy Technology Data Exchange (ETDEWEB)

    Golpe, Rafael; Llano, Luis A. Perez de; Olalla, Castro-Anon [The Respiratory Service, Hospital Lucus Augusti, Lugo (Spain)], e-mail: Rafael.golpe.gomez@sergas.es; Vazquez-Caruncho, Manuel [The Radiology Service, Hospital Lucus Augusti, Lugo (Spain); Gonzalez-Juanatey, Carlos [The Cardiology Service, Hospital Lucus Augusti, Lugo (Spain); Farinas, Maria Carmen [Internal Medicine Dept., Hospital Univ. Marques de Valdecilla, Santander (Spain)

    2012-09-15

    Background: The incidence and clinical significance of pulmonary residual thrombosis 6 months after an acute pulmonary embolism (PE) are still not well-known. Purpose: To evaluate the association between residual vascular obstruction and the risk of venous thromboembolism (VTE) recurrence or death. Material and Methods: Computed tomography pulmonary angiography (CTPA) was repeated in 97 consecutive patients 6 months after an acute episode of hemodynamically stable pulmonary embolism. We assessed the long-term consequences of residual thrombosis on vital status and incidence of recurrent VTE. Results: Six patients were lost for follow-up. The remaining 91 patients were classified according to the presence (Group 1: 18 cases) or absence (Group 2: 73 cases) of residual pulmonary vascular obstruction. After a mean {+-}SD of 2.91 {+-}0.99 years, there were eight (8.8%) deaths and 11 (12.1%) VTE recurrences. Groups 1 and 2 did not differ in the incidence of death or VTE recurrence. Conclusion: Persistent pulmonary vascular obstruction on 6-month CTPA did not predict long-term adverse outcome events.

  10. Are there differences in acute phase inflammation markers regarding the type of heart failure?

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    Jaime Agüero-Ramón-Llin

    2011-09-01

    Full Text Available This study aimed to determine if there are differences in inflammatory markers in the acute phase between systolic heart failure and heart failure with preserved systolic function. One hundred and thirty-one patients with acute heart failure were recruited consecutively. At admission, plasma fibrinogen, Creactive protein, sialic acid, von Willebrand factor, vascular endothelial growth factor, interleukin-6 and NTproBNP were all evaluated. If the ejection fraction was 45% or over patients were included in the HF-PSF group; the remaining patients were included in the SHF group. The HF-PSF patients were older (72±10 vs 63±12 years, P<0.001, presented a higher rate of atrial fibrillation (56.1 vs 21.3%, P<0.001, and had a lower rate of hemoglobin (12.2±2 vs 13.3±2.1 g/dL, P<0.01. No significant differences were observed in the inflammation markers analyzed among SHF and HFPSF groups. In the acute phase of heart failure there is a marked elevation of inflammatory markers but there are no differences in the inflammatory markers analyzed between the two different types of heart failure

  11. Acticoat™ stimulates inflammation, but does not delay healing, in acute full-thickness excisional wounds.

    Science.gov (United States)

    Hartmann, Carol A; Rode, Heinz; Kramer, Beverley

    2016-12-01

    Acticoat™ has antimicrobial and anti-inflammatory effects which aid wound healing. However, in vitro studies indicate that Acticoat™ is cytotoxic and clinical and in vivo studies suggest that it may delay healing in acute wounds. Therefore, this study investigated the effects of Acticoat™ on healing in acute full-thickness excisional wounds. Using a porcine model, healing was assessed on days 3, 6, 9 and 15 post-wounding. Five wounds dressed with Acticoat™ and five wounds dressed with polyurethane film (control) were assessed per day (n = 40 wounds). The rate of healing, inflammatory response, restoration of the epithelium and blood vessel and collagen formation were evaluated. No difference was found in the rate of healing between wounds treated with Acticoat™ and the control wounds. Inflammation was increased in Acticoat™-treated wounds on day 3 post-wounding compared to the control wounds. However, by day 15 post-wounding, the epithelium of the Acticoat™-treated wounds closely resembled normal epithelium. Acticoat™-treated wounds also contained a higher proportion of mature blood vessels, and differences in collagen deposition were apparent. Despite inducing an inflammatory response, Acticoat™ did not delay healing in acute wounds. Conversely, the improved quality of the epithelium and blood vessels within Acticoat™-treated wounds indicates that Acticoat™ has a beneficial effect on healing. © 2015 Medicalhelplines.com Inc and John Wiley & Sons Ltd.

  12. Nutritional status of chronic obstructive pulmonary disease patients admitted in hospital with acute exacerbation.

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    Gupta, Barkha; Kant, Surya; Mishra, Rachna; Verma, Sanjay

    2010-03-20

    Patients with Chronic Obstructive Pulmonary Disease (COPD) are frequently hospitalized with an acute exacerbation. Patients with COPD often lose weight. Consequently, deterioration in nutritional status (loss of lean body mass) is a likely repercussion of acute exacerbation in hospitalized COPD patients. The study was carried out to assess the nutritional status of COPD patients with acute exacerbation, during the period of hospital admission, and to evaluate the relationships between the nutritional indices and the pulmonary function parameters. A cross sectional observation study constituting 83 COPD patients consecutively hospitalized with acute exacerbation on accrual during a period of one year. Lung function was measured by routine spirometry. Nutritional status was assessed by the measurement of anthropometric parameters. Hospital outcome was also assessed. Statistical analysis was performed using SPSS version 16.0 Independent t-tests and Pearsons correlation coefficient was used. Mean body weight was 50.03 ± 9.23 kg. Subjects had approximately 5 kg weight loss in previous six months. All the subjects had low BMI (19.38 ± 3.10) and MUAC (21.18 ± 2.31) that was significantly below the predicted levels. The correlation between body weight and FEV(1)/FVC% was good (r = 0.648, p = 0.003). BMI was negatively correlated (r = - 0.0103, p= 0.03) with duration of hospital stay. The high prevalence of malnutrition among hospitalized COPD patients with acute exacerbation is related to their lung function and hospital outcome such as duration of hospital stay. Nutritional status; COPD; Acute exacerbation; Hospitalization.

  13. Diagnóstico por imagem do tromboembolismo pulmonar agudo Imaging of acute pulmonary thromboembolism

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    C. Isabela S. Silva

    2004-10-01

    Full Text Available O diagnóstico do tromboembolismo pulmonar agudo é baseado na probabilidade clínica, uso do dímero D (quando disponível e na avaliação por imagem. Os principais métodos de imagem utilizados no diagnóstico são representados por cintilografia ventilação-perfusão, angiografia pulmonar e tomografia computadorizada (TC. Na última década vários estudos têm demonstrado que a TC espiral apresenta elevada sensibilidade e especificidade no diagnóstico de tromboembolismo pulmonar agudo. Uma melhor avaliação das artérias pulmonares tornou-se possível com a recente introdução dos equipamentos de TC espirais com multidetectores. Vários pesquisadores têm sugerido que a angiografia pulmonar por TC espiral deve substituir a cintilografia na avaliação de pacientes com suspeita clinica de tromboembolismo pulmonar agudo. Os autores discutem os principais métodos de imagem utilizados no diagnóstico de tromboembolismo pulmonar agudo enfatizando o papel da TC espiral.The diagnosis of acute pulmonary thromboembolism is based on the clinical probability, use of D-dimer (when available and imaging. The main imaging modalities used in the diagnosis are ventilation-perfusion (V/Q, scintigraphy, angiography, and computed tomography (CT. In the last decade several studies have demonstrated that spiral CT has a high sensitivity and specificity in the diagnosis of acute pulmonary thromboembolism. The evaluation of the pulmonary arteries has further improved with the recent introduction of multidetector spiral CT scanners. Various investigators have suggested that spiral CT pulmonary angiography should replace scintigraphy in the assessment of patients whose symptoms are suggestive of acute PE. This article discusses the role of the various imaging modalities in the diagnosis of acute pulmonary thromboembolism with emphasis on the role of spiral CT.

  14. Roger S. Mitchell lecture. Uses of expression microarrays in studies of pulmonary fibrosis, asthma, acute lung injury, and emphysema.

    Science.gov (United States)

    Sheppard, Dean

    2002-03-01

    Expression microarrays are a powerful tool that could provide new information about the molecular pathways regulating common lung diseases. To exemplify how this tool can be useful, selected examples of informative experiments are reviewed. In studies relevant to asthma, the cytokine interleukin-13 has been shown to produce many of the phenotypic features of this disease, but the cellular targets in the airways and the molecular pathways activated are largely unknown. We have used microarrays to begin to dissect the different transcriptional responses of primary lung cells to this cytokine. In experiments designed to identify global transcriptional programs responsible for regulating lung inflammation and pulmonary fibrosis, we performed microarray experiments on lung tissue from wild-type mice and mice lacking a member of the integrin family know to be involved in activation of latent transforming growth factor (TGF)-beta. In addition to identifying distinct cluster of genes involved in each of these processes, these studies led to the identification of novel pathways by which TGF-beta can regulate acute lung injury and emphysema. Together, these examples demonstrate how careful application and thorough analysis of expression microarrays can facilitate the discovery of novel molecular targets for intervening in common lung diseases.

  15. Receptor Interacting Protein 3-Mediated Necroptosis Promotes Lipopolysaccharide-Induced Inflammation and Acute Respiratory Distress Syndrome in Mice.

