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Sample records for adhesion molecule-1 icam-1

  1. Signaling through intercellular adhesion molecule 1 (ICAM-1) in a B cell lymphoma line

    DEFF Research Database (Denmark)

    Holland, J; Owens, T

    1997-01-01

    Intercellular adhesion molecule 1 (ICAM-1) (CD54) is an adhesion molecule of the immunoglobulin superfamily. The interaction between ICAM-1 on B lymphocytes and leukocyte function-associated antigen 1 on T cells plays a major role in several aspects of the immune response, including T-dependent B...

  2. Association of Intercellular Adhesion Molecule 1 (ICAM1 with Diabetes and Diabetic Nephropathy

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    Harvest F Gu

    2013-01-01

    Full Text Available Diabetes and diabetic nephropathy are complex diseases affected by genetic and environmental factors. Identification of the susceptibility genes and investigation of their roles may provide useful information for better understanding of the pathogenesis and for developing novel therapeutic approaches. Intercellular adhesion molecule 1 (ICAM1 is a cell surface glycoprotein expressed on endothelial cells and leukocytes in the immune system. The ICAM1 gene is located on chromosome 19p13 within the linkage region of diabetes. In the recent years, accumulating reports have implicated that genetic polymorphisms in the ICAM1 gene are associated with diabetes and diabetic nephropathy. Serum ICAM1 levels in diabetes patients and the icam1 gene expression in kidney tissues of diabetic animals are increased compared to the controls. Therefore, ICAM1 may play a role in the development of diabetes and diabetic nephropathy. In this review, we present genomic structure, variation and regulation of the ICAM1 gene, summarized genetic and biological studies of this gene in diabetes and diabetic nephropathy and discussed about the potential application using ICAM1 as a biomarker and target for prediction and treatment of diabetes and diabetic nephropathy.

  3. Transfected HEK293 Cells Expressing Functional Recombinant Intercellular Adhesion Molecule 1 (ICAM-1) - A Receptor Associated with Severe Plasmodium falciparum Malaria

    DEFF Research Database (Denmark)

    Bengtsson, Anja; Joergensen, Louise; Barbati, Zachary R;

    2013-01-01

    Intercellular adhesion molecule 1 (ICAM-1) is a membrane-bound glycoprotein expressed on endothelial cells and cells of the immune system. Human ICAM-1 mediates adhesion and migration of leucocytes, and is implicated in inflammatory pathologies, autoimmune diseases and in many cancer processes....... Additionally, ICAM-1 acts as receptor for pathogens like human rhinovirus and Plasmodium falciparum malaria parasites. A group of related P. falciparum erythrocyte membrane protein 1 (PfEMP1) domains, the DBLβ, mediates ICAM-1 binding of P. falciparum-infected erythrocytes. This ICAM‑1-binding phenotype has...... as vaccine candidates and go into clinical trials. Such studies require availability of functional recombinant ICAM-1 in large quantities. In this study, we compared recombinant ICAM-1 expressed in HEK293 and COS-7 cells with mouse myeloma NS0 ICAM-1 purchased from a commercial vendor in terms of protein...

  4. FRET based quantification and screening technology platform for the interactions of leukocyte function-associated antigen-1 (LFA-1 with intercellular adhesion molecule-1 (ICAM-1.

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    Sandeep Chakraborty

    Full Text Available The interaction between leukocyte function-associated antigen-1(LFA-1 and intercellular adhesion molecule-1 (ICAM-1 plays a pivotal role in cellular adhesion including the extravasation and inflammatory response of leukocytes, and also in the formation of immunological synapse. However, irregular expressions of LFA-1 or ICAM-1 or both may lead to autoimmune diseases, metastasis cancer, etc. Thus, the LFA-1/ICAM-1 interaction may serve as a potential therapeutic target for the treatment of these diseases. Here, we developed one simple 'in solution' steady state fluorescence resonance energy transfer (FRET technique to obtain the dissociation constant (Kd of the interaction between LFA-1 and ICAM-1. Moreover, we developed the assay into a screening platform to identify peptides and small molecules that inhibit the LFA-1/ICAM-1 interaction. For the FRET pair, we used Alexa Fluor 488-LFA-1 conjugate as donor and Alexa Fluor 555-human recombinant ICAM-1 (D1-D2-Fc as acceptor. From our quantitative FRET analysis, the Kd between LFA-1 and D1-D2-Fc was determined to be 17.93±1.34 nM. Both the Kd determination and screening assay were performed in a 96-well plate platform, providing the opportunity to develop it into a high-throughput assay. This is the first reported work which applies FRET based technique to determine Kd as well as classifying inhibitors of the LFA-1/ICAM-1 interaction.

  5. Soluble intercellular adhesion molecule-1 (sICAM-1) and soluble interleukin-2 receptors (sIL-2R) in scleroderma skin

    DEFF Research Database (Denmark)

    Søndergaard, Klaus; Deleuran, Mette; Heickendorff, Lene;

    1998-01-01

    In order to investigate whether soluble intercellular adhesion molecule-1 (sICAM-1) and soluble interleukin-2 receptors (sIL-2R) were present in scleroderma skin, and to compare their levels to concentrations measured in plasma and clinical parameters, we examined suction blister fluid and plasma...... from 13 patients with systemic sclerosis and 11 healthy volunteers. Suction blisters and biopsies were from the transition zone between normal skin and scleroderma, and uninvolved abdominal skin. The levels of sICAM-1 and sIL-2R were significantly increased in both plasma and suction blister fluid from...... systemic sclerosis patients compared with healthy volunteers. ICAM-1 was localized to vessels and perivascular mononuclear infiltrates by immunohistochemical methods. IL-2R was expressed by CD3-positive cells. The elevated levels of sICAM-1 and sIL-2R in suction blister fluid point towards activation...

  6. Study on the serum levels of soluble intercellular adhesion molecule-1 (sICAM-1) in patients with Helicobacter pylori Infection

    Institute of Scientific and Technical Information of China (English)

    吴勤动; 朱永良; 石益海

    2002-01-01

    Objective: To evaluate the interaction between serum levels of soluble intercellular adhesion molecule-1 (sICAM-1) and Helicobacter pylori (H. pylori) infection in patients with chronic gastritis and peptic ulcer. Methods: The serum levels of sICAM-1 in 205 patients with chronic gastric diseases were detected by ELISA method and the status of H. pylori was determined by histologic examination, RUT, 14C - UBT, and serology. The sera obtained from 18 healthy volunteers served as controls. Results: The serum levels of sICAM-1 were significantly higher in patients with H. pylori positive than those of H. pylori negative (889.43±32.52 ng/ml vs. 747.07±30.45 ng/ml, P<0.05). The serum levels of sICAM-1 in patients with mild, moderate and severe infection of H. pylori were 841.68±72.36 ng/ml, 905.43±37.59 ng/ml and 1012.54±49.34 ng/ml,respectively (P<0.05). The serum levels of sICAM-1 proved to be significantly correlated with the density of H. pylori colonization in gastric mucosa (rs =0.316, P<0.001). The serum levels of sICAM-1 in patients with chronic gastritis and peptic ulcer were significantly higher than those in healthy controls (P<0.05). Conclusions: These results indicated that H. pylori infection up-regulates the expression of sICAM-1.

  7. Lauric acid abolishes interferon-gamma (IFN-γ)-induction ofIntercellular AdhesionMolecule-1 (ICAM-1) andVascularCellAdhesionMolecule-1 (VCAM-1) expression in human macrophages

    Institute of Scientific and Technical Information of China (English)

    Wei-Siong Lim; Mary-Shi-Ying Gan; Melissa-Hui-Ling Ong; Choy-Hoong Chew

    2015-01-01

    Objective:To investigate the effect of different concentrations of lauric acid on Intercellular Adhesion Molecule-1 (ICAM-1) and Vascular Cell Adhesion Molecule-1 (VCAM-1) expression in IFN-γ stimulated human monocytic THP-1 cell line.Methods:THP-1 cell were cultured using Roswell Park Memorial Institute medium supplemented with 10% fetal bovine serum. THP-1 monocytes were firstly differentiated into macrophages by using phorbol-12-myristate-13-acetate. IFN-γ response test was perfomed and total cellular RNA was extracted using TRI Reagent®LS before q-RT-PCR was carried out. Subsequently, IFN-γ treated THP-1 macrophages were stimulated with increasing doses of lauric acid for another 24 hour, before q-RT-PCR. MTT assay was carried out to investigate the effect of lauric acid on undifferentiated and differentiated THP-1 cells.Results:The mRNA expression levels of ICAM-1 and VCAM-1 were normalized toβ-actin and relatived to the untreated cells. The expressions of ICAM-1 and VCAM-1 were significantly induced in cells treated with 10 ng/mL of IFN-γ. This showed that IFN-γ could up-regulate inflammatory process and may cause atheroma formation. Although lauric acid did not have any significant impact on undifferentiated and differentiated THP-1 cell viability, the normalized fold expressions of ICAM-1 and VCAM-1 in IFN-γ-treated THP-1 macrophages were decreased significantly in a dose dependent manner with the presence of increasing doses of lauric acid.Conclusions:This study successfully proved that lauric acid was able to antagonize the up-regulatory effect of IFN-γ on ICAM-1 and VCAM-1 expressions in THP-1 macrophages. This indicates that lauric acid may be an anti-inflammatory therapeutic and prophylaxis agent for atherosclerosis.

  8. The influence of propofol on the expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) in reoxygenated human umbilical vein endothelial cells.

    LENUS (Irish Health Repository)

    Corcoran, T B

    2012-02-03

    BACKGROUND: Leucocytes are a pivotal component of the inflammatory cascade that results in tissue injury in a large group of disorders. Free radical production and endothelial activation promote leucocyte-endothelium interactions via endothelial expression of vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) which augment these processes, particularly in the setting of reperfusion injury. Propofol has antioxidant properties which may attenuate the increased expression of these molecules that is observed. METHODS: Cultured human umbilical vein endothelial cells were exposed to 20 h of hypoxia, then returned to normoxic conditions. Cells were treated with saline, Diprivan 5 microg mL(-1) or propofol 5 microg mL(-1), for 4 h after reoxygenation and were examined for ICAM-1 and VCAM-1 expression. RESULTS: Hypoxia did not increase the expression of ICAM-1\\/VCAM-1. ICAM-1 expression peaked 12 h after reoxygenation (21.75(0.6) vs. 9.6(1.3), P = 0.02). Propofol, but not Diprivan, prevented this increase (8.2(2.9) vs. 21.75(0.6), P = 0.009). VCAM-1 expression peaked 24 h after reoxygenation (9.8(0.9) vs. 6.6(0.6), P = 0.03). Propofol and Diprivan prevented this increase, with no difference between the two treatments observed (4.3(0.3) and 6.4(0.5) vs. 9.8(0.9), P = 0.001, 0.02, respectively). CONCLUSION: These effects are likely to be attributable to the antioxidant properties of propofol, and suggest that propofol may have a protective role in disorders where free radical mediated injury promotes leucocyte-endothelium adhesive interactions.