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    Linlin Wang

    Full Text Available Necrosis amplifies inflammation and plays important roles in acute respiratory distress syndrome (ARDS. Necroptosis is a newly identified programmed necrosis that is mediated by receptor interacting protein 3 (RIP3. However, the potential involvement and impact of necroptosis in lipopolysaccharide (LPS-induced ARDS remains unknown. We therefore explored the role and mechanism of RIP3-mediated necroptosis in LPS-induced ARDS. Mice were instilled with increasing doses of LPS intratracheally to induce different degrees of ARDS. Lung tissues were harvested for histological and TUNEL staining and western blot for RIP3, p-RIP3, X-linked inhibitor of apoptosis protein (XIAP, mixed lineage kinase domain-like protein (MLKL, total and cleaved caspases-3/8. Then, wild-type and RIP3 knock-out mice were induced ARDS with 30 mg/kg LPS. Pulmonary cellular necrosis was labeled by the propidium Iodide (PI staining. Levels of TNF-a, Interleukin (IL-1β, IL-6, IL-1α, IL-10 and HMGB1, tissue myeloperoxidase (MPO activity, neutrophil counts and total protein concentration were measured. Results showed that in high dose LPS (30mg/kg and 40mg/kg -induced severe ARDS, RIP3 protein was increased significantly, accompanied by increases of p-RIP3 and MLKL, while in low dose LPS (10mg/kg and 20mg/kg -induced mild ARDS, apoptosis was remarkably increased. In LPS-induced severe ARDS, RIP3 knock-out alleviated the hypothermia symptom, increased survival rate and ameliorated the lung tissue injury RIP3 depletion also attenuated LPS-induced increase in IL-1α/β, IL-6 and HMGB1 release, decreased tissue MPO activity, and reduced neutrophil influx and total protein concentration in BALF in severe ARDS. Further, RIP3 depletion reduced the necrotic cells in the lung and decreased the expression of MLKL, but had no impact on cleaved caspase-3 in LPS-induced ARDS. It is concluded that RIP3-mediated necroptosis is a major mechanism of enhanced inflammation and lung tissue injury in

  16. Myeloid differentiation factor 88-dependent signaling is critical for acute organic dust-induced airway inflammation in mice.

    Science.gov (United States)

    Bauer, Christopher; Kielian, Tammy; Wyatt, Todd A; Romberger, Debra J; West, William W; Gleason, Angela M; Poole, Jill A

    2013-06-01

    Organic dust exposure within agricultural environments results in airway diseases. Toll-like receptor 2 (TLR2) and TLR4 only partly account for the innate response to these complex dust exposures. To determine the central pathway in mediating complex organic dust-induced airway inflammation, this study targeted the common adaptor protein, myeloid differentiation factor 88 (MyD88), and investigated the relative contributions of receptors upstream from this adaptor. Wild-type, MyD88, TLR9, TLR4, IL-1 receptor I (RI), and IL-18R knockout (KO) mice were challenged intranasally with organic dust extract (ODE) or saline, according to an established protocol. Airway hyperresponsiveness (AHR) was assessed by invasive pulmonary measurements. Bronchoalveolar lavage fluid was collected to quantitate leukocyte influx and cytokine/chemokine (TNF-α, IL-6, chemokine [C-X-C motif] ligands [CXCL1 and CXCL2]) concentrations. Lung tissue was collected for histopathology. Lung cell apoptosis was determined by a terminal deoxynucleotidyl transferase dUTP nick-end labeling assay, and lymphocyte influx and intercellular adhesion molecule-1 (ICAM-1) expression were assessed by immunohistochemistry. ODE-induced AHR was significantly attenuated in MyD88 KO mice, and neutrophil influx and cytokine/chemokine production were nearly absent in MyD88 KO animals after ODE challenges. Despite a near-absent airspace inflammatory response, lung parenchymal inflammation was increased in MyD88 KO mice after repeated ODE exposures. ODE-induced epithelial-cell ICAM-1 expression was diminished in MyD88 KO mice. No difference was evident in the small degree of ODE-induced lung-cell apoptosis. Mice deficient in TLR9, TLR4, and IL-18R, but not IL-1IR, demonstrated partial protection against ODE-induced neutrophil influx and cytokine/chemokine production. Collectively, the acute organic dust-induced airway inflammatory response is highly dependent on MyD88 signaling, and is dictated, in part, by important

  17. Free Floating Right Heart Thrombus Associated with Acute Pulmonary Embolism: An Unsettled Therapeutic Difficulty

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    Nkoke, Clovis; Faucher, Olivier; Camus, Lise; Flork, Laurence

    2015-01-01

    Free floating right heart thrombus is a rare phenomenon in the context of acute pulmonary embolism and it is associated with a poor outcome. The increased use of echocardiography has led to an increased detection of right heart thrombi. However, optimal management of free floating right heart thrombus remains controversial with no clear consensus. We present the case of a 74-year-old woman who presented to the emergency department with acute onset dyspnea on minimal exertion which had developed over a period of 1 day. A computed tomography of the chest demonstrated massive bilateral proximal pulmonary embolism. A bedside transthoracic echocardiography performed showed a moderately dilated, poorly functioning right ventricle with visible highly mobile serpiginous thrombus moving to and fro across the tricuspid valve. Thrombolytic therapy was immediately initiated with tenecteplase which resulted in excellent results. Although there is no clear consensus for the management of right heart thrombus associated with pulmonary embolism, thrombolysis is readily available and can be effective in carefully selected patients. PMID:26078887

  18. Recurrent acute pulmonary embolism and paroxysmal atrial fibrillation associated with subclinical hyperthyroidism.

    Science.gov (United States)

    Patanè, Salvatore; Marte, Filippo; Currò, Alessio; Cimino, Claudia

    2010-07-09

    Subclinical hyperthyroidism is an increasingly recognized entity that is defined as a normal serum free thyroxine and free triiodothyronine levels with a thyroid-stimulating hormone level suppressed below the normal range and usually undetectable. It has been reported that subclinical hyperthyroidism is not associated with coronary heart disease or mortality from cardiovascular causes but it is sufficient to induce arrhythmias including atrial fibrillation and atrial flutter. It has also been reported that increased factor X activity in patients with subclinical hyperthyroidism represents a potential hypercoagulable state. Elevated D-dimer levels have been reported in acute pulmonary embolism and it has also been reported that right ventricular overload and hypoxia in acute pulmonary embolism may lead to right ventricular myocardium injury reflected by elevated cardiac troponin levels too. We present a case of recurrent pulmonary embolism associated with subclinical hyperthyroidism, in an 81-year-old Italian woman. Also this case focuses attention on the importance of a correct evaluation of subclinical hyperthyroidism.

  19. Free Floating Right Heart Thrombus Associated with Acute Pulmonary Embolism: An Unsettled Therapeutic Difficulty

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    Clovis Nkoke

    2015-01-01

    Full Text Available Free floating right heart thrombus is a rare phenomenon in the context of acute pulmonary embolism and it is associated with a poor outcome. The increased use of echocardiography has led to an increased detection of right heart thrombi. However, optimal management of free floating right heart thrombus remains controversial with no clear consensus. We present the case of a 74-year-old woman who presented to the emergency department with acute onset dyspnea on minimal exertion which had developed over a period of 1 day. A computed tomography of the chest demonstrated massive bilateral proximal pulmonary embolism. A bedside transthoracic echocardiography performed showed a moderately dilated, poorly functioning right ventricle with visible highly mobile serpiginous thrombus moving to and fro across the tricuspid valve. Thrombolytic therapy was immediately initiated with tenecteplase which resulted in excellent results. Although there is no clear consensus for the management of right heart thrombus associated with pulmonary embolism, thrombolysis is readily available and can be effective in carefully selected patients.

  20. CASE REPORT Acute Compartment Syndrome of the Forearm Following Blood Gas Analysis Postthrombolysis for Pulmonary Embolism.

    Science.gov (United States)

    Bisarya, Kamal; George, Samuel; El Sallakh, Sam

    2013-01-01

    Acute compartment syndrome is an important condition with potentially serious consequences if not diagnosed and treated promptly. This report highlights a case of acute compartment syndrome of the forearm after radial artery blood gas analysis in a patient who had been thrombolyzed for a pulmonary embolus. Methods/Case Report: We present a case of a 54-year-old lady, admitted and treated for a pulmonary embolism with tenecteplase for thrombolysis. As per routine management, she had taken an arterial blood gas sample, which caused hematoma in the wrist and a few hours later developed pain and a tense right forearm being diagnosed with compartment syndrome. She underwent fasciotomies and subsequent split skin grafting. We discuss the different etiologies of compartment syndrome, clinical signs, and available investigations as well as immediate and definitive management options including fasciotomy techniques. We present the latest literature on the subject and extract valuable learning points from this case. With the common use of thrombolysis for the management of a myocardial infarction or pulmonary embolus, compartment syndrome is an uncommon but potentially associated problem. Furthermore, with blood gas sampling being part of daily clinical practice and a potential cause of this condition, the compartment syndrome becomes iatrogenic and potentiates serious litigation. As many junior doctors are performing blood gas analysis postthrombolysis, they need to assess patients adequately and realize the risk of possible sequelae such as compartment syndrome in this group and inform patients of such complications.

  1. Invasive Pulmonary Aspergillosis in a Patient with Acute Lymphoblastic Leukemia

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    Orhan Ayyıldız

    2004-01-01

    Full Text Available Fungal infections are common and life-threatening among immunosupressive patients.Invasive pulmonar aspergilloz (IPA generally occurs when Aspergillus inhaled, but rarelywith the hematogen spread of dermal or gastrointestinal Aspergillus. We present here, IPA ina 58 year-old male patient with acute lymphoblastic leukemia (ALL. He was admitted to ourclinic with fatigue, weakness, pansitopenia, and with petechia. Supportive treatment,vincristine and prednisone was initiated. Chest roentgenogram was normal. Dyspnea andfever (39.5’C were seen after 1 month of therapy. Thorax high resolution computerizedtomography was obtained and cavitary lesion was seen in the left upper-anterior segment oflung. Sputum and blood culture were negative. In spite of the empiric use of Meropenem 3gr/d, Vancomycin 2 gr/d and fluconazole 200 mg/d, fever was not turned to normal andclinical symptoms were not healed. On the fifth days of therapy amphotericin-B was initiatedand the other antibiotics were stopped after 3 days. General symptoms were healed on the 8thdays. Radiologic findings were improved partially after 20 days. The patient clinically is welland remains in remission and radiologic findings were turn to near normal after 10 monthsof treatment. We aimed to emphasis about treatment of empirical Amphotericin-B incritically ill patient with ALL.