  9. G241R and K469E polymorphisms of intercellular adhesion molecule 1 (ICAM-1) could predispose to Hashimoto thyroiditis.

    Science.gov (United States)

    Akman, Fevziye Emin; Kanmaz-Özer, Müge; Vural, Pervin; Özderya, Ayşenur; Karadağ, Berrin; Doğru-Abbasoğlu, Semra; Uysal, Müjdat

    2012-12-01

    This study examined firstly the possible association of G241R and K469E single nucleotide polymorphisms (SNPs) of ICAM-1 gene with the occurrence of Hashimoto thyroiditis (HT). G241R and K469E SNPs in DNA from peripheral blood leukocytes of 190 HT and 247 healthy controls were investigated by real-time PCR combined with melting curve analysis using fluorescence-labeled hybridization probes. There was a significant increase of ICAM-1 241R allele frequency in patients with HT compared with healthy controls (P = 0.04, OR = 1.84, 95 % CI = 1.00-3.37). Regarding ICAM-1 K469E polymorphism, patients homozygous for E allele had 1.73-fold increased risk for developing HT according to KK homozygotes (P = 0.04, 95 % CI = 1.00-3.01). The 469E allele frequency was higher in HT patients according to controls, however the difference was at borderline significance (P = 0.05, OR = 1.30, 95 % CI = 1.00-1.70). No associations between polymorphisms and HT phenotypes were observed. We suggest that the G241R and K469E SNPs of ICAM-1 gene may be related to occurrence of HT. However, more studies with larger sample size including other loci of the ICAM-1 gene are necessary to support our findings before any definite statement can be made about the relationship between HT and ICAM-1 polymorphism.

  10. Decreased expression of intercellular adhesion molecule-1 (ICAM-1) and urokinase-type plasminogen activator receptor (uPAR) is associated with tumor cell spreading in vivo.

    Science.gov (United States)

    Donadio, Ana C; Remedi, María M; Frede, Silvia; Bonacci, Gustavo R; Chiabrando, Gustavo A; Pistoresi-Palencia, María C

    2002-01-01

    The development of an effective antitumor immune response to control tumor growth is influenced by the tumor cell itself and/or by the tumor microenvironment. Tumor invasion and tumor cell spreading require a finely tuned regulation of the formation and loosening of adhesive contacts of tumor cells with the extracellular matrix (ECM). In our laboratory, a rat tumor cell line derived from a spontaneous rat sarcoma revealed, by flow cytometry, a high frequency of intercellular adhesion molecule-1 (ICAM-1, 70.1 +/- 8.7%) and urokinase-type plaminogen activator receptor (uPAR, 51.2 +/- 5.2%) positive cells, while a weak expression of MHC class II (IA, 2.2 +/- 0.2% and IE, 17.4 +/- 3.7%) and B7 (12.1 +/- 2.2%) antigens was detected. In our tumor experimental model, after implantation of tumor cells, visible tumor masses were present at days 5-7 with a relatively fast tumor growth until day 15 (progressive phase) followed by a suppression of the tumor growth (regressive phase). Here we present data that correlates a significant decrease in the frequency of ICAM-1 and uPAR expressing tumor cells with the appearance of tumor cells in sites distant from that of the primary tumor. In addition we describe the development of a cellular immune response which controls the tumor progression and is associated with an increase in the expression of major histocompatibility complex (MHC) class II IA antigen during tumor development. The histological examination at tumor progressive and regressive time points revealed the relevant presence of polymorphonuclear neutrophils (PMNs) evidencing colliquative necrosis in tumor growth areas. Taken together, these results support the idea that the balance between adhesive interactions, proteolytic activity and tumorigenicity may lead to a tumor invasive phenotype.

  11. The Effect of Dexmedetomidine on Oxidative Stress Response Following Cerebral Ischemia-Reperfusion in Rats and the Expression of Intracellular Adhesion Molecule-1 (ICAM-1) and S100B

    Science.gov (United States)

    Li, Yanwen; Liu, Shikun

    2017-01-01

    Background Ischemia-reperfusion injury of whole brain involves a complicated pathophysiology mechanism. Dexmedetomidine (Dex) has been shown to have neuro protective functions. This study observed the effect of Dex on serum S100B and cerebral intracellular adhesion molecule-1 (ICAM-1) in a rat model of cerebral ischemia-reperfusion. Material/Methods Healthy Sprague Dawley (SD) rats (males, 7 weeks old) were randomly divided into sham, model, and Dex groups (n=20 each). A cerebral ischemia-reperfusion model was prepared by clipping of the bilateral common carotid artery combined with hypotension. Dex (9 μg/kg) was infused intravenously immediately after reperfusion in the Dex group, while the other two groups received an equal volume of saline. Neural defect score (NDS) was measured at 6 hours, 24 hours, and 72 hours after surgery, with pathological observation of brain tissues. ELISA was then used to test serum S100B protein level. Malondialdehyde (MDA) and superoxide dismutase (SOD) were assayed by spectrometry. Nuclear factor-kappa B (NF-κB) and ICAM-1 levels were determined by real-time (RT)-PCR. Results Model rats had significant injury in the hippocampal CA1 region as shown by elevated NDS, S100B, and MDA levels, higher NF-κB and ICAM-1 mRNA expression, and lower SOD levels (poxidative stress and inflammatory response. PMID:28212354

  12. Lauric acid abolishes interferon-gamma (IFN-γ-induction of intercellular adhesion molecule-1 (ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1 expression in human macrophages

    Directory of Open Access Journals (Sweden)

    Wei-Siong Lim

    2015-09-01

    Conclusions: This study successfully proved that lauric acid was able to antagonize the up-regulatory effect of IFN-γ on ICAM-1 and VCAM-1 expressions in THP-1 macrophages. This indicates that lauric acid may be an anti-inflammatory therapeutic and prophylaxis agent for atherosclerosis.

  13. Angiogenic Effect of Intercellular Adhesion Molecule-1

    Institute of Scientific and Technical Information of China (English)

    DENG Chenguo; ZHANG Duanlian; SHAN Shengguo; WU Jingwen; YANG Hong; YU Ying

    2007-01-01

    In order to investigate the angiogenic effect of intercellular adhesion molecule-1 (ICAM-1), two parts of experiment were performed. Chick embryo chorioallantoic membrane (CAM) assay was used for in vivo angiogenic research. The chick embryos were divided into 4 groups: ICAM-1 group (divided into 3 subgroups, Ⅰ, Ⅱ and Ⅲ) for screening the angiogenic effect of ICAM-1 by adding different concentrations of ICAM-1 (0.1, 0.2 and 0.3 μg/μL) 5 μL into the chick embryo CAMs on the day 10 after incubation for every subgroup; Anti-ICAM-1 group A (divided into 2 subgroups, Ⅰ and Ⅱ) by adding different concentrations of Anti-ICAM-1 (1:100, 1:50) 5 μL into the chick embryo CAMs on the day 10 after incubation for every subgroup to evaluate the effect of ICAM-1 on the survival of microvessels through observing whether Anti-ICAM-1 could induce involution of the microvessels on CAMs; Anti-ICAM-1 group B (divided into 2 subgroups, Ⅰ and Ⅱ ) by adding different concentrations of Anti-ICAM-1 (1:100, 1:50) 5 μL into the chick embryo CAMs on the day 6 after incubation for every subgroup to evaluate whether ICAM-1 involved in embryonic angiogenesis through observing the growth of microvessels on CAMs; Control group: ICAM-1 or Anti-ICAM-1 was substituted by PBS 5 μL on the day 10 or day 6 after incubation. Three days later, the CAMs were photographed in vivo, excised, sectioned and the number of microvessels was counted. In ICAM-1 group, there was increased number of microvessels arranged radially with "spoked-wheel" pattern around the gelatin sponges. The new microvessels growing perpendicularly to gelatin sponges were observed. The number of the microvessels growing in the CAM mesenchymes around the sponges in 3 subgroups was higher than that in control group (P<0.01), however, there was no significant difference among the 3 subgroups (P>0.05). In anti-ICAM-1 group A, the radially arranged microvessels were very unclear around the sponges contrast to that of ICAM

  14. Blockage of intercellular adhesion molecule-1 (ICAM-1 in the prevention of reperfusion lesion in the skeletal musculature of EPM-1 Wistar rats Bloqueio das moléculas de adesão intercelular-1 (ICAM-1 na prevenção da lesão de reperfusão na musculatura esquelética de ratos Wistar EPM-1

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    Roberto David Filho

    2004-12-01

    Full Text Available Purpose: Ischemia-reperfusion lesions are a form of acute inflammation in which leukocytes are considered to play a pivotal role. This study was made with the objective of determining whether the blockage of intracellular adhesion molecule-1, involved in the diapedesis of leukocytes, is efficacious in minimizing this lesions in the skeletal musculature of the posterior limbs of rats. Methods: The juxta-infrarenal aorta of three groups of six adult rats was clipped for six hours. After this, one group was sacrificed (control group and the others underwent 24 hours of reperfusion, one with 0.9% physiological saline (reperfusion group and the other with anti-ICAM-1 monoclonal antibodies (ICAM-1 group. A myeloperoxidase assay was utilized for estimating the infiltrate of neutrophils. Biopsies were obtained to make thin sections of hematoxylin-eosin and NADH. Blood samples were collected for making assays of biochemical parameters (creatinine; potassium; DHL; leukogram; venous pH; CK. Results: The myeloperoxidase levels were raised in the reperfusion (p Objetivo: As lesões de isquemia-reperfusão (I/R são uma forma de inflamação aguda na qual os leucócitos são considerados como tendo um papel fundamental. Este estudo foi feito com o objetivo de determinar se o bloqueio das Moléculas de Adesão Intercelular -1 (ICAM-1, envolvidas na diapedese dos leucócitos, é eficaz em minimizar estas lesões na musculatura esquelética dos membros posteriores de ratos. Métodos: A aorta infra-renal de três grupos de seis ratos adultos foi clampeada por seis horas. Logo após, um grupo foi sacrificado (grupo controle e os outros foram submetidos a 24 horas de reperfusão, um com solução salina fisiológica 0,9% (grupo reperfusão e outro com anticorpos monoclonais anti-ICAM-1 (grupo ICAM-1. A quantificação da enzima mieloperoxidase foi utilizada para estimar o infiltrado de leucócitos na musculatura. Biópsias foram obtidas e coradas com hematoxilina

  15. Intercellular adhesion molecule-1 in patients with idiopathic interstitial pneumonia.

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    Takehara H

    2001-08-01

    Full Text Available This study focuses on a possible role of intercellular adhesion molecule-1 (ICAM-1 in interstitial pulmonary diseases. We determined a soluble form of ICAM-1 in serum and bronchoalveolar lavage fluid (BALF using ELISA in patients with usual interstitial pneumonia (UIP, bronchiolitis obliterance organizing pneumonia (BOOP, or nonspecific interstitial pneumonia (NSIP. In addition, we investigated the expression of ICAM-1 in the lung tissues of these patients by means of immunohistochemical staining. Serum levels of soluble ICAM-1 were significantly higher in patients with UIP or NSIP than in healthy subjects, and were also high in patients with BOOP. The soluble ICAM-1 in BALF tended to be higher in patients with UIP, BOOP, or NSIP than in normal subjects. A significant correlation was seen between soluble levels of ICAM-1 in serum and BALF. In the immunostaining of ICAM-1 of the lung tissues, ICAM-1 expression was more pronounced in patients with UIP than in those with BOOP or NSIP. The increased expression of ICAM-1 was seen in type II alveolar epithelium and vascular endothelium in patients with interstitial pneumonia. A positive correlation was observed between the degree of ICAM-1 expression in the lung tissues and the BALF levels of soluble ICAM-1. The expression of ICAM-1 in type II alveolar epithelium suggests that ICAM-1 plays a specific role in the fibrotic process of the lung, and that the measurement of soluble ICAM-1 in sera and BALF could be a useful marker for evaluating the progression of fibrosis.

  16. Engagement of PSGL-1 enhances β2-integrin-involved adhesion of neutrophils to recombinant ICAM-1

    Institute of Scientific and Technical Information of China (English)

    Xiao-guang WANG; Yan-ping CHENG; Xue-qing BA

    2006-01-01

    Aim: The interactions of selectins and their ligands initiate the process of leukocyte migrating into inflamed tissue. P-selectin glycoprotein ligand 1 (PSGL-1) is the best characterized ligand of selectins, and has been demonstrated to mediate the adhesion of leukocytes to all three selectins in vivo. PSGL-1 not only functions as an anchor molecule to capture the leukocytes to the activated endothelial cells by its interaction with selectins, but also transduces the signals to activate leukocytes. Our present work aimed to investigate the mechanism by which PSGL-1-mediated signal activates neutrophils and enhances the adhesion to the endothelial cells. Methods: We detected the effects of the engagement of PSGL-1 with monoclonal antibodies (mAb) or P-selectin on the adhesion of neutrophils to the recombinant intercellular adhesion molecule-1 (ICAM-1), and on the expression of β2-integrin. Additionally, the role of cytoskeleton in these process was studied by using inhibitor cytochalasin B. Results: The engagement of PSGL-1 increased the expression of β2-integrin on the surface of neutrophils and enhanced the adhesion of neutrophils to the recombinant ICAM-1. mAb against CD 18 impaired the adhesion of PSGL-1 -engaged neutrophils to ICAM-1. Moreover, the inhibitor cytochalasin B largely blocked the increase of CD 18 expression as well as the adhesion of PSGL-1-engaged neutrophils to ICAM-1. Conclusion: The PSGL-1-transduced signals can enhance β2-integrin-involved adhesion of neutrophils to the recombinant ICAM-1, and this process depends on the dynamics of cytoskeleton.

  17. Intercellular adhesion molecule-1 expression by skeletal muscle cells augments myogenesis

    Energy Technology Data Exchange (ETDEWEB)

    Goh, Qingnian; Dearth, Christopher L.; Corbett, Jacob T. [Department of Kinesiology, The University of Toledo, Toledo, OH (United States); Pierre, Philippe [Centre d’Immunologie de Marseille-Luminy U2M, Aix-Marseille Université, Marseille (France); INSERM U631, Institut National de la Santé et Recherche Médicale, Marseille (France); CNRS UMR6102, Centre National de la Recherche Scientifique, Marseille (France); Chadee, Deborah N. [Department of Biological Sciences, The University of Toledo, Toledo, OH (United States); Pizza, Francis X., E-mail: Francis.Pizza@utoledo.edu [Department of Kinesiology, The University of Toledo, Toledo, OH (United States)

    2015-02-15

    We previously demonstrated that the expression of intercellular adhesion molecule-1 (ICAM-1) by skeletal muscle cells after muscle overload contributes to ensuing regenerative and hypertrophic processes in skeletal muscle. The objective of the present study is to reveal mechanisms through which skeletal muscle cell expression of ICAM-1 augments regenerative and hypertrophic processes of myogenesis. This was accomplished by genetically engineering C2C12 myoblasts to stably express ICAM-1, and by inhibiting the adhesive and signaling functions of ICAM-1 through the use of a neutralizing antibody or cell penetrating peptide, respectively. Expression of ICAM-1 by cultured skeletal muscle cells augmented myoblast–myoblast adhesion, myotube formation, myonuclear number, myotube alignment, myotube–myotube fusion, and myotube size without influencing the ability of myoblasts to proliferate or differentiate. ICAM-1 augmented myotube formation, myonuclear accretion, and myotube alignment through a mechanism involving adhesion-induced activation of ICAM-1 signaling, as these dependent measures were reduced via antibody and peptide inhibition of ICAM-1. The adhesive and signaling functions of ICAM-1 also facilitated myotube hypertrophy through a mechanism involving myotube–myotube fusion, protein synthesis, and Akt/p70s6k signaling. Our findings demonstrate that ICAM-1 expression by skeletal muscle cells augments myogenesis, and establish a novel mechanism through which the inflammatory response facilitates growth processes in skeletal muscle. - Highlights: • We examined mechanisms through which skeletal muscle cell expression of ICAM-1 facilitates events of in vitro myogenesis. • Expression of ICAM-1 by cultured myoblasts did not influence their ability to proliferate or differentiate. • Skeletal muscle cell expression of ICAM-1 augmented myoblast fusion, myotube alignment, myotube–myotube fusion, and myotube size. • ICAM-1 augmented myogenic processes through

  18. EXPRESSION OF INTERCELLULAR ADHESION MOLECULE-1 BY MYOFIBERS IN mdx MICE

    Science.gov (United States)

    TORRES-PALSA, MARIA J.; KOZIOL, MATTHEW V.; GOH, QINGNIAN; CICINELLI, PETER A.; PETERSON, JENNIFER M.; PIZZA, FRANCIS X.

    2017-01-01

    Introduction We investigated the extent to which intercellular adhesion molecule-1 (ICAM-1), a critical protein of the inflammatory response, is expressed in skeletal muscles of mdx mice (a murine model of Duchenne muscular dystrophy). Methods Muscles were collected from control and mdx mice at 2–24 weeks of age and analyzed for ICAM-1 expression by means of Western blot and immunofluorescence. Results Western blot revealed higher expression of ICAM-1 in mdx compared with control muscles through 24 weeks of age. In contrast to control muscles, ICAM-1 was expressed on the membrane of damaged, regenerating, and normal myofibers of mdx mice. CD11b+ myeloid cells also expressed ICAM-1 in mdx muscles, and CD11b+ cells were closely associated with the membrane of myofibers expressing ICAM-1. Conclusions These findings support a paradigm in which ICAM-1 and its localization to myofibers in muscles of mdx mice contributes to the dystrophic pathology. PMID:25728314

  19. Increased Expression of Intercellular Adhesion Molecule-1, Vascular Cellular Adhesion Molecule-1 and Leukocyte Common Antigen in Diabetic Rat Retina

    Institute of Scientific and Technical Information of China (English)

    Ningyan Bai; Shibo Tang; Jing Ma; Yan Luo; Shaofeng Lin

    2003-01-01

    Purpose: To understand the expression and distribution of intercellular adhesion molecule- 1(ICAM- 1),vascular cellular adhesion molecule- 1 (VCAM- 1)and CD45 (Leukocyte Common Antigen) in the control nondiabetic and various courses of diabetic rats retina. To explore the role of adhesion molecules (Ams) and the adhesion of leukocytes to vascular endothelial cells via Ams in diabetic retinopathy(DR).Methods: Sixty healthy adult male Wistar rats were randomly divided into diabetic groups(induced by Streptozotocin, STZ) and normal control groups. Rats in these two groups were further randomly divided into 3, 7, 14, 30, 90 and 180 days-group,including 5 rats respectively. The immunohistochemical studies of ICAM-1, VCAM-1 and CD45 were carried out in the retinal digest preparations or retinal paraffin sections, and the results were analyzed qualitatively, semi-quantitatively.Results: No positive reaction of VCAM-1 was found, and weak reactions of ICAM-1,CD45 were found in nondiabetic rats retina. The difference of 6 control groups had no statistical significance(P > 0.05). The increased ICAM-1 and CD45 staining pattern were detectable 3 days after diabetes induction, and a few VCAM-1 positive cells were observed in the retinal blood capillaries. The difference of diabetes and control is significant( P < 0.05).Following the course, the expressions of ICAM-1, VCAM-1 and CD45 were increasingly enhanced, reaching a peak at the 14th day.Conclusion: Increased expression of ICAM-1, VCAM-1 and leukocytes adhering and stacking in retinal capillaries are the very early events in DR. Coherence of expression and distribution of the three further accounts for it is the key point for the onset of DR that Ams mediates leukocytes adhesion and endothelial cell injury.

  20. Inhibitors of 5-lipoxygenase inhibit expression of intercellular adhesion molecule-1 in human melanoma cells

    Institute of Scientific and Technical Information of China (English)

    Yin WANG; Bin ZHOU; Ji LI; Yong-bing CAO; Xin-sheng CHEN; Ming-he CHENG; Ming YIN

    2004-01-01

    AIM: To study the effect of 5-lipoxygenase inhibitors on the expression of intercellular adhesion molecule-1 (ICAM-1) in melanoma cells. METHODS: ICAM-1 protein of human melanoma cell a375 was detected by enzyme-linked immunosorbent, flow cytometry and Western blot analysis. Level of ICAM-1 mRNA in a375 was evaluated by Northern blot analysis. Adhesion of a375 to endothelial cell EC304 was analyzed by isotopic tracing. RESULTS:5-Lipoxygenase inhibitors nordihydroguaiaretic acid, AA861 and MK886, could suppress the expression of ICAM-1 protein as well as of its mRNA in a375 cells and reduce the adhesion of a375 to EC304. CONCLUSION:5-Lipoxygenase inhibitors can inhibit the expression of ICAM-1 in human melanoma cells and may be valuable for treatment of melanoma metastasis.