  2. Pulmonary infection control window as a switching point for consequential ventilation: an encouraging finding in treatment of acute respiratory failure of chronic obstructive pulmonary disease

    Institute of Scientific and Technical Information of China (English)

    ZHANG Xi-long

    2005-01-01

    @@ I read with great interest the article by Collaborating Research Group for Noninvasive Mechanical Ventilation of Chinese Respiratory Society.1 Based on the concept mentioned in this paper, I have found that it is really an encouraging new finding in the field of clinical application of mechanical ventilation and treatment of acute respiratory failure (ARF) of chronic obstructive pulmonary disease (COPD).

  3. Unilateral pulmonary edema: a rare initial presentation of cardiogenic shock due to acute myocardial infarction.

    Science.gov (United States)

    Shin, Jeong Hun; Kim, Seok Hwan; Park, Jinkyu; Lim, Young-Hyo; Park, Hwan-Cheol; Choi, Sung Il; Shin, Jinho; Kim, Kyung-Soo; Kim, Soon-Gil; Hong, Mun K; Lee, Jae Ung

    2012-02-01

    Cardiogenic unilateral pulmonary edema (UPE) is a rare clinical entity that is often misdiagnosed at first. Most cases of cardiogenic UPE occur in the right upper lobe and are caused by severe mitral regurgitation (MR). We present an unusual case of right-sided UPE in a patient with cardiogenic shock due to acute myocardial infarction (AMI) without severe MR. The patient was successfully treated by percutaneous coronary intervention and medical therapy for heart failure. Follow-up chest Radiography showed complete resolution of the UPE. This case reminds us that AMI can present as UPE even in patients without severe MR or any preexisting pulmonary disease affecting the vasculature or parenchyma of the lung.

  4. [Pulmonary contusion and acute respiratory distress syndrome (ARDS) as complications of blunt chest trauma].

    Science.gov (United States)

    Michalska, Agata; Jurczyk, Agnieszka P; Machała, Waldemar; Szram, Stefan; Berent, Jarosław

    2009-01-01

    Blunt chest traumas are common nowadays due to development of motor transport. They are associated with high mortality rates because of serious injuries of internal organs. The mechanisms of injuries are complex and may cause damages ranging from small ones, such as bruises or abrasions, to life-threatening trauma. Among typical injuries there are rib fractures, sternal fractures, pneumothorax, hemothorax, diaphragm lacerations, pulmonary contusions, cardiac tamponade, cardiac rupture and many others. The authors of the article would like to emphasize the pathophysiology and diagnostic difficulties in such blunt chest trauma complications as pulmonary contusions and acute respiratory distress syndrome, for which no causal treatment is available and only early diagnosis and administration of symptomatic treatment may increase the patients' chances to survive. In Forensic Medicine Department, Medical University of Łódź, an opinion was issued on a case which illustrates the clinical problem.

  5. Java interface to a computer-aided diagnosis system for acute pulmonary embolism using PIOPED findings

    Science.gov (United States)

    Frederick, Erik D.; Tourassi, Georgia D.; Gauger, Matthew; Floyd, Carey E., Jr.

    1999-05-01

    An interface to a Computer Aided Diagnosis (CAD) system for diagnosis of Acute Pulmonary Embolism (PE) from PIOPED radiographic findings was developed. The interface is based on Internet technology which is user-friendly and available on a broad range of computing platforms. It was designed to be used as a research tool and as a data collection tool, allowing researchers to observe the behavior of a CAD system and to collect radiographic findings on ventilation-perfusion lung scans and chest radiographs. The interface collects findings from physicians in the PIOPED reporting format, processes those findings and presents them as inputs to an artificial neural network (ANN) previously trained on findings from 1,064 patients from the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) study. The likelihood of PE predicted by the ANN and by the physician using the system is then saved for later analysis.

  6. Genetics of acute inflammation: inflammatory reactions in inbred lines of mice and in their interline crosses.

    Science.gov (United States)

    Stiffel, C; Ibanez, O M; Ribeiro, O G; Decreusefond, C; Mouton, D; Siqueira, M; Biozzi, G

    1990-01-01

    Acute inflammation is induced by the subcutaneous injection of swollen polyacrylamide microbeads, its intensity measured by the cell and protein concentration of the local exudates. A large and continuous range of responses is obtained in different inbred strains of mice, which suggests a polygenic control of the inflammatory response. The variable levels of the global dominance observed in F1 hybrids issued from several parental combinations indicated that the pattern of alleles controlling high or low response was different in each parental strain. Balanced intercrossing of the 8 inbred strains studied has provided a genetically heterogeneous F3 population, presenting a high variability of responses. The value of the genetic part of F3 phenotypic variance, the spread of the interstrain differences, as well as the polygenic nature of the regulation of inflammatory responses pointed out the possibility to perform a bidirectional genetic selection by using the F3 mice as the foundation population, and response to microbeads as the selective phenotypic character.

  7. An unusual presentation of massive pulmonary embolism mimicking septal acute myocardial infarction treated with tenecteplase.

    Science.gov (United States)

    Fasullo, Sergio; Paterna, Salvatore; Di Pasquale, Pietro

    2009-02-01

    A 31-year-old man (175 cm, 82 kg) was referred to the emergency department 2 h after the sudden onset of acute dyspnea. Immediate ECG showed sinus tachycardia with ST elevations from V1 through V2 and a diagnosis of septal acute myocardial infarction was made. ECG on admission to the cardiology department showed the same results plus the S1-Q3-T3 pattern. Echocardiogram revealed a normally contracting left ventricle, a distended right ventricle with free wall hypokinesia and displacement of the interventricular septum towards the left ventricle. Thrombolytic therapy with tenecteplase 8000 IU and heparin 5000 IU was administered 5-10 min after hospitalisation and the patient was haemodynamically stable 30 min later. Echocardiogram performed 12 h after thrombolysis showed a normal left ventricle and a less distended right ventricle. Lung spiral computed tomography (CT) and lower abdominal CT on the fourth day showed large emboli in the inferior pulmonary arteries of the right and left lung. Rarely, massive pulmonary embolism may mimic anteroseptal acute myocardial infarction on ECG and this case demonstrates the utility of echocardiography for a differential diagnosis, as well as the efficacy of tenecteplase for thrombolytic therapy.

  8. Activation of the contact system and inflammation after thrombolytic therapy in patients with acute myocardial infarction.

    Science.gov (United States)

    Merlini, Piera Angelica; Cugno, Massimo; Rossi, Marco L; Agricola, Pietro; Repetto, Alessandra; Fetiveau, Raffaella; Diotallevi, Paolo; Canosi, Umberto; Mannucci, Pier Mannuccio; Ardissino, Diego

    2004-04-01

    Thrombolytic therapy activates the contact system, and factor XII activation may activate the coagulation cascade and inflammation. It is not known whether an early inflammatory response is induced by thrombolytic therapy in patients with acute myocardial infarction (AMI). We prospectively measured the plasma levels of activated factor XII, cleaved kininogen, prothrombin fragment 1 + 2 (as indexes of the contact phase and coagulation activation), and interleukin-6 and C-reactive protein (CRP) (as indexes of inflammation) in 39 patients hospitalized for AMI within 12 hours of symptom onset: 26 receiving thrombolytic therapy and 13 heparin alone. Blood samples were collected at baseline and after 90 minutes and 24 hours. Patients undergoing thrombolysis had a significant early increase in activated factor XII (from 2.2 ng/ml at baseline to 4.7 ng/ml after 90 minutes; p = 0.0001), cleaved kininogen (from 26% to 37%; p = 0.001), and fragment 1 + 2 (from 1.4 to 2.1 nmol/L; p = 0.0001), whereas the 24-hour levels were similar to baseline levels. The levels of interleukin-6 significantly increased during the first 90 minutes (from 3.9 to 6.3 microg/ml; p = 0.001), and were even higher after 24 hours (11.9 ng/ml, p = 0.0001). CRP levels increased only after 24 hours (p = 0.0001). There were no changes in these parameters in patients receiving heparin alone, except for a 24-hour increase in interleukin-6 and CRP levels. Thus, in patients with AMI receiving thrombolytic therapy, early activation of inflammation parallels the activation of the contact system and the coagulation cascade, which might contribute to microvascular obstruction and reperfusion injury.