  1. Role of ICAM-1 in the aggregation and adhesion of human alveolar macrophages in response to TNF-α and INF-γ

    Directory of Open Access Journals (Sweden)

    Masahiro Sasaki

    2001-01-01

    Full Text Available Intracellular adhesion molecule-1 (ICAM-1-mediated cell-cell adhesion is thought to play an important role at sites of inflammation. Recent evidence suggests that ICAM-1 surface expression on alveolar macrophages is increased in pulmonary sarcoidosis and that inflammatory granuloma formation is characterized by the aggregation of macrophages. The present study shows that ICAM-1 expression is significantly elevated on alveolar macrophages from patients with sarcoidosis in response to tumor necrosis factor-α (TNF-α and interferon- γ (INF-γ compared with healthy controls. Aggregation and adhesion were significantly increased in alveolar macrophages treated with TNF-α and INF-γ, and significantly inhibited in those pretreated with a monoclonal antibody to ICAM-1. Similarly, aggregation and adhesion were inhibited in macrophages treated with heparin, which then exhibited a wide range of biological activities relevant to inflammation. These results suggested that the surface expression of ICAM-1 on alveolar macrophages in response to TNF-α and INF-γ is important in mediating aggregation and adhesion. Additionally, heparin may be useful for developing novel therapeutic agents for fibrotic lung disease.

  2. S108抑制大鼠肾移植排斥反应时细胞间粘附分子-1的表达%S108 inhibits the expression of cell adhesion molecule-1 (ICAM-1) during the rejection of renal allograft in rat

    Institute of Scientific and Technical Information of China (English)

    沈文律; 黄孝伦; 周泽清; 李幼平; 王学; 杜成友

    1998-01-01

    观测细胞间粘附分子-1(ICAM-1)在大鼠移植肾的表达,旨在探索S108抗排斥作用的机理以及对ICAM-1的表达有无抑制作用.共分5个实验组:即同品系移植组、不用药对照组、短期单用环孢素A(CsA)组、小剂量CsA联合S108组及单用S108组.采用小鼠抗大鼠单克隆抗体(IA29)测定移植肾内ICAM-1的表达,每一标本采用计算机图象分析定量测定.结果表明,ICAM-1在同品系移植肾肾小管周围的毛细血管内皮细胞、静脉和肾小管仅呈微弱阳性表达,不表达于肾间质组织.排斥时ICAM-1在移植肾血管内皮细胞、组织间质和肾小管上广泛表达,表达水平高低与移植肾排斥强弱有相关性,S108可降低ICAM-1抗原分子在移植肾的表达水平,呈现抗排斥效应.%In order to explore the anti-rejection mechanism of S108 and its inhibition on the ICAM-1 expression, the "expression of ICAM-1 in rat renal isografts and allografts was studied.The rats were divided into 5 experimental groups. The expression of ICAM-1 in the renal grafts was determined using mouse anti-rat monoclonal antibody (IA29). Quantitative measurement was performed in each samples using computer imaging analysis. The results showed that the expression of ICAM-1 presented faint positive inthe capillary endothelial cells, veins around the tubules and the tubules in the same strain renal grafts. No ICAM-1 expression was found in the renal intestitial tissue. The extensive expression of ICAM-1 was found in the endothelial cells, intestitial tissue and tubules of the renal grafts during the rejection with the expression level relative to the severity of the rejection of the renal grafts. S108 could reduce the expression level of ICAM-1 in the renal grafts, so as to present anti-rejection reaction.

  3. Soluble adhesion molecules ICAM-1, VCAM-1, P-selectin in children with Helicobacter pylori infection

    Institute of Scientific and Technical Information of China (English)

    Elzbieta Maciorkowska; Maciej Kaczmarski; Anatol Panasiuk; Katarzyna Kondej-Muszynska; Andrzej Kemonai

    2005-01-01

    AIM: To assess the sICAM-1, sVCAM-1, and sP-selectin levels in children withHelicobacter pylori(H pylori)infection and to evaluate their significance for the morphological changes found in gastric mucosa.METHODS: The study included 106 children: 59children (55.7%) with chronic gastritis and positive IgG against H pylori, 29 children (27.3%) after previous H pylori infection without the bacterium colonization but with positive IgG against H pylori, and 18 children (17%) with functional disorders of the gastrointestinal system but with normal IgG against H pylori. Endoscopic and histopathological evaluation of gastric mucosa was performed based on the Sydney System classification.The evaluation of sP-selectin, sIC AM-1, sVCAM-1 levels in the sera of children was carried out using ELISA test.RESULTS: The assessment of gastritis activity degrees indicated statistically significant values in the antrum and corpus (P<0.001) of children examined. Serum sVCAM-1 levels were higher in group with gastritis due to H pylori infection than in group without infection and differed statistically (P<0.05). Serum sVCAM-1 levels proved to be the highest among other adhesive molecules in infected children and decreased after eradication of H pylori. Serum sICAM-1 levels were similar in all examined groups. Serum sP-selectin levels were similar in children with and without H pylori infection.CONCLUSION: Assessment of adhesive molecules (sPselectin, sICAM-1, sVCAM-1) in the sera of children with active H pylori infection can show the participation of sVCAM-1 in the pathogenesis of gastric mucosal inflammation, sP-selectin and sICAM-1 concentrations in the sera of children with H pylori infection after eradication cannot reveal any significant differences as compared to healthy children.

  4. Lipid Raft is required for PSGL-1 ligation induced HL-60 cell adhesion on ICAM-1.

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    Tingshuang Xu

    Full Text Available P-selectin glycoprotein ligand-1 (PSGL-1 and integrins are adhesion molecules that play critical roles in host defense and innate immunity. PSGL-1 mediates leukocyte rolling and primes leukocytes for integrin-mediated adhesion. However, the mechanism that PSGL-1 as a rolling receptor in regulating integrin activation has not been well characterized. Here, we investigate the function of lipid raft in regulating PSGL-1 induced β2 integrin-mediated HL-60 cells adhesion. PSGL-1 ligation with antibody enhances the β2 integrin activation and β2 integrin-dependent adhesion to ICAM-1. Importantly, with the treatment of methyl-β-cyclodextrin (MβCD, we confirm the role of lipid raft in regulating the activation of β2 integrin. Furthermore, we find that the protein level of PSGL-1 decreased in raft fractions in MβCD treated cells. PSGL-1 ligation induces the recruitment of spleen tyrosine kinase (Syk, a tyrosine kinase and Vav1 (the pivotal downstream effector of Syk signaling pathway involved in cytoskeleton regulation to lipid raft. Inhibition of Syk activity with pharmacologic inhibitor strongly reduces HL-60 cells adhesion, implicating Syk is crucial for PSGL-1 mediated β2 integrin activation. Taken together, we report that ligation of PSGL-1 on HL-60 cells activates β2 integrin, for which lipid raft integrity and Syk activation are responsible. These findings have shed new light on the mechanisms that connect leukocyte initial rolling with subsequent adhesion.

  5. Matrix stiffness exerts biphasic control over monocyte-endothelial adhesion via Rho-mediated ICAM-1 clustering.

    Science.gov (United States)

    Scott, Harry A; Quach, Boi; Yang, Xiao; Ardekani, Soroush; Cabrera, Andrea P; Wilson, Randall; Messaoudi-Powers, Ilhem; Ghosh, Kaustabh

    2016-08-01

    Leukocyte-endothelial adhesion is a critical early step in chronic vascular inflammation associated with diabetes, emphysema, and aging. Importantly, these conditions are also marked by abnormal subendothelial matrix crosslinking (stiffness). Yet, whether and how abnormal matrix stiffness contributes to leukocyte-endothelial adhesion remains poorly understood. Using a co-culture of human monocytic cells and human microvascular endothelial cells (ECs) grown on matrices of tunable stiffness, we demonstrate that matrix stiffness exerts biphasic control over monocyte-EC adhesion, with both matrix softening and stiffening eliciting a two-fold increase in this adhesive interaction. This preferential endothelial adhesivity on softer and stiffer matrices was consistent with a significant increase in α-actinin-4-associated endothelial ICAM-1 clustering, a key determinant of monocyte-EC adhesion. Further, the enhanced ICAM-1 clustering on soft and stiff matrices correlated strongly with an increase in Rho activity and ROCK2 expression. Importantly, inhibition of Rho/ROCK activity blocked the effects of abnormal matrix stiffness on ICAM-1 clustering and monocyte-EC adhesion. Thus, these findings implicate matrix stiffness-dependent ICAM-1 clustering as an important regulator of vascular inflammation and provide the rationale for closely examining mechanotransduction pathways as new molecular targets for anti-inflammatory therapy.

  6. Nd:YAG激光联合牙周基础治疗对慢性牙周炎患牙龈沟液中sICAM-1的影响%Effects of conventional periodontal treatment combined with pulsed Nd:YAG laser on the expression of Soluble Intercellular Adhesion Molecule-1 in gingival crevicular fluid of patients with chronic periodontitis

    Institute of Scientific and Technical Information of China (English)

    冯萍; 王青; 余晓燕; 戴海燕; 伍燕; 高丽

    2016-01-01

    目的 检测慢性牙周炎患者经过牙周基础治疗后,联合Nd:YAG激光,观察牙周临床指标的改变,同时通过对龈沟液中可溶性细胞间粘附分子-1(sICAM-1)的检测,探讨Nd:YAG激光在牙周治疗中的应用.方法 14例慢性牙周炎患者(40颗观察牙)分为观察组(8例患者20颗患牙)和对照组(6例患者20例患牙),观察组采用Nd:YAG激光联合牙周基础治疗,采用龈下刮治+根面平整(SRP);对照组仅进行牙周基础治疗术.在治疗前以及治疗后1周、4周分别采用滤纸条法采集龈沟液样本,用酶联免疫吸附测定法(ELISA)检测样本中sICAM-1的含量.分别于治疗前及治疗后4周检查牙周临床指数的变化.结果 慢性牙周炎患者龈沟液中sICAM-1的含量在治疗后第1周、4周,观察组和对照组均低于治疗前(P<0.05),在治疗后第4周,观察组与对照组之间比较,sICAM-1的含量降低差异有统计学意义(P<0.05).治疗后4周,除临床附着丧失(CAL)外,观察组与对照组牙周探诊深度(PD)、出血指数(BI)与治疗前相比,均有明显降低(P<0.05),观察组与对照组之间比较,仅BI的改变差异有统计学意义(P<0.05).结论 龈沟液中sICAM-1的水平与牙周炎症密切相关,可作为反映牙周状态的客观指标.使用Nd:YAG激光能够有效地减少龈沟液中sICAM-1的表达,减轻牙周炎症反应,尤其是改善牙龈出血症状效果明显.

  7. Skeletal muscle cells express ICAM-1 after muscle overload and ICAM-1 contributes to the ensuing hypertrophic response.

    Directory of Open Access Journals (Sweden)

    Christopher L Dearth

    Full Text Available We previously reported that leukocyte specific β2 integrins contribute to hypertrophy after muscle overload in mice. Because intercellular adhesion molecule-1 (ICAM-1 is an important ligand for β2 integrins, we examined ICAM-1 expression by murine skeletal muscle cells after muscle overload and its contribution to the ensuing hypertrophic response. Myofibers in control muscles of wild type mice and cultures of skeletal muscle cells (primary and C2C12 did not express ICAM-1. Overload of wild type plantaris muscles caused myofibers and satellite cells/myoblasts to express ICAM-1. Increased expression of ICAM-1 after muscle overload occurred via a β2 integrin independent mechanism as indicated by similar gene and protein expression of ICAM-1 between wild type and β2 integrin deficient (CD18-/- mice. ICAM-1 contributed to muscle hypertrophy as demonstrated by greater (p<0.05 overload-induced elevations in muscle protein synthesis, mass, total protein, and myofiber size in wild type compared to ICAM-1-/- mice. Furthermore, expression of ICAM-1 altered (p<0.05 the temporal pattern of Pax7 expression, a marker of satellite cells/myoblasts, and regenerating myofiber formation in overloaded muscles. In conclusion, ICAM-1 expression by myofibers and satellite cells/myoblasts after muscle overload could serve as a mechanism by which ICAM-1 promotes hypertrophy by providing a means for cell-to-cell communication with β2 integrin expressing myeloid cells.

  8. Expression of intercellular adhesion molecule-1 in UVA-irradiated human skin cells in vitro and in vivo

    Energy Technology Data Exchange (ETDEWEB)

    Treina, G.; Scaletta, C.; Frenk, E.; Applegate, L.A. [University Hospital-CHUV, Lausanne (Switzerland). Laboratory of Photobiology; Fourtanier, A.; Seite, S. [L`Oreal-Centre de Recherche Charles Zviak (France). Recherche Avancee Biologie

    1996-08-01

    Ultraviolet A (UVA) radiation represents an important oxidative stress to human skin and certain forms of oxidative stress have been shown to modulate intercellular adhesion molecule-1 (ICAM-1) expression. ICAM-1 has been shown to play an important part in many immune reactions and the perturbations of this molecule by ultraviolet radiation could have implications in many inflammatory responses. An enhancement immunohistochemical method with avidin/biotin was used for analysing the early effects of UVA radiation on human cell cultures and human skin (340-400 nm). Both in vitro and in vivo data show that ICAM-1 staining in epidermal keratinocytes, which was expressed constitutively, decreased in a UVA dose-dependent manner. The decrease was most noted at 3-6 h following UVA radiation with some ICAM-1 staining returning by 48 h post-UVA. ICAM-1 positive staining in the dermis was specific for vascular structures and was increased 24 h after UVA radiation. Cultured dermal fibroblasts exhibited ICAM-1 staining which increased slightly within 6-48 h post-UVA radiation. As epidermal ICAM-1 expression is depleted following UVA radiation and dermal expression increases due to an increase in the vascular structures, ICAM-1 provides a valuable marker following UVA radiation in human skin that can be readily measured in situ. (author).

  9. Discrimination among rhinovirus serotypes for a variant ICAM-1 receptor molecule.

    Science.gov (United States)

    Xiao, Chuan; Tuthill, Tobias J; Bator Kelly, Carol M; Challinor, Lisa J; Chipman, Paul R; Killington, Richard A; Rowlands, David J; Craig, Alister; Rossmann, Michael G

    2004-09-01

    Intercellular adhesion molecule 1 (ICAM-1) is the cellular receptor for the major group of human rhinovirus serotypes, including human rhinovirus 14 (HRV14) and HRV16. A naturally occurring variant of ICAM-1, ICAM-1Kilifi, has altered binding characteristics with respect to different HRV serotypes. HRV14 binds to ICAM-1 only transiently at physiological temperatures but forms a stable complex with ICAM-1Kilifi. Conversely, HRV16 forms a stable complex with ICAM-1 but does not bind to ICAM-1Kilifi. The three-dimensional structures of HRV14 and HRV16, complexed with ICAM-1, and the structure of HRV14, complexed with ICAM-1Kilifi, have been determined by cryoelectron microscopy (cryoEM) image reconstruction to a resolution of approximately 10 angstroms. Structures determined by X-ray crystallography of both viruses and of ICAM-1 were fitted into the cryoEM density maps. The interfaces between the viruses and receptors contain extensive ionic networks. However, the interactions between the viruses and ICAM-1Kilifi contain one less salt bridge than between the viruses and ICAM-1. As HRV16 has fewer overall interactions with ICAM-1 than HRV14, the absence of this charge interaction has a greater impact on the binding of ICAM-1Kilifi to HRV16 than to HRV14.

  10. Intraocular soluble intracellular adhesion molecule-1 correlates with subretinal fluid height of diabetic macular edema

    Directory of Open Access Journals (Sweden)

    Dan Zhu

    2014-01-01

    Full Text Available Objective: To investigate the correlations between aqueous concentrations of vascular endothelial growth factor (VEGF, monocyte chemoattractant protein-1 (MCP-1, soluble intracellular adhesion molecule-1 (sICAM-1 and diabetic macular edema (DME. Materials and Methods: VEGF, MCP-1 and sICAM-1 concentrations in aqueous humor samples of 22 patients with DME and 23 patients with cataract of a control group were measured with solid-phase chemiluminescence immunoassay. Results: Aqueous VEGF (89.2 ± 58.5 pg/ml versus 48.5 ± 27.8 pg/ml, P = 0.006, MCP-1 (684.2 ± 423.4 pg/ml versus 432.4 ± 230.4 pg/ml, P = 0.019 and sICAM-1 (3213.8 ± 2581.6 pg/ml versus 260.2 ± 212.2 pg/ml, P < 0.001 all vary significantly between DME group and control group. Maximum height of submacular fluid measured by Optical coherence tomography (OCT was significantly associated with aqueous sICAM-1 (r = -0.45, P = 0.034. The maximum height of macular thickness measured by OCT was not significantly associated with either VEGF (P = 0.300, MCP-1 (P = 0.320 or sICAM-1 (P = 0.285. Conclusions: Our results suggest that sICAM-1 may majorly contribute to the formation of subretinal fluid in DME patients and imply that MCP-1 and sICAM-1 may be the potential therapy targets, besides VEGF.

  11. Expression of intercellular adhesion molecule-1and HLA-DR antigens in uveitis

    Institute of Scientific and Technical Information of China (English)

    1999-01-01

    目的:研究细胞间粘附分子-1(intellular adhesion molecule-1,ICAM-1)和人体组织相关抗原(human leudocyte antigen,HLA-DR)在萄萄膜炎免疫反应中的作用.方法:应用免疫组织化学染色检查20只正常眼和54例葡萄糖膜炎眼球摘除眼(其中外源性33例和内源性21例)的脉络膜和视网膜组织中ICAM-1和HLA-DR的表达.结果:正常眼的脉络膜和视网膜组织没有ICAM-1的阳性染色,没有或较少有HLA-DR的表达,葡萄膜炎眼中二者有增高表达(P<0.01),而外源性和内源性葡萄膜炎眼组间表达统计学上无显著差异(P>0.05).结论:ICAM-1、HLA-DR分子能够介导白细胞和炎症部位组织细胞的识别和粘附,二者的共同表达说明它们在葡萄糖膜炎脉络膜视网膜组织的免疫性损伤中具有重要意义.%Objective :To study the effects of intercellular adhesion molecule-1 (ICAM-1) and human leukocyte antigen (HAL-DR) on the immunopathologic process of uveitis. Methods:Imn- munohistochemical techniques were applied to detect their expression in eyes of both the health (20 cases from eye bank) and patients with uveitis (54 cases with 54 eyes which included 33 ex- ogenous uveitis and 21 endogenous one). Results:Both the two ant igens were detectable in the choroidal and retinal tissues in eyes of uveitis while all the normal eyes showed negative expres- sion of ICAM-1 and negative or little expression of HLA-DR (P<0. 01). However,there was no statistically significant difference between exogenous and endogenous types (P>0. 05). Conclu- sion: Both ICAM-1 and HLA-DR may be responsible for cell recognition and binding in the in- flarnmatory tissues. The co-expression of ICAM-1 and HAL-DR showed that these two factors might play an important role in the immunologic damage of the choroid and retina in uveitis.

  12. Intercellular adhesion molecule 1 serves as a primary cognate receptor for the Type IV pilus of nontypeable Haemophilus influenzae.

    Science.gov (United States)

    Novotny, Laura A; Bakaletz, Lauren O

    2016-08-01

    Nontypeable Haemophilus influenzae (NTHI) utilizes the Type IV pilus (Tfp) to adhere to respiratory tract epithelial cells thus colonizing its human host; however, the host cell receptor to which this adhesive protein binds is unknown. From a panel of receptors engaged by Tfp expressed by other bacterial species, we showed that the majority subunit of NTHI Tfp, PilA, bound to intercellular adhesion molecule 1 (ICAM1) and that this interaction was both specific and of high affinity. Further, Tfp-expressing NTHI inoculated on to polarized respiratory tract epithelial cells that expressed ICAM1 were significantly more adherent compared to Tfp-deficient NTHI or NTHI inoculated on to epithelial cells to which ICAM1 gene expression was silenced. Moreover, pre-incubation of epithelial cells with recombinant soluble PilA (rsPilA) blocked adherence of NTHI, an outcome that was abrogated by admixing rsPilA with ICAM1 prior to application on to the target cells. Epithelial cells infected with adenovirus or respiratory syncytial virus showed increased expression of ICAM1; this outcome supported augmented adherence of Tfp-expressing NTHI. Collectively, these data revealed the cognate receptor for NTHI Tfp as ICAM1 and promote continued development of a Tfp-targeted vaccine for NTHI-induced diseases of the airway wherein upper respiratory tract viruses play a key predisposing role.