  9. Characterisation of leukocytes in a human skin blister model of acute inflammation and resolution.

    Science.gov (United States)

    Jenner, William; Motwani, Madhur; Veighey, Kristin; Newson, Justine; Audzevich, Tatsiana; Nicolaou, Anna; Murphy, Sharon; Macallister, Raymond; Gilroy, Derek W

    2014-01-01

    There is an increasing need to understand the leukocytes and soluble mediators that drive acute inflammation and bring about its resolution in humans. We therefore carried out an extensive characterisation of the cantharidin skin blister model in healthy male volunteers. A novel fluorescence staining protocol was designed and implemented, which facilitated the identification of cell populations by flow cytometry. We observed that at the onset phase, 24 h after blister formation, the predominant cells were CD16hi/CD66b+ PMNs followed by HLA-DR+/CD14+ monocytes/macrophages, CD11c+ and CD141+ dendritic cells as well as Siglec-8+ eosinophils. CD3+ T cells, CD19+ B cells and CD56+ NK cells were also present, but in comparatively fewer numbers. During resolution, 72 h following blister induction, numbers of PMNs declined whilst the numbers of monocyte/macrophages remain unchanged, though they upregulated expression of CD16 and CD163. In contrast, the overall numbers of dendritic cells and Siglec-8+ eosinophils increased. Post hoc analysis of these data revealed that of the inflammatory cytokines measured, TNF-α but not IL-1β or IL-8 correlated with increased PMN numbers at the onset. Volunteers with the greatest PMN infiltration at onset displayed the fastest clearance rates for these cells at resolution. Collectively, these data provide insight into the cells that occupy acute resolving blister in humans, the soluble mediators that may control their influx as well as the phenotype of mononuclear phagocytes that predominate the resolution phase. Further use of this model will improve our understanding of the evolution and resolution of inflammation in humans, how defects in these over-lapping pathways may contribute to the variability in disease longevity/chronicity, and lends itself to the screen of putative anti-inflammatory or pro-resolution therapies.

  10. ACUTE AND SUBACUTE MODELS OF INFLAMMATION OF NYCTANTHES ARBOR TRISTIS AND MAHARASNADI GHAN

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    Abhijeet R. Bhalerao

    2011-10-01

    Full Text Available Aqueous Methanolic extracts of Nyctanthes Arbor tristis and Maharasnadi ghan were studied for a  inflammation   parameter using   carrageenin induced hind paw edema   and cotton pellet granuloma . The natural plant was screened for acute toxicity and it did not show any toxic or deleterious effects indicating low toxicity of the extract even at high doses at two different dose levels. In carrageenin induced hind paw edema a  significant reduction in paw volume was observed  as  compared  to  control  group  whereas  in  cotton  pellet  granuloma  model  marked inhibition in granuloma formation, reduction in the elevated levels of serum lysosomal enzymes (SGPT, SGOT, and ALP and lipid peroxidation was noted as compared to control group. The extracts exhibited profound anti-inflammatory activity in both acute and subacute animal models warranting further  investigations to establish its anti-inflammatory potential. The activity was thought  due  to  flavonoids  which  might  be  present  in  the  formulation  which  could  play  a significant role in preventing the release of histamine, leukotreins and prostaglandins. In future the extract needs to be studied for cellular line models of inflammation.

  11. Protectin D1 promotes resolution of inflammation in a murine model of lipopolysaccharide-induced acute lung injury via enhancing neutrophil apoptosis

    Institute of Scientific and Technical Information of China (English)

    Li Xingwang; Li Chunlai; Liang Wandong; Bi Yuntian; Chen Maohua; Dong Sheng

    2014-01-01

    Background Protectin D1 (PD1),derived from docosahexaenoic acid,has been shown to control and resolve inflammation in some experimental models of inflammatory disorders.We investigated the protective roles of protectin D1 in pulmonary inflammation and lung injury induced by lipopolysaccharide (LPS).Methods Mice were randomly assigned to six groups (n=6 per group):sham-vehicle group,sham-PD1 group,shamzVAD-fmk group,LPS-vehicle group,LPS-PD1 group,and LPS-PD1-zVAD-fmk group.Mice were injected intratracheally with 3 mg/kg LPS or saline,followed 24 hours later by intravenous injection of 200 μg/mouse PD1 or vehicle.At the same time,some mice were also injected intraperitoneally with the pan-caspase inhibitor zVAD-fmk.Seventy-two hours after LPS challenge,samples of pulmonary tissue and bronchoalveolar lavage fluid were collected.Optical microscopy was used to examine pathological changes in lungs.Cellularity and protein concentration in bronchoalveolar lavage fluid were analyzed.Lung wet/dry ratios and myeloperoxidase activity were measured.Apoptosis of neutrophils in bronchoalveolar lavage fluid (BALF) was also evaluated by flow cytometry.Results Intratracheal instillation of LPS increased neutrophil counts,protein concentration in bronchoalveolar lavage fluid and myeloperoxidase activity,it induced lung histological injury and edema,and also suppressed apoptosis of neutrophils in BALF.Posttreatment with PD1 inhibited LPS-evoked changes in BALF neutrophil counts and protein concentration and lung myeloperoxidase activity,with the outcome of decreased pulmonary edema and histological injury.In addition,PD1 promoted apoptosis of neutrophils in BALF.The beneficial effects of PD1 were blocked by zVAD-fmk.Conclusion Posttreatment with PD1 enhances resolution of lung inflammation during LPS-induced acute lung injury by enhancing apoptosis in emigrated neutrophils,which is,at least in part,caspase-dependent.

  12. 5-lipoxygenase is a key determinant of acute myocardial inflammation and mortality during Trypanosoma cruzi infection.

    Science.gov (United States)

    Pavanelli, Wander R; Gutierrez, Fredy R S; Mariano, Flávia S; Prado, Cibele M; Ferreira, Beatriz Rossetti; Teixeira, Mauro Martins; Canetti, Cláudio; Rossi, Marcos A; Cunha, Fernando Q; Silva, João S

    2010-08-01

    This study provides evidence supporting the idea that although inflammatory cells migration to the cardiac tissue is necessary to control the growth of Trypanosoma cruzi, the excessive influx of such cells during acute myocarditis may be deleterious to the host. Production of lipid mediators of inflammation like leukotrienes (LTs) along with cytokines and chemokines largely influences the severity of inflammatory injury in response to tissue parasitism. T. cruzi infection in mice deficient in 5-lipoxygenase (5-LO), the enzyme responsible for the synthesis of LTs and other lipid inflammatory mediators, resulted in transiently increased parasitemia, and improved survival rate compared with WT mice. Myocardia from 5-LO(-/-) mice exhibited reduced inflammation, collagen deposition, and migration of CD4(+), CD8(+), and IFN-gamma-producer cells compared with WT littermates. Moreover, decreased amounts of TNF-alpha, IFN-gamma, and nitric oxide synthase were found in the hearts of 5-LO(-/-) mice. Interestingly, despite of early higher parasitic load, 5-LO(-/-) mice survived, and controlled T. cruzi infection. These results show that efficient parasite clearance is possible in a context of moderate inflammatory response, as occurred in 5-LO(-/-) mice, in which reduced myocarditis protects the animals during T. cruzi infection. Copyright 2010 Elsevier Masson SAS. All rights reserved.

  13. Toll-like receptors elicit different recruitment kinetics of monocytes and neutrophils in mouse acute inflammation.

    Science.gov (United States)

    Imhof, Beat A; Jemelin, Stephane; Emre, Yalin

    2017-03-16

    Leukocyte recruitment is an important process in combatting pathogens. The largest class of circulating leukocytes are neutrophils, which rapidly invade inflamed tissue, followed by inflammatory Ly6C(+) monocytes. Ly6C(low) monocytes patrol the endothelial wall routinely in the steady state. We recently reported early luminal recruitment of Ly6C(low) monocytes, which preceded and orchestrated neutrophil arrival and extravasation in response to TLR7/8-mediated vascular inflammation. Here we dissected the kinetics of recruitment of monocytes and neutrophils and examined the dynamics of Ly6C(low) monocytes in response to several other Toll-like receptor (TLR) agonists, using intravital confocal microscopy. We observed two types of kinetics in mesenteric veins. TLR2, TLR5 and TLR9 agonists caused early monocyte and neutrophil influx whereas TLR3 and TLR4 agonists rapidly recruited neutrophils and caused Ly6C(low) monocytes to arrive at low levels later on. All TLR agonists, except TLR9, led Ly6C(low) monocytes to meticulously patrol the vascular wall. Finally, these monocytes released pro-inflammatory cytokines and chemokines implicated in neutrophil recruitment in response to TLR2, TLR4 and TLR9 stimulation but not to TLR3 and TLR5 agonists. These results refine our understanding of the early events in the leukocyte recruitment cascade, including the patrolling behaviour of Ly6C(low) monocytes, in TLR-mediated acute vascular inflammation. This article is protected by copyright. All rights reserved.

  14. N-Arachidonoyl Dopamine Modulates Acute Systemic Inflammation via Nonhematopoietic TRPV1

    Science.gov (United States)

    Lawton, Samira K.; Xu, Fengyun; Tran, Alphonso; Wong, Erika; Schumacher, Mark; Wilhelmsen, Kevin

    2017-01-01

    N-Arachidonoyl dopamine (NADA) is an endogenous lipid that potently activates the transient receptor potential vanilloid 1 (TRPV1), which mediates pain and thermosensation. NADA is also an agonist of cannabinoid receptors 1 and 2. We have reported that NADA reduces the activation of cultured human endothelial cells by LPS and TNF-α. Thus far, in vivo studies using NADA have focused on its neurologic and behavioral roles. In this article, we show that NADA potently decreases in vivo systemic inflammatory responses and levels of the coagulation intermediary plasminogen activator inhibitor 1 in three mouse models of inflammation: LPS, bacterial lipopeptide, and polymicrobial intra-abdominal sepsis. We also found that the administration of NADA increases survival in endotoxemic mice. Additionally, NADA reduces blood levels of the neuropeptide calcitonin gene-related peptide but increases the neuropeptide substance P in LPS-treated mice. We demonstrate that the anti-inflammatory effects of NADA are mediated by TRPV1 expressed by nonhematopoietic cells and provide data suggesting that neuronal TRPV1 may mediate NADA’s anti-inflammatory effects. These results indicate that NADA has novel TRPV1-dependent anti-inflammatory properties and suggest that the endovanilloid system might be targeted therapeutically in acute inflammation. PMID:28701511