  13. ICAM-1 and Acute Pancreatitis Complicated by Acute Lung Injury

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    XiPing Zhang

    2009-01-01

    Full Text Available One of the most common complications of acute pancreatitis is acute lung injury, during which intercellular adhesion molecule-1 (ICAM-1 plays an important role by participating in leukocyte adhesion and activation as well as by inducing the “cascade effect” of inflammatory mediators, pulmonary microcirculation dysfunction and even acute respiratory distress syndrome, multiple organ failure or death. Although it is generally believed that the modulatory mechanism of ICAM-1 during this process is associated with the activation of nuclear transcription factor kappa B which is mediated by IL-1, IL-6, IL-18 and oxygen free radical, etc., further studies are still required to clarify it. Since the upregulation of ICAM-1 expression in the lung during acute lung injury is one of main pathogeneses, the early detection of the ICAM-1 expression level may contribute to the prevention and treatment of acute lung injury. Moreover, reducing pulmonary ICAM-1 expression levels through treatment with anti-ICAM-1 monoclonal antibody (aICAM-1 and antagonists of the neurokinin 1 receptor, etc., should have a positive effect on protecting the lungs during acute pancreatitis. This review aims to further clarify the relationship between ICAM-1 and acute pancreatitis complicated by acute lung injury, and therefore provides a theoretical basis for the formulation of corresponding therapeutic measures in clinical practice for acute pancreatitis.

  14. Association of ICAM-1 K469E polymorphism with neurocysticercosis.

    Science.gov (United States)

    Singh, Amrita; Singh, Aloukick K; Singh, Satyendra K; Paliwal, Vimal K; Gupta, Rakesh K; Prasad, Kashi N

    2014-11-15

    Neurocysticercosis (NCC), a central nervous system (CNS) disease is caused by the larval stage of Taenia solium. The disease is heterogeneous in clinical presentation; some infected individuals develop symptoms and others may remain symptom free. Impaired blood brain barrier allows recruitment of immune cells in the CNS during infection and soluble intercellular adhesion molecule-1 (sICAM-1) plays an important role in the recruitment of immune cells. We studied ICAM-1 K469E polymorphism among symptomatic and asymptomatic NCC patients. The study revealed that individuals with variant (EE) genotype were more susceptible to symptomatic NCC and also had an elevated level of sICAM-1.

  15. Differential effects of heme oxygenase isoforms on heme mediation of endothelial intracellular adhesion molecule 1 expression.

    Science.gov (United States)

    Wagener, F A; da Silva, J L; Farley, T; de Witte, T; Kappas, A; Abraham, N G

    1999-10-01

    Heme oxygenase (HO), by catabolizing heme to bile pigments, down-regulates cellular hemoprotein, hemoglobin, and heme; the latter generates pro-oxidant products, including free radicals. Two HO isozymes, the products of distinct genes, have been described; HO-1 is the inducible isoform, whereas HO-2 is suggested to be constitutively expressed. We studied the inducing effect of several metal compounds (CoCl(2), stannic mesoporphyrin, and heme) on HO activity. Additionally, we studied HO-1 expression in experimental models of adhesion molecule expression produced by heme in endothelial cells, and the relationship of HO-1 expression to the induced adhesion molecules. Flow cytometry analysis showed that heme induces intracellular adhesion molecule 1 (ICAM-1) expression in a concentration (10-100 microM)- and time (1-24 h)-dependent fashion in human umbilical vein endothelial cells. Pretreatment with stannic mesoporphyrin, an inhibitor of HO activity, caused a 2-fold increase in heme-induced ICAM-1 expression. In contrast, HO induction by CoCl(2) decreased heme-induced ICAM-1 expression by 33%. To examine the contribution of HO-1 and HO-2 to endothelial HO activity, specific antisense oligonucleotides (ODNs) of each isoform were tested for their specificity to inhibit HO activity in cells exposed to heme. Endothelial cells exposed to heme elicited increased HO activity, which was prevented (70%) by HO-1 antisense ODNs. HO-2 antisense ODN inhibited heme-induced HO activity by 21%. Addition of HO-1 antisense ODNs prevented heme degradation and resulted in elevation of microsomal heme. Western blot analysis showed that HO-1 antisense ODNs selectively inhibited HO-1 protein and failed to inhibit HO-2 protein. Incubation of endothelial cells with HO-1 antisense enhanced heme-dependent increase of ICAM-1. In contrast, addition of HO-2 antisense to endothelial cells failed to increase adhesion molecules. The role of glutathione, an important antioxidant, was examined on heme

  16. Effect of thalidomide dithiocarbamate analogs on the intercellular adhesion molecule-1 expression.

    Science.gov (United States)

    Guirgis, Adel A; Zahran, Magdy A H; Mohamed, Amr S; Talaat, Roba M; Abdou, Bishoy Y; Agwa, Hussein S

    2010-07-01

    Thalidomide has been reported to have anti-angiogenic and antimetastatic effects. Intercellular adhesion molecule-1 (ICAM-1) was shown to be involved in monocyte adherence to epithelial cells and cancer cell invasion. Novel thalidomide dithiocarbamate analogs (containing 2 sulfur atoms) were designed and synthesized as potential anti-tumor agents. The aim of this work is to investigate their anti-tumor effect against transplantable experimental tumor, Ehrlich ascites carcinoma (EAC), in mice by studying the changes in cell's biochemical profile, the expression of ICAM-1 and nitric oxide (NO) and their association with tumor burden. As shown in our results, treatment of solid tumor-bearing mice with thalidomide 1 resulted in a significant reduction in tumor volume with 75.4% inhibition, a significant decrease in lactate dehydrogenase (LDH), ICAM-1 expression and NO. Thalidomide dithiocarbamate analogs 2 and 3 exhibited a potent effect to reduce the volume of solid tumor with 96.7% and 96.5% inhibition, respectively, a significant ability to increase the albumin, alanine aminotransferase (ALT) and glucose levels and to diminish LDH, ICAM-1 expression and NO. Thalidomide dithiocarbamate analog 3 has more potent anti-tumor activity as compared with thalidomide 1 or its dithiocarbamate analog 2. Taken together, our study improved that the dithiocarbamate analogs 2 and 3 are more potent anti-tumor agents with more pronounced effect than thalidomide 1 itself.

  17. Cardiotrophin-1 induces intercellular adhesion molecule-1 expression by nuclear factor κB activation in human umbilical vein endothelial cells

    Institute of Scientific and Technical Information of China (English)

    2008-01-01

    Background In addition to elevated concentrations of cytokines, patients with congestive heart failure (CHF) show endothelial dysfunction and increased plasma concentrations of adhesion molecules like intercellular adhesion molecule-1 (ICAM-1). Furthermore, the concentration of cardiotrophin-1 (CT-1) - a cytokine of the interleukin-6 superfamily - is increased in CHF. We tested the hypothesis whether CT-1 is able to induce ICAM-1 in human umbilical vein endothelial cells (HUVEC). Furthermore we examined the signalling mechanisms of CT-1 mediated ICAM-1 expression. Methods Confluent layers of HUVEC were incubated with increasing concentrations of CT-1 (5 to 100 ng/ml) for different periods. ICAM-1 mRNA was determined by real-time polymerase chain reaction (PCR) and ICAM-1 surface expression by fluorescence-activated cell sorter (FACS) analysis and soluble ICAM-1 (slCAM-1) in the culture supematant by enzyme linked immunosorbent assay (ELISA). To clarify the signalling pathway of CT-1 induced ICAM-1 expression we used various inhibitors of possible signal transducing molecules, electromobility shift assay (EMSA) and Western blot analysis. Results CT-1 induced ICAM-1 mRNA (1.8i-0.8 fold increase compared to unstimulated cells after 6 hours) and protein (1.4~-0.2 fold increase compared to unstimulated cells after 48 hours) in HUVEC in a time- and concentration-dependent manner. EMSA experiments show that CT-1 causes nuclear factor (NF) KB activation. Because parthenolide could inhibit CT-1 induced ICAM-1 expression NFKB activation is required in this pathway. CT-1 did not activate extraceUular signal regulated kinases (ERK), c-Jun N-terminal kinase (JNK) and p38. Conclusion CT-1 is able to induce ICAM-1 in endothelial cells by NFKB activation. These results may explain in part elevated ICAM-1 concentrations in patients with CHF and endothelial dysfunction.

  18. Clinical evaluation of serum concentrations of intercellular adhesion molecule-1 in patients with colorectal cancer

    Institute of Scientific and Technical Information of China (English)

    Xu Kang; Fang Wang; Jin-Dong Xie; Jun Cao; Pei-Zhong Xian

    2005-01-01

    AIM: To investigate the correlation between the serum soluble intercellular adhesion molecule-1 (sICAM-1) and the clinicopathologic features and to evaluate the possible prognostic significance of sICAM-1 concentration in colorectal cancer.METHODS: A total of 56 patients (mean age 57.3 years)having transitional cell carcinoma of the colorectal and 25 control patients (mean age 42.6 years) were enrolled in the study. The serum samples of the patients were obtained on the day before surgery. Sera were obtained by centrifugation, and stored at -80 ℃ until assay. Serumconcentrations of ICAM-1 were measured with enzymelinked immunoassay. Differences between the two groups were analyzed by Student's t-test.RESULTS: No significant increase of serum sICAM-1 could be demonstrated in the Dukes A1 patients (352.63±61.82μg/L) compared to the control group (345.72±49.81 μg/L,P>0.05), Dukes A1 patients (352.63±61.82 μg/L)compared to Dukes A2,3 patients (491.17±86.36 μg/L,P<0.05). Furthermore, the patients with Dukes B had significantly higher serum concentrations of sICAM-1than those of the control group (496.82±93.04 μg/L vs 345.72±49.81 μg/L, P<0.01). Compared with Dukes A2,3,B colorectal cancer patients, patients with more advanced clinical stage (Dukes C and D) had higher levels of sICAM-1 (743.68±113.74 μg/L vs491.17±86.36 μg/L and 496.82±93.04 μg/L, P<0.001). The difference was statistically significant in sICAM-1 levels between patients with positive lymph node status and those without lymph node involvement (756.25±125.57 μg/L vs445.62±69.18 μg/L, P<0.001).Patients with poorly differentiated colorectal cancer had a higher level of sICAM-1 than those with differentiated and highly differentiated cancer (736.49±121.97 μg/Lvs 410.23±67.47 μg/L, P<0.001).CONCLUSION: In this study, serum ICAM-1 levels were found to be related to tumor presence, clinical stages,and grade. Increased ICAM-1 in patients with colorectal cancer which should

  19. Expression of ICAM-1 in colon epithelial cells

    DEFF Research Database (Denmark)

    Vainer, Ben; Sørensen, Susanne; Seidelin, Jakob;

    2003-01-01

    Studies have suggested that in ulcerative colitis (UC), intercellular adhesion molecule-1 (ICAM-1) is involved in migration of leukocytes toward the colonic epithelium. A suitable in vitro model of chronic colonic inflammation does not exist, and the role of the epithelium is based on monolayers ...... of cancer cells. Conflicting results exist on epithelial ICAM-1 expression, and the aim of this study was to compare the expression in various models of colonic epithelium.......Studies have suggested that in ulcerative colitis (UC), intercellular adhesion molecule-1 (ICAM-1) is involved in migration of leukocytes toward the colonic epithelium. A suitable in vitro model of chronic colonic inflammation does not exist, and the role of the epithelium is based on monolayers...

  20. Sesamin attenuates intercellular cell adhesion molecule-1 expression in vitro in TNF-alpha-treated human aortic endothelial cells and in vivo in apolipoprotein-E-deficient mice.

    Science.gov (United States)

    Wu, Wen-Huey; Wang, Shu-Huei; Kuan, I-I; Kao, Ya-Shi; Wu, Pei-Jhen; Liang, Chan-Jung; Chien, Hsiung-Fei; Kao, Chiu-Hua; Huang, Ching-Jang; Chen, Yuh-Lien

    2010-09-01

    Sesame lignans have antioxidative and anti-inflammatory properties. We focused on the effects of the lignans sesamin and sesamol on the expression of endothelial-leukocyte adhesion molecules in tumor necrosis factor-alpha (TNF-alpha)-treated human aortic endothelial cells (HAECs). When HAECs were pretreated with sesamin (10 or 100 microM), the TNF-alpha-induced expression of intercellular cell adhesion molecule-1 (ICAM-1) was significantly reduced (35 or 70% decrease, respectively) by Western blotting. Sesamol was less effective at inhibiting ICAM-1 expression (30% decrease at 100 microM). Sesamin and sesamol reduced the marked TNF-alpha-induced increase in human antigen R (HuR) translocation and the interaction between HuR and the 3'UTR of ICAM-1 mRNA. Both significantly reduced the binding of monocytes to TNF-alpha-stimulated HAECs. Sesamin significantly attenuated TNF-alpha-induced ICAM-1 expression and cell adhesion by downregulation of extracellular signal-regulated kinase 1/2 and p38. Furthermore, in vivo, sesamin attenuated intimal thickening and ICAM-1 expression seen in aortas of apolipoprotein-E-deficient mice. Taken together, these data suggest that sesamin inhibits TNF-alpha-induced extracellular signal-regulated kinase/p38 phosphorylation, nuclear translocation of NF-kappaB p65, cytoplasmic translocalization of HuR and thereby suppresses ICAM-1 expression, resulting in reduced adhesion of leukocytes. These results also suggest that sesamin may prevent the development of atherosclerosis and inflammatory responses.

  1. Expression of lung vascular and airway ICAM-1 after exposure to bacterial lipopolysaccharide

    DEFF Research Database (Denmark)

    Beck-Schimmer, B; Schimmer, R C; Warner, R L

    1997-01-01

    ]anti-ICAM-1 to airway surfaces increased 11-fold in a TNF-alpha-dependent manner. In situ hybridization and immunohistochemical analyses of lung tissue revealed ICAM-1 upregulation in the bronchiolar epithelium and in peribronchiolar smooth muscle. Soluble ICAM-1 could also be detected in bronchoalveolar......Airway instillation of bacterial lipopolysaccharide (LPS) into rat lungs induces neutrophil accumulation, which is known to be intercellular adhesion molecule-1 (ICAM-1)-dependent. In the present study, ICAM-1 messenger RNA (mRNA) of whole lung was found to increase by 20-fold in this inflammatory...... model. This increase was reduced by 81% after treatment of animals with anti-tumor necrosis factor-alpha (TNF-alpha) antibody and by 37% after treatment with anti-interleukin-1 (IL-1) antibody. The same interventions reduced whole-lung ICAM-1 protein by 85% and 25%, respectively. The studies were...

  2. Correlation of Serum Concentrations of Soluble Thrombomodulin, Soluble Vascular Cell Adhesion Molecule-1,Intracellular Adhesion Molecule -1 And E-Selectin In Patients WithSystemic Lupus Erythematosus

    Directory of Open Access Journals (Sweden)

    Malak., A. Mohsen*, Magda.A.Gamil*,Maha. I.Shehata

    2003-09-01

    Full Text Available To date no specific serological parameters are available to assess disease activity in systemic lupus erythematosus (SLE. The objective of this study was to correlate serum levels of thrombomodulin (TM, intracellular adhesion molecule-1 sICAM-1, vascular cell adhesion molecule-1 sVCAM-1, and E-selectin with standard laboratory tests and clinical indices of disease activity in 40 patients with SLE and 20 apparently healthy persons as controls. According to British Isles Lupus Assessment Group (BILAG disease activity index, the 40 patients were divided into two groups, the first consisted of 22 with active disease, and the second consisted of 18 patients with inactive SLE. Serum sTM, sICAM-1, sVCAM-I, and E-selectin were measured in their sera, using enzyme linked immuonosorbent assay (ELISA technique.C-reactiv protein (CRP, Erythrocyte sedimentation rates (ESR and serum creatinines were measured by standard laboratory tests. Total leukocytic count and hemoglobin concentration were detected by coulter counter. Levels of sTM and sVCAM were highly elevated in the group of patients with active SLE as compared to the inactive one (P0.05. In SLE, the BILAG disease activity index, ESR and serum creatinine correlated best with sTM, sVCAM-1 and E-selectin levels while there was a weak association between CRP levels and the adhesion molecules, and no correlation between CRP level and disease activity. In conclusion, sTM and sVCAM were the most important serological indices of disease activity in SLE and might be valuable serological parameters for monitoring therapy.

  3. Soluble intercellular adhesion molecule 1 and flow-mediated dilatation are related to the estimated risk of coronary heart disease independently from each other

    NARCIS (Netherlands)

    Witte, D.R.; Broekmans, W.M.R.; Kardinaal, A.F.M.; Klöpping-Ketelaars, I.A.A.; Poppel, G. van; Bots, M.L.; Kluft, C.; Princen, J.M.G.

    2003-01-01

    Background: Flow mediated dilatation (FMD) of the brachial artery and soluble intercellular adhesion molecule 1 (sICAM-1) are measures of distinct functions of the endothelium, reflecting nitric oxide (NO)-mediated and pro-inflammatory status, respectively. The comparative value of the two measures

  4. Control of islet intercellular adhesion molecule-1 expression by interferon-alpha and hypoxia.

    Science.gov (United States)

    Chakrabarti, D; Huang, X; Beck, J; Henrich, J; McFarland, N; James, R F; Stewart, T A

    1996-10-01

    The ability of interferon-alpha (IFN-alpha) to induce the adhesion molecules that characterize the islets of patients with type I diabetes has been investigated. We have found that all tested recombinant IFN-as will induce major histocompatibility complex (MHC) class I on arterial endothelial cells. Some but not all IFN-as will induce intercellular adhesion molecule-1 (ICAM-1). However, there is only a transient and modest increase in VCAM on arterial endothelial cells. IFN-alpha has very little effect on endothelial MHC class II expression but will induce these proteins on monocytes. Thus, there is a close concordance between the biological actions of IFN-alpha and the appearance of those adhesion molecules induced in the islets of patients with type I diabetes. IFN-alpha is also produced in normal human islets during short-term cultures, probably as a result of the ischemia present at the center of the islet. This induction of IFN-alpha by hypoxia may explain the previously reported spontaneous induction of ICAM-1 in human islets and may also be a contributing factor to the failure of islet grafts.

  5. Nitric oxide pretreatment enhances atheroma component highlighting in vivo with intercellular adhesion molecule-1-targeted echogenic liposomes.

    Science.gov (United States)

    Kee, Patrick H; Kim, Hyunggun; Huang, Shaoling; Laing, Susan T; Moody, Melanie R; Vela, Deborah; Klegerman, Melvin E; McPherson, David D

    2014-06-01

    We present an ultrasound technique for the detection of inflammatory changes in developing atheromas. We used contrast-enhanced ultrasound imaging with (i) microbubbles targeted to intercellular adhesion molecule-1 (ICAM-1), a molecule of adhesion involved in inflammatory processes in lesions of atheromas in New Zealand White rabbits, and (ii) pretreatment with nitric oxide-loaded microbubbles and ultrasound activation at the site of the endothelium to enhance the permeability of the arterial wall and the penetration of ICAM-1-targeted microbubbles. This procedure increases acoustic enhancement 1.2-fold. Pretreatment with nitric oxide-loaded echogenic liposomes and ultrasound activation can potentially facilitate the subsequent penetration of targeted echogenic liposomes into the arterial wall, thus allowing improved detection of inflammatory changes in developing atheromas.

  6. Combined measurement of soluble and cellular ICAM-1 among children with Plasmodium falciparum malaria in Uganda

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    Cserti-Gazdewich Christine M

    2010-08-01

    Full Text Available Abstract Background Intercellular adhesion molecule-1 (ICAM-1 is a cytoadhesion molecule implicated in the pathogenesis of Plasmodium falciparum malaria. Elevated levels of soluble ICAM-1 (sICAM-1 have previously been reported with increased malaria disease severity. However, studies have not yet examined both sICAM-1 concentrations and monocyte ICAM-1 expression in the same cohort of patients. To better understand the relationship of soluble and cellular ICAM-1 measurements in malaria, both monocyte ICAM-1 expression and sICAM-1 concentration were measured in children with P. falciparum infection exhibiting a spectrum of clinical severity. Methods Samples were analysed from 160 children, aged 0.5 to 10.8 years, with documented P. falciparum malaria in Kampala, Uganda. The patients belonged to one of three pre-study defined groups: uncomplicated malaria (UM, severe non-fatal malaria (SM-s, and fatal malaria (SM-f. Subset analysis was done on those with cerebral malaria (CM or severe malaria anaemia (SMA. Monocyte ICAM-1 was measured by flow cytometry. sICAM-1 was measured by enzyme immunoassay. Results Both sICAM-1 and monocyte cell-surface ICAM-1 followed a log-normal distribution. Median sICAM-1 concentrations increased with greater severity-of-illness: 279 ng/mL (UM, 462 ng/mL (SM-s, and 586 ng/mL (SM-f, p Conclusion In this cohort of children with P. falciparum malaria, sICAM-1 levels were associated with severity-of-illness. Patients with UM had higher monocyte ICAM-1 expression consistent with a role for monocyte ICAM-1 in immune clearance during non-severe malaria. Among the subsets of patients with either SMA or CM, monocyte ICAM-1 levels were higher in CM, consistent with the role of ICAM-1 as a marker of cytoadhesion. Categories of disease in pediatric malaria may exhibit specific combinations of soluble and cellular ICAM-1 expression.