  15. Anti-inflammatory effects of Asparagus cochinchinensis extract in acute and chronic cutaneous inflammation.

    Science.gov (United States)

    Lee, Do Yeon; Choo, Byung Kil; Yoon, Taesook; Cheon, Myeong Sook; Lee, Hye Won; Lee, A Yeong; Kim, Ho Kyoung

    2009-01-12

    Although Asparagus cochinchinensis Merrill (Liliaceae) has long been used in traditional Korean and Chinese medicine to treat inflammatory diseases, the underlying mechanism(s) by which these effects are induced remains to be defined. We investigated the effects of 70% ethanolic extract from Asparagus cochinchinensis Merrill (ACE) on skin inflammation in mice. Production of pro-inflammatory cytokines (tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta), activation of myeloperoxidase, and histological assessment were examined in acute and chronic skin inflammation using 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced mouse ear edema. We also performed acetic acid-induced vascular permeability test. ACE inhibited topical edema in the mouse ear, following administration at 200mg/kg (i.p.), leading to substantial reductions in skin thickness and tissue weight, inflammatory cytokine production, neutrophil-mediated myeloperoxidase (MPO) activity, and various histopathological indicators. Furthermore, ACE was effective at reducing inflammatory damage induced by chronic TPA exposure and evoked a significant inhibition of vascular permeability induced by acetic acid in mice. These results demonstrate that ACE is an effective anti-inflammatory agent in murine phorbol ester-induced dermatitis, and suggest that the compound may have therapeutic potential in a variety of immune-related cutaneous diseases.

  16. Evaluation of a Western Blot Test in an Outbreak of Acute Pulmonary Histoplasmosis

    Science.gov (United States)

    Pizzini, Claudia V.; Zancopé-Oliveira, Rosely M.; Reiss, Errol; Hajjeh, Rana; Kaufman, Leo; Peralta, José Mauro

    1999-01-01

    A western blot (WB) test was evaluated for detection of antibodies against native glycosylated and chemically deglycosylated M and H antigens of Histoplasma capsulatum in serum obtained from patients during the acute phase of pulmonary histoplasmosis that occurred during an outbreak. Of 275 serum samples tested by immunodiffusion and complement fixation (CF) samples from 40 patients affected during this outbreak and from 37 negative controls were tested by WB test. A group of patients whose sera were negative for CF antibodies and precipitins early in the acute stage of histoplasmosis but who all seroconverted during convalescence 6 weeks later were tested with the WB test. Antibodies against untreated H and M antigens were detected at a 1:100 dilution by WB test in 45% of the 20 acute-phase serum samples and in all 20 of the convalescent-phase specimens. The WB test’s sensitivity for acute-phase specimens increased to 90% (18 of 20 specimens) when H and M antigens were treated by periodate oxidation to inactivate susceptible carbohydrate epitopes. When native glycosylated antigens were used in the WB test, positive reactions were observed in negative control serum specimens (3 of 37 specimens; 8%) and in serum specimens obtained from asymptomatic persons screened as part of the outbreak investigation (13 of 20 specimens; 65%). These positive reactions were also attributed to glycosidic epitopes since the specificity of the WB test increased from 78 to 100% when periodate-treated H and M antigens were used. WB test with deglycosylated H and M antigens of histoplasmin provides a rapid, sensitive, and specific test to diagnose acute pulmonary histoplasmosis before precipitins can be detected. PMID:9874658

  17. Does urinary trypsin inhibitor have a role in acute lung injury induced by pulmonary contusion: a basic research in a model of rats.

    Science.gov (United States)

    Wang, Shaohua; Wang, Jin; Chen, Xi; Ruan, Zheng; Zheng, Jin; Zhang, Jie

    2014-01-01

    We evaluate the efficacy of urinary trypsin inhibitor (UTI) on inflammation, oxidative stress, hypoxemia, and diseased lesion in a rat model of acute lung injury induced by blunt trauma. Rats were allocated to 4 groups. One group served as normal control. The other 3 groups had a moderate pulmonary contusion. Except for 1 sham group administrated saline, 1 group was administrated low-dose UTI (20,000 U/kg), and another group was administrated high-dose UTI (50,000 U/kg). Twelve hours after contusion, neutrophil counting in bronchoalveolar lavage fluid (BALF) was performed and tumor necrosis factor α level and albumin level in BALF was tested. Lung tissue malondialdehyde levels, superoxide dismutase, and catalase activity was investigated, and blood gas analysis and contusion volume quantification using 3-dimensional computed tomography were performed. High-dose UTI significantly decreased neutrophil count and tumor necrosis factor α level in BALF (Pcontusion volume by UTI (P>0.05). UTI has a dose-dependent trend to ameliorate inflammatory and oxygen stress in pulmonary contusion-induced acute lung injury. However, the effect on hypoxemia and contusion lesion and the best administration regime should be investigated in future study.

  18. Pulmonary inflammation is regulated by the levels of the vesicular acetylcholine transporter.

    Directory of Open Access Journals (Sweden)

    Nathalia M Pinheiro

    Full Text Available Acetylcholine (ACh plays a crucial role in physiological responses of both the central and the peripheral nervous system. Moreover, ACh was described as an anti-inflammatory mediator involved in the suppression of exacerbated innate response and cytokine release in various organs. However, the specific contributions of endogenous release ACh for inflammatory responses in the lung are not well understood. To address this question we have used mice with reduced levels of the vesicular acetylcholine transporter (VAChT, a protein required for ACh storage in secretory vesicles. VAChT deficiency induced airway inflammation with enhanced TNF-α and IL-4 content, but not IL-6, IL-13 and IL-10 quantified by ELISA. Mice with decreased levels of VAChT presented increased collagen and elastic fibers deposition in airway walls which was consistent with an increase in inflammatory cells positive to MMP-9 and TIMP-1 in the lung. In vivo lung function evaluation showed airway hyperresponsiveness to methacholine in mutant mice. The expression of nuclear factor-kappa B (p65-NF-kB in lung of VAChT-deficient mice were higher than in wild-type mice, whereas a decreased expression of janus-kinase 2 (JAK2 was observed in the lung of mutant animals. Our findings show the first evidence that cholinergic deficiency impaired lung function and produce local inflammation. Our data supports the notion that cholinergic system modulates airway inflammation by modulation of JAK2 and NF-kB pathway. We proposed that intact cholinergic pathway is necessary to maintain the lung homeostasis.

  19. Histologic and biochemical alterations predict pulmonary mechanical dysfunction in aging mice with chronic lung inflammation.

    Science.gov (United States)

    Massa, Christopher B; Groves, Angela M; Jaggernauth, Smita U; Laskin, Debra L; Gow, Andrew J

    2017-08-01

    Both aging and chronic inflammation produce complex structural and biochemical alterations to the lung known to impact work of breathing. Mice deficient in surfactant protein D (Sftpd) develop progressive age-related lung pathology characterized by tissue destruction/remodeling, accumulation of foamy macrophages and alteration in surfactant composition. This study proposes to relate changes in tissue structure seen in normal aging and in chronic inflammation to altered lung mechanics using a computational model. Alterations in lung function in aging and Sftpd -/- mice have been inferred from fitting simple mechanical models to respiratory impedance data (Zrs), however interpretation has been confounded by the simultaneous presence of multiple coexisting pathophysiologic processes. In contrast to the inverse modeling approach, this study uses simulation from experimental measurements to recapitulate how aging and inflammation alter Zrs. Histologic and mechanical measurements were made in C57BL6/J mice and congenic Sftpd-/- mice at 8, 27 and 80 weeks of age (n = 8/group). An anatomic computational model based on published airway morphometry was developed and Zrs was simulated between 0.5 and 20 Hz. End expiratory pressure dependent changes in airway caliber and recruitment were estimated from mechanical measurements. Tissue elements were simulated using the constant phase model of viscoelasticity. Baseline elastance distribution was estimated in 8-week-old wild type mice, and stochastically varied for each condition based on experimentally measured alteration in elastic fiber composition, alveolar geometry and surfactant composition. Weighing reduction in model error against increasing model complexity allowed for identification of essential features underlying mechanical pathology and their contribution to Zrs. Using a maximum likelihood approach, alteration in lung recruitment and diminished elastic fiber density were shown predictive of mechanical alteration at

  20. Histologic and biochemical alterations predict pulmonary mechanical dysfunction in aging mice with chronic lung inflammation.

    Directory of Open Access Journals (Sweden)

    Christopher B Massa

    2017-08-01

    Full Text Available Both aging and chronic inflammation produce complex structural and biochemical alterations to the lung known to impact work of breathing. Mice deficient in surfactant protein D (Sftpd develop progressive age-related lung pathology characterized by tissue destruction/remodeling, accumulation of foamy macrophages and alteration in surfactant composition. This study proposes to relate changes in tissue structure seen in normal aging and in chronic inflammation to altered lung mechanics using a computational model. Alterations in lung function in aging and Sftpd -/- mice have been inferred from fitting simple mechanical models to respiratory impedance data (Zrs, however interpretation has been confounded by the simultaneous presence of multiple coexisting pathophysiologic processes. In contrast to the inverse modeling approach, this study uses simulation from experimental measurements to recapitulate how aging and inflammation alter Zrs. Histologic and mechanical measurements were made in C57BL6/J mice and congenic Sftpd-/- mice at 8, 27 and 80 weeks of age (n = 8/group. An anatomic computational model based on published airway morphometry was developed and Zrs was simulated between 0.5 and 20 Hz. End expiratory pressure dependent changes in airway caliber and recruitment were estimated from mechanical measurements. Tissue elements were simulated using the constant phase model of viscoelasticity. Baseline elastance distribution was estimated in 8-week-old wild type mice, and stochastically varied for each condition based on experimentally measured alteration in elastic fiber composition, alveolar geometry and surfactant composition. Weighing reduction in model error against increasing model complexity allowed for identification of essential features underlying mechanical pathology and their contribution to Zrs. Using a maximum likelihood approach, alteration in lung recruitment and diminished elastic fiber density were shown predictive of mechanical

  1. Dynamic expression of leukocyte innate immune genes in whole blood from horses with lipopolysaccharide-induced acute systemic inflammation

    DEFF Research Database (Denmark)

    Vinther, Anne Mette L.; Skovgaard, Kerstin; Heegaard, Peter M. H.

    2015-01-01

    ) and sepsis. Therefore, the aim of this study was to investigate the expression of 31 selected blood leukocyte immune genes in an equine model of acute systemic inflammation to identify significantly regulated genes and to describe their expression dynamics during a 24-h experimental period. Systemic...

  2. January 2015 Phoenix pulmonary journal club: noninvasive ventilation in acute respiratory failure

    Directory of Open Access Journals (Sweden)

    Mathew M

    2015-01-01

    Full Text Available No abstract available. Article truncated after 150 words. Noninvasive positive pressure ventilation has expanded its role in the treatment of both chronic and acute respiratory failure. Its initial use in conditions such as obstructive sleep apnea, neuromuscular disease and tracheobronchomalacia, have been shown to improve quality of life and reduce mortality. Over the past 20 years studies have looked at using noninvasive ventilation in the management of acute respiratory failure from pulmonary edema, asthma and COPD exacerbations. During this month's journal club we reviewed 3 articles evaluating the efficacy of noninvasive ventilation in acute respiratory failure. Gupta D, Nath A, Agarwal R, Behera D. A prospective randomized controlled trial on the efficacy of noninvasive ventilation in severe acute asthma. Respir Care. 2010;55(5:536-43. [PubMed] This was a small unblinded randomized controlled trial (RCT looking at the efficacy using noninvasive ventilation (NIV in acute asthma. A total of 53 patients were included and divided into 2 groups of 28 patients ...

  3. Concurrent early-onset peripartum cardiomyopathy in a preeclampsia patient with acute pulmonary edema.

    Science.gov (United States)

    Belen, Erdal; Tipi, Fahri Fatih; Helvaci, Aysen; Bayyigit, Akif

    2015-01-01

    We herein report the case of a preeclampsia patient with comorbid peripartum cardiomyopathy (PPCMP). A 22-year-old woman in the 26th week of gestation was admitted with acute pulmonary edema. Hypertension and proteinuria were detected, and echocardiography showed an ejection fraction of 33%. It is remarkable that PPCMP particularly that associated with preeclampsia was observed in the early gestational period. In conclusion, while dyspnea and pretibial edema are often noted during normal pregnancies, the potential for PPCMP should be considered if these symptoms are excessive and/or comorbid paroxysmal nocturnal dyspnea and orthopnea are present, even in patients with preeclampsia.

  4. Undiagnosed chronic obstructive pulmonary diseases in patients admittet to an acute assessment unit

    DEFF Research Database (Denmark)

    Eikhof, Karin Dam; Olsen, Kristine R; Wrengler, NCH

    2017-01-01

    % were offered follow-up visit after 6 weeks. Results: Of the 1145 admitted patients, 46% were eligible: 28% of those had an abnormal spirometry. The offered follow-up visit was attended by 51% and in this group 17% were diagnosed with lung disease. COPD was the most prevalent diagnosis (73%), and 2......Introduction: Chronic obstructive pulmonary disease (COPD) is very prevalent worldwide, yet underdiagnosed. Aim: This study investigates feasibility of performing spirometry in patients in need of acute hospital admission as well as the prevalence of undiagnosed COPD in the same cohort. Methods...

  5. Treatment of Acute Pulmonary Embolism: Update on Newer Pharmacologic and Interventional Strategies

    Directory of Open Access Journals (Sweden)

    Francesco Pelliccia

    2014-01-01

    Full Text Available Acute pulmonary embolism (PE is a common complication in hospitalized patients, spanning multiple patient populations and crossing various therapeutic disciplines. Current treatment paradigm in patients with massive PE mandates prompt risk stratification with aggressive therapeutic strategies. With the advent of endovascular technologies, various catheter-based thrombectomy and thrombolytic devices are available to treat patients with massive or submassive PE. In this paper, a variety of newer treatment strategies for PE are analyzed, with special emphasis on various interventional treatment strategies. Clinical evidence for utilizing endovascular treatment modalities, based on our institutional experience as well as a literature review, is provided.

  6. Isocitrate treatment of acute anemia of inflammation in a mouse model.

    Science.gov (United States)

    Kim, Airie; Fung, Eileen; Parikh, Sona G; Gabayan, Victoria; Nemeth, Elizabeta; Ganz, Tomas

    2016-01-01

    Acute and severe anemia of inflammation (AI) is a common complication of various clinical syndromes, including fulminant infections, critical illness with multiorgan failure, and exacerbations of autoimmune diseases. Building on recent data showing beneficial results with isocitrate treatment for chronic low-grade AI in a rat model, we used a mouse model of acute and severe AI induced by intraperitoneal heat-killed Brucella abortus to determine if isocitrate would be effective in this more stringent application. Inflamed mice treated with isocitrate developed an early but transient improvement in hemoglobin compared to solvent-treated controls, with a robust improvement on day 7, and only a trend towards improvement by day 14. Reticulocyte counts were increased in treated mice transiently, with no significant difference by day 21. Serum erythropoietin (EPO) levels were similar in treated versus control mice, indicating that isocitrate increased sensitivity to EPO. Serum and tissue iron levels showed no significant differences between the treated and control mice, ruling out improved iron availability as the cause of the increased response to endogenous EPO. Compared to the milder rat model, much higher doses of isocitrate were required for a relatively modest benefit.

  7. Neurotrauma: The Crosstalk between Neurotrophins and Inflammation in the Acutely Injured Brain

    Directory of Open Access Journals (Sweden)

    Lindolfo da Silva Meirelles

    2017-05-01

    Full Text Available Traumatic brain injury (TBI is a major cause of morbidity and mortality among young individuals worldwide. Understanding the pathophysiology of neurotrauma is crucial for the development of more effective therapeutic strategies. After the trauma occurs, immediate neurologic damage is produced by the traumatic forces; this primary injury triggers a secondary wave of biochemical cascades together with metabolic and cellular changes, called secondary neural injury. In the scenario of the acutely injured brain, the ongoing secondary injury results in ischemia and edema culminating in an uncontrollable increase in intracranial pressure. These areas of secondary injury progression, or areas of “traumatic penumbra”, represent crucial targets for therapeutic interventions. Neurotrophins are a class of signaling molecules that promote survival and/or maintenance of neurons. They also stimulate axonal growth, synaptic plasticity, and neurotransmitter synthesis and release. Therefore, this review focuses on the role of neurotrophins in the acute post-injury response. Here, we discuss possible endogenous neuroprotective mechanisms of neurotrophins in the prevailing environment surrounding the injured areas, and highlight the crosstalk between neurotrophins and inflammation with focus on neurovascular unit cells, particularly pericytes. The perspective is that neurotrophins may represent promising targets for research on neuroprotective and neurorestorative processes in the short-term following TBI.

  8. O-Methylated flavonol isorhamnetin prevents acute inflammation through blocking of NF-κB activation.

    Science.gov (United States)

    Yang, Ji Hye; Kim, Sang Chan; Shin, Bo Yeon; Jin, So Hee; Jo, Mi Jeong; Jegal, Kyung Hwan; Kim, Young Woo; Lee, Jong Rok; Ku, Sae Kwang; Cho, Il Je; Ki, Sung Hwan

    2013-09-01

    Here, we isolated isorhamnetin, a natural 3'-O-methylated flavonoid, from water dropwort (Oenanthe javanica, Umbelliferae) and investigated its ability to protect against acute inflammation in vivo and in vitro. To induce paw swelling, the hind paw of each rat was injected with a carrageenan 1h after vehicle or isorhamnetin treatment. In vitro effect and mechanism studies were performed in lipopolysaccharide (LPS)-activated macrophages. Administration of isorhamnetin markedly inhibited the swelling volume and the thickness of hind paws. Moreover, isorhamnetin significantly reduced inflammatory cell infiltration and pro-inflammatory gene expression in rats. Isorhamnetin pretreatment inhibited inducible nitric oxide synthase (iNOS) expression and NO release in LPS-stimulated cells. Activation of nuclear factor-kappa B (NF-κB) and activating protein-1 (AP-1) is the key step in the iNOS gene induction. Isorhamnetin specifically inhibited NF-κB luciferase activity, but not AP-1. Pretreatment with isorhamnetin suppressed NF-κB nuclear translocation in accordance with decreased phosphorylation and degradation of inhibitory-κB. Consistently, TNF-α, IL-1β and IL-6 expression, representative NF-κB target genes, were almost completely prohibited by isorhamnetin. Furthermore, isorhamnetin inhibited LPS-induced JNK and AKT/IKKα/β phosphorylation. Our results suggest that isorhamnetin inhibited JNK, and AKT/IKKα/β activation, leading to NF-κB inactivation, which might contribute to the inhibition of the acute inflammatory response.

  9. A novel anti-inflammatory and pro-resolving role for resolvin D1 in acute cigarette smoke-induced lung inflammation.

    Directory of Open Access Journals (Sweden)

    Hsi-Min Hsiao

    Full Text Available Cigarette smoke is a profound pro-inflammatory stimulus that contributes to acute lung injuries and to chronic lung disease including COPD (emphysema and chronic bronchitis. Until recently, it was assumed that resolution of inflammation was a passive process that occurred once the inflammatory stimulus was removed. It is now recognized that resolution of inflammation is a bioactive process, mediated by specialized lipid mediators, and that normal homeostasis is maintained by a balance between pro-inflammatory and pro-resolving pathways. These novel small lipid mediators, including the resolvins, protectins and maresins, are bioactive products mainly derived from dietary omega-3 and omega-6 polyunsaturated fatty acids (PUFA. We hypothesize that resolvin D1 (RvD1 has potent anti-inflammatory and pro-resolving effects in a model of cigarette smoke-induced lung inflammation.Primary human lung fibroblasts, small airway epithelial cells and blood monocytes were treated with IL-1β or cigarette smoke extract in combination with RvD1 in vitro, production of pro-inflammatory mediators was measured. Mice were exposed to dilute mainstream cigarette smoke and treated with RvD1 either concurrently with smoke or after smoking cessation. The effects on lung inflammation and lung macrophage populations were assessed.RvD1 suppressed production of pro-inflammatory mediators by primary human cells in a dose-dependent manner. Treatment of mice with RvD1 concurrently with cigarette smoke exposure significantly reduced neutrophilic lung inflammation and production of pro-inflammatory cytokines, while upregulating the anti-inflammatory cytokine IL-10. RvD1 promoted differentiation of alternatively activated (M2 macrophages and neutrophil efferocytosis. RvD1 also accelerated the resolution of lung inflammation when given after the final smoke exposure.RvD1 has potent anti-inflammatory and pro-resolving effects in cells and mice exposed to cigarette smoke. Resolvins

  10. microRNA-1246 mediates lipopolysaccharide-induced pulmonary endothelial cell apoptosis and acute lung injury by targeting angiotensin-converting enzyme 2

    Science.gov (United States)

    Fang, Yue; Gao, Fengying; Hao, Jing; Liu, Zhenwei

    2017-01-01

    In this study, we aimed to identify potential microRNA (miRNA) regulators of angiotensin-converting enzyme 2 (ACE2) and to explore their roles in lipopolysaccharide (LPS)-induced acute lung injury (ALI). The expression of predicted miRNA regulators of ACE2 was examined in LPS-exposed pulmonary microvascular endothelial cells (PMVECs). Gain- and loss-of-function studies were performed to determine the functions of candidate miRNAs in LPS-induced PMVEC apoptosis and inflammatory response. The roles of the miRNAs in LPS-induced lung inflammation and permeability were investigated in a mouse model. Notably, LPS (1 μg/mL) significantly induced the expression of miR-1246 in PMVECs. ACE2 was validated as a target gene of miR-1246. Silencing of miR-1246 prevented LPS-induced inhibition of ACE2, which was accompanied by reduced apoptosis and production of IL-1β and TNF-α. In contrast, ectopic expression of miR-1246 triggered apoptosis in PMVECs and promoted IL-1β and TNF-α release. MiR-1246-mediated apoptosis of PMVECs was impaired by overexpression of ACE2. Depletion of miR-1246 attenuated lung inflammation, neutrophil infiltration, and vascular permeability and restored pulmonary expression of ACE2 in LPS-exposed mice. Taken together, miR-1246 meditates LPS-induced pulmonary endothelial cell apoptosis in vitro and ALI in mouse models, which are, at least partially, ascribed to repression of ACE2.

  11. Acute hemodynamic responses to adenosine and iloprost in patients with congenital heart defects and severe pulmonary arterial hypertension.

    Science.gov (United States)

    Zhang, Duan-zhen; Zhu, Xian-yang; Meng, Jing; Xue, Hong-mei; Sheng, Xiao-tang; Han, Xiu-min; Cui, Chun-sheng; Wang, Qi-guang; Zhang, Po

    2011-03-17

    Detection of pulmonary vasoreactivity is important for the evaluation of patient with pulmonary arterial hypertension (PAH). The present study aimed to investigate the acute hemodynamic responses to adenosine and iloprost in patients with congenital heart defects (CHDs) and severe PAH. From Mar 2007 to Nov 2009, 75 patients with severe PAH secondary to left-to-right shunt CHDs underwent acute vasodilator test using aerosolized iloprost (n = 50) or intravenous adenosine (n = 25). The hemodynamics were detected and analyzed. Decreased mean pulmonary arterial pressure (PAP) and pulmonary vascular resistance (PVR) were observed in 39 and 43 patients in the iloprost group, and in 16 and 19 patients in the adenosine group, respectively. However, the mean PAP was higher than 40 mm Hg in both groups. No significant difference was observed in the age and baseline hemodynamics between the patients with the decrease of PVR and mean pulmonary-to-aortic pressure (Pp/Ps) ratio greater than 10% and the remaining patients. Adenosine decreased both PAP and systemic arterial pressure significantly, while iloprost inhalation selectively reduced the PAP and increased the oxygen saturation of femoral arterial blood and the pulmonary-to-systemic flow (Qp/Qs) ratio. Compared with adenosine, iloprost caused a more profound decline in the Pp/Ps ratio, PVR and pulmonary-to-systemic vascular resistance ratio, and increase in the Qp/Qs ratio. The acute haemodynamic responses to adenosine and iloprost varied among the patients with CHDs and severe PAH. Different to adenosine, inhaled iloprost exerted selective pulmonary vasodilative effects and was beneficial for pulmonary gas exchange. Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.

  12. MRI for short-term follow-up of acute pulmonary embolism. Assessment of thrombus appearance and pulmonary perfusion: a feasibility study

    Energy Technology Data Exchange (ETDEWEB)

    Kluge, Alexander; Gerriets, Tibo; Bachman, George [Kerckhoff Heart Center, Department of Diagnostic Radiology, Bad Nauheim (Germany); Lange, Uwe [Kerckhoff Heart Center, Department of Diagnostic Radiology, Bad Nauheim (Germany); Kerckhoff Heart Center, Department of Rheumatology, Bad Nauheim (Germany)

    2005-09-01

    Tha aim of this study was to demonstrate the feasibility of MRI for short-term follow-up examinations in patients with acute pulmonary embolism (PE), and to assess temporal changes of pulmonary perfusion and thrombus characteristics that may be helpful in determining thrombus age. Thirty-three patients (15 female, 18 male, mean age 59.4 years) with acute PE were examined initially and 1 week later using both 16-row computed tomography (CT) and MRI with magnetic resonance angiography (MRA), real-time MRI and magnetic resonance (MR) pulmonary perfusion imaging. MRA and MR pulmonary perfusion used contrast-enhanced 3D flash sequences, and real-time MRI used true fast imaging with steady-state precession sequences (repetition time/echo time 3.1/1.5, bandwidth 975 Hz, 256 matrix size, acquisition time 0.4 s per image) in three orthogonal planes. Follow-up examinations were feasible for all patients. Diagnosis of PE was concordant between MRI and CT in all patients. The signal intensity of embolic material increased after 1 week for real-time MRI [132{+-}5 vs. 232{+-}22 (standard error of the mean), p<0.001], but not significantly for MRA. MR pulmonary perfusion of areas affected by PE increased (area under the curve initially 9.6{+-}7.4, at follow-up 40.7{+-}7.6, p<0.001). A decreasing time-to-peak in normal lung areas (15.7{+-}0.96 and 13.2{+-}0.55, respectively, p<0.05) indicated systemic circulatory effects of PE, and subsiding pulmonary artery obstruction improved arterial inflow for the entire lung. Follow-up examinations of patients with acute PE are feasible with MRI, and a relation between thrombus appearance and thrombus age can be implied. (orig.)

  13. 慢性阻塞性肺疾病与慢性炎症%Chronic obstructive pulmonary disease and chronic inflammation

    Institute of Scientific and Technical Information of China (English)

    何馨; 王浩彦

    2011-01-01

    慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患病率高、病程长、病死率高,已成为严重的社会负担.小气道炎症是COPD的主要病变及导致肺功能进行性损害的主要原因,同时大量研究证明COPD患者存在系统性炎症,但目前对于COPD气道炎症与系统性炎症的关系尚不十分明确.%With an increased prevalence,chronic obstructive pulmonary disease (COPD),which is characterized by airflow obstruction, has represented an increasing burden throughout the world.Inflammation of small airway is the primary lesions of COPD. It has been confirmed that airwayinflammation is the major reason which caused the damage of lung function in COPD. And lots of studies has proved that patients with COPD had systemic inflammation. However, the reason of systemic inflammation in COPD and the relationship between airway inflammation and systemic inflammation in COPD are still unclear.

  14. The effects of acute inflammation on cognitive functioning and emotional processing in humans: A systematic review of experimental studies.

    Science.gov (United States)

    Bollen, Jessica; Trick, Leanne; Llewellyn, David; Dickens, Chris

    2017-03-01

    The cognitive neuropsychological model of depression proposes that negative biases in the processing of emotionally salient information have a central role in the development and maintenance of depression. We have conducted a systematic review to determine whether acute experimental inflammation is associated with changes to cognitive and emotional processing that are thought to cause and maintain depression. We identified experimental studies in which healthy individuals were administered an acute inflammatory challenge (bacterial endotoxin/vaccination) and standardised tests of cognitive function were performed. Fourteen references were identified, reporting findings from 12 independent studies on 345 participants. Methodological quality was rated strong or moderate for 11 studies. Acute experimental inflammation was triggered using a variety of agents (including endotoxin from E. coli, S. typhi, S. abortus Equi and Hepatitis B vaccine) and cognition was assessed over hours to months, using cognitive tests of i) attention/executive functioning, ii) memory and iii) social/emotional processing. Studies found mixed evidence that acute experimental inflammation caused changes to attention/executive functioning (2 of 6 studies showed improvements in attention executive function compared to control), changes in memory (3 of 5 studies; improved reaction time: reduced memory for object proximity: poorer immediate and delayed memory) and changes to social/emotional processing (4 of 5 studies; reduced perception of emotions, increased avoidance of punishment/loss experiences, and increased social disconnectedness). Acute experimental inflammation causes negative biases in social and emotional processing that could explain observed associations between inflammation and depression. Copyright © 2017 Elsevier Inc. All rights reserved.

  15. Mesenchymal Stem Cell Attenuates Neutrophil-predominant Inflammation and Acute Lung Injury in an In Vivo Rat Model of Ventilator-induced Lung Injury

    Institute of Scientific and Technical Information of China (English)

    Tian-Shun Lai; Zhi-Hong Wang; Shao-Xi Cai

    2015-01-01

    Background:Subsequent neutrophil (polymorphonuclear neutrophil [PMN])-predominant inflammatory response is a predominant feature of ventilator-induced lung injury (VILI),and mesenchymal stem cell (MSC) can improve mice survival model of endotoxin-induced acute lung injury,reduce lung impairs,and enhance the repair of VILI.However,whether MSC could attenuate PMN-predominant inflammatory in the VILI is still unknown.This study aimed to test whether MSC intervention could attenuate the PMN-predominate inflammatory in the mechanical VILI.Methods:Sprague-Dawley rats were ventilated for 2 hours with large tidal volume (20 mL/kg).MSCs were given before or after ventilation.The inflammatory chemokines and gas exchange were observed and compared dynamically until 4 hours after ventilation,and pulmonary pathological change and activation of PMN were observed and compared 4 hours after ventilation.Results:Mechanical ventilation (MV) caused significant lung injury reflected by increasing in PMN pulmonary sequestration,inflammatory chemokines (tumor necrosis factor-alpha,interleukin-6 and macrophage inflammatory protein 2) in the bronchoalveolar lavage fluid,and injury score of the lung tissue.These changes were accompanied with excessive PMN activation which reflected by increases in PMN elastase activity,production of radical oxygen series.MSC intervention especially pretreatment attenuated subsequent lung injury,systemic inflammation response and PMN pulmonary sequestration and excessive PMN activation initiated by injurious ventilation.Conclusions:MV causes profound lung injury and PMN-predominate inflammatory responses.The protection effect of MSC in the VILI rat model is related to the suppression of the PMN activation.

  16. Acute Amiodarone Pulmonary Toxicity after Drug Holiday: A Case Report and Review of the Literature

    Directory of Open Access Journals (Sweden)

    Ahmed Abuzaid

    2015-01-01

    Full Text Available Amiodarone is reported to cause a wide continuum of serious clinical effects. It is often challenging to detect Amiodarone-induced pulmonary toxicity (AIPT. Typically, the diagnosis is made based on the clinical settings and may be supported by histopathology results, if available. We describe a 57-year-old patient who developed severe rapidly progressive respiratory failure secondary to AIPT with acute bilateral infiltrates and nodular opacities on chest imaging. Interestingly, Amiodarone was discontinued 3 weeks prior to his presentation. He had normal cardiac filling pressures confirmed by echocardiography. To our knowledge, this is the first case of isolated acute lung injury induced by Amiodarone, three weeks after therapy cessation, with adequate clinical improvement after supportive management and high dose steroid therapy.

  17. Particle-induced pulmonary acute phase response correlates with neutrophil influx linking inhaled particles and cardiovascular risk

    DEFF Research Database (Denmark)

    Saber, Anne Thoustrup; Lamson, Jacob Stuart; Jacobsen, Nicklas Raun

    2013-01-01

    at a biofuel plant. Mice were exposed to single or multiple doses of particles by inhalation or intratracheal instillation and pulmonary mRNA expression of Saa3 was determined at different time points of up to 4 weeks after exposure. Also hepatic mRNA expression of Saa3, SAA3 protein levels in broncheoalveolar......, whereas hepatic Saa3 levels were much less affected. Pulmonary Saa3 expression correlated with the number of neutrophils in BAL across different dosing regimens, doses and time points. Conclusions Pulmonary acute phase response may constitute a direct link between particle inhalation and risk...

  18. Fatal course of pulmonary Absidia sp. infection in a 4-year-old girl undergoing treatment for acute lymphoblastic leukemia.

    Science.gov (United States)

    Krauze, Agnieszka; Krenke, Katarzyna; Matysiak, Michal; Kulus, Marek

    2005-07-01

    Absidia sp. is a rare etiologic agent responsible for infectious complications in immunosuppressed patients. The authors describe a 4-year-old girl with acute lymphoblastic leukemia complicated with pleuropneumonia caused by an Absidia infection during the induction of remission. A review of the published reports in current literature is included for comparison. To the authors' knowledge only six cases of primary pulmonary absidiomycosis have been published. Despite its uncommon pulmonary presentation, mucormycosis should be considered in patients with an immunosuppressing illness and positive risk factors and when a pulmonary lesion is not responding to appropriate antibiotic therapy.

  19. Lung inflammation and genotoxicity in mice lungs after pulmonary exposure to candle light combustion particles

    DEFF Research Database (Denmark)

    Skovmand, Astrid; Damiao Gouveia, Ana Cecilia; Koponen, Ismo Kalevi

    2017-01-01

    Candle burning produces a large amount of particles that contribute substantially to the exposure to indoor particulate matter. The exposures to various types of combustion particles, such as diesel exhaust particles, have been associated with increased risk of lung cancer by mechanisms that invo......Candle burning produces a large amount of particles that contribute substantially to the exposure to indoor particulate matter. The exposures to various types of combustion particles, such as diesel exhaust particles, have been associated with increased risk of lung cancer by mechanisms...... a significant influx of alveolar macrophages and polymorphonuclear leukocytes and increased concentrations of proteins and lactate dehydrogenase activity in bronchoalveolar fluid. Lower levels of these markers of inflammation and cytotoxicity were observed after i.t. instillation of the same dose of A...

  20. IKKi: a novel regulator of Act1, IL-17 signaling and pulmonary inflammation

    Institute of Scientific and Technical Information of China (English)

    Noula Shembade; Edward W Harhaj

    2011-01-01

    TH17 inflammatory helper cells constitute an important subset of T lymphocytes that secrete the cytokine interleukin 17(IL-17) and thereby drive inflammation in response to microbial antigens.Dysregulation of TH 17 cells,characterized by increased IL-17 production,is a hallmark of many inflammatory and autoimmune diseases such as asthma,multiple sclerosis and rheumatoid arthritis.1 The adaptor molecule and E3 ubiquitin ligase Actl is a key signaling molecule downstream of the IL-17 receptor (IL-17R)that triggers activation of the NF-κB and mitogen-activated protein kinase (MAPK)signaling pathways,which in turn coordinate the induction of cytokine and chemokine genes that are central to the inflammatory response.

  1. Can a chronic disease management pulmonary rehabilitation program for COPD reduce acute rural hospital utilization?

    Science.gov (United States)

    Rasekaba, T M; Williams, E; Hsu-Hage, B

    2009-01-01

    Chronic obstructive pulmonary disease (COPD) imposes a costly burden on healthcare. Pulmonary rehabilitation (PR) is the best practice to better manage COPD to improve patient outcomes and reduce acute hospital care utilization. To evaluate the impact of a once-weekly, eight-week multidisciplinary PR program as an integral part of the COPD chronic disease management (CDM) Program at Kyabram District Health Services. The study compared two cohorts of COPD patients: CDM-PR Cohort (4-8 weeks) and Opt-out Cohort (0-3 weeks) between February 2006 and March 2007. The CDM-PR Program involved multidisciplinary patient education and group exercise training. Nonparametric statistical tests were used to compare acute hospital care utilization 12 months before and after the introduction of CDM-PR. The number of patients involved in the CDM-PR Cohort was 29 (n = 29), and that in the Opt-out Cohort was 24 (n = 24). The CDM-PR Cohort showed significant reductions in cumulative acute hospital care utilization indicators (95% emergency department presentations, 95% inpatient admissions, 99% length of stay; effect sizes = 0.62-0.66, P indicators were statistically insignificant for the Opt-out Cohort (emergency department presentations decreased by 5%, inpatient admissions decreased by 12%, length of stay increased by 30%; effect size = 0.14-0.40, P > 0.05). Total costs associated with the hospital care utilization decreased from $130,000 to $7,500 for the CDM-PR Cohort and increased from $77,700 to $101,200 for the Opt-out Cohort. Participation in the CDM-PR for COPD patients can significantly reduce acute hospital care utilization and associated costs in a small rural health service.

  2. VALIDATION OF PULMONARY SCORE IN THE EVALUATION OF ACUTE EXACERBATION OF ASTHMA

    Directory of Open Access Journals (Sweden)

    Chandrakala

    2014-03-01

    Full Text Available BACKGROUND & OBJECTIVES: Numerous asthma scoring systems have been devised which combine a number of physical signs to estimate the severity of an acute asthma exacerbation. Although more than 16 scoring systems exist, many are difficult to use. The pulmonary score was developed to provide ‘‘user-friendly’’ measure of asthma severity for children with acute asthma exacerbation. The objective of the study is to study the efficacy of pulmonary score in assessing the severity of acute exacerbation of asthma in comparison to peak expiratory flow rate. METHODS: The study sampled 50 children, aged 5–18 years, with mild to moderate acute exacerbation of asthma. The PEFR (best of three attempts and the PS were measured before and after treatme