  7. Effects of anisodamine on the expressions of vascular endothelial growth factor and intercellular adhesion molecule 1 in experimental infusion phlebitis

    Institute of Scientific and Technical Information of China (English)

    ZHANG Zhen-xiang; WANG Peng; ZHANG Qiu-shi; PAN Xue; ZHAO Qing-xia; WANG Xiao-kai

    2012-01-01

    Background Infusion phlebitis is the most common side effect of clinical intravenous drug therapy and several clinical studies have demonstrated that anisodamine can effectively prevent the occurrence of infusion phlebitis.This study was designed to investigate effects of anisodamine on the expressions of vascular endothelial growth factor (VEGF) and intercellular adhesion molecule 1 (ICAM-1) in a rabbit model of infusion phlebitis and to analyze the mechanisms of anisodamine effect on the prevention and treatment of experimental infusion phlebitis.Methods Twenty-four specific pathogen-free male Japanese white rabbits were randomly assigned to the control group,the model group,the magnesium sulfate group and the anisodamine group.The rabbit model of infusion phlebitis,induced by intravenous administration,was established and expressions of VEGF and ICAM-1 were determined and contrasted with the control group treated with normal saline.We evaluated expression by histopathology,immunohistochemistry,reverse transcription-polymerase chain reaction,and Western blotting assay.Results Pathohistological changes of the model group were observed,such as loss of venous endothelial cells,inflammatory cell infiltration,edema and thrombus.The magnesium sulfate group and the anisodamine group showed significant protective effects on vascular congestion,inflammatory cell infiltration,proliferation,swelling of endothelium and perivascular hemorrhage.The model group showed the highest expressions of VEGF and ICAM-1 of the four groups (P<0.01).On the contrary,anisodamine alleviated the inflammatory damage by significantly reducing the expressions of VEGF and ICAM-1 compared with the model group (P <0.01).There was no significant difference in the expressions of VEGF and ICAM-1 between the magnesium sulfate group and the anisodamine group (P >0.05).Conclusion Anisodamine alleviates inflammatory damage by significantly reducing the expressions of VEGF and ICAM-1,and shows

  8. Overexpression of sICAM-1 in the Alveolar Epithelial Space Results in an Exaggerated Inflammatory Response and Early Death in Gram Negative Pneumonia

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    Curtis Jeffery L

    2011-01-01

    Full Text Available Abstract Background A sizeable body of data demonstrates that membrane ICAM-1 (mICAM-1 plays a significant role in host defense in a site-specific fashion. On the pulmonary vascular endothelium, mICAM-1 is necessary for normal leukocyte recruitment during acute inflammation. On alveolar epithelial cells (AECs, we have shown previously that the presence of normal mICAM-1 is essential for optimal alveolar macrophage (AM function. We have also shown that ICAM-1 is present in the alveolar space as a soluble protein that is likely produced through cleavage of mICAM-1. Soluble intercellular adhesion molecule-1 (sICAM-1 is abundantly present in the alveolar lining fluid of the normal lung and could be generated by proteolytic cleavage of mICAM-1, which is highly expressed on type I AECs. Although a growing body of data suggesting that intravascular sICAM-1 has functional effects, little is known about sICAM-1 in the alveolus. We hypothesized that sICAM-1 in the alveolar space modulates the innate immune response and alters the response to pulmonary infection. Methods Using the surfactant protein C (SPC promoter, we developed a transgenic mouse (SPC-sICAM-1 that constitutively overexpresses sICAM-1 in the distal lung, and compared the responses of wild-type and SPC-sICAM-1 mice following intranasal inoculation with K. pneumoniae. Results SPC-sICAM-1 mice demonstrated increased mortality and increased systemic dissemination of organisms compared with wild-type mice. We also found that inflammatory responses were significantly increased in SPC-sICAM-1 mice compared with wild-type mice but there were no difference in lung CFU between groups. Conclusions We conclude that alveolar sICAM-1 modulates pulmonary inflammation. Manipulating ICAM-1 interactions therapeutically may modulate the host response to Gram negative pulmonary infections.

  9. Priming by chemokines restricts lateral mobility of the adhesion receptor LFA-1 and restores adhesion to ICAM-1 nano-aggregates on human mature dendritic cells.

    Directory of Open Access Journals (Sweden)

    Kyra J E Borgman

    Full Text Available LFA-1 is a leukocyte specific β2 integrin that plays a major role in regulating adhesion and migration of different immune cells. Recent data suggest that LFA-1 on mature dendritic cells (mDCs may function as a chemokine-inducible anchor during homing of DCs through the afferent lymphatics into the lymph nodes, by transiently switching its molecular conformational state. However, the role of LFA-1 mobility in this process is not yet known, despite that the importance of lateral organization and dynamics for LFA-1-mediated adhesion regulation is broadly recognized. Using single particle tracking approaches we here show that LFA-1 exhibits higher mobility on resting mDCs compared to monocytes. Lymphoid chemokine CCL21 stimulation of the LFA-1 high affinity state on mDCs, led to a significant reduction of mobility and an increase on the fraction of stationary receptors, consistent with re-activation of the receptor. Addition of soluble monomeric ICAM-1 in the presence of CCL21 did not alter the diffusion profile of LFA-1 while soluble ICAM-1 nano-aggregates in the presence of CCL21 further reduced LFA-1 mobility and readily bound to the receptor. Overall, our results emphasize the importance of LFA-1 lateral mobility across the membrane on the regulation of integrin activation and its function as adhesion receptor. Importantly, our data show that chemokines alone are not sufficient to trigger the high affinity state of the integrin based on the strict definition that affinity refers to the adhesion capacity of a single receptor to its ligand in solution. Instead our data indicate that nanoclustering of the receptor, induced by multi-ligand binding, is required to maintain stable cell adhesion once LFA-1 high affinity state is transiently triggered by inside-out signals.

  10. Priming by chemokines restricts lateral mobility of the adhesion receptor LFA-1 and restores adhesion to ICAM-1 nano-aggregates on human mature dendritic cells.

    Science.gov (United States)

    Borgman, Kyra J E; van Zanten, Thomas S; Manzo, Carlo; Cabezón, Raquel; Cambi, Alessandra; Benítez-Ribas, Daniel; Garcia-Parajo, Maria F

    2014-01-01

    LFA-1 is a leukocyte specific β2 integrin that plays a major role in regulating adhesion and migration of different immune cells. Recent data suggest that LFA-1 on mature dendritic cells (mDCs) may function as a chemokine-inducible anchor during homing of DCs through the afferent lymphatics into the lymph nodes, by transiently switching its molecular conformational state. However, the role of LFA-1 mobility in this process is not yet known, despite that the importance of lateral organization and dynamics for LFA-1-mediated adhesion regulation is broadly recognized. Using single particle tracking approaches we here show that LFA-1 exhibits higher mobility on resting mDCs compared to monocytes. Lymphoid chemokine CCL21 stimulation of the LFA-1 high affinity state on mDCs, led to a significant reduction of mobility and an increase on the fraction of stationary receptors, consistent with re-activation of the receptor. Addition of soluble monomeric ICAM-1 in the presence of CCL21 did not alter the diffusion profile of LFA-1 while soluble ICAM-1 nano-aggregates in the presence of CCL21 further reduced LFA-1 mobility and readily bound to the receptor. Overall, our results emphasize the importance of LFA-1 lateral mobility across the membrane on the regulation of integrin activation and its function as adhesion receptor. Importantly, our data show that chemokines alone are not sufficient to trigger the high affinity state of the integrin based on the strict definition that affinity refers to the adhesion capacity of a single receptor to its ligand in solution. Instead our data indicate that nanoclustering of the receptor, induced by multi-ligand binding, is required to maintain stable cell adhesion once LFA-1 high affinity state is transiently triggered by inside-out signals.

  11. EXPRESSION OF ICAM-1 AND LFA-1 MOLECULES IN RELATION TO RENAL ALLOGRAFT REJECTION IN RATS

    Institute of Scientific and Technical Information of China (English)

    1999-01-01

    Objective.The purpose of this study was to assess the renal graft expression of ICAM-1(intercellular adhesion molecule-1) nd LFA-1(lymphocyte function-associated antigen-1)molecule with relation to graft rejection.Methods.Rat kiney transplantation was performed according to the procedure of Kamada with some modification.Experimental rats were divided into 5 groups.The survival time of recipient rats and function of grafts after renal transplantation were observed.The sections of renal graft were stained for monoclonal antibody ICAM-1 and LFA-1, and then quantification of ICAM-1 and LFA-1 expression was accomplished by computer image analysis.Results.ICAM-1 and LFA-1 increased significantly in the renal allograft rejection group as compared with the non-rejection groups(P<0.05).Conluson.Both biopsy of renal graft and monitoring of ICAM-1 and LFA-1 are useful tools in diagnosing and treating acute rejection.

  12. The structure of the two amino-terminal domains of human intercellular adhesion molecule-1 suggests how it functions as a rhinovirus receptor.

    Science.gov (United States)

    Bella, J; Kolatkar, P R; Marlor, C W; Greve, J M; Rossmann, M G

    1999-08-01

    The normal function of human intercellular adhesion molecule-1 (ICAM-1) is to provide adhesion between endothelial cells and leukocytes after injury or stress. ICAM-1 binds to leukocyte function-associated antigen (LFA-1) or macrophage-1 antigen (Mac-1). However, ICAM-1 is also utilized as a receptor by the major group of human rhinoviruses and is a catalyst for the subsequent viral uncoating during cell entry. The three-dimensional atomic structure of the two amino-terminal domains (D1 and D2) of ICAM-1 has been determined to 2.2 A resolution and fitted into a cryo-electron microscopy reconstruction of a rhinovirus-ICAM-1 complex. Rhinovirus attachment is confined to the BC, CD, DE and FG loops of the amino-terminal immunoglobulin-like domain (D1) at the end distal to the cellular membrane. The loops are considerably different in structure to those of human ICAM-2 or murine ICAM-1 which do not bind rhinoviruses. There are extensive charge interactions between ICAM-1 and human rhinoviruses, which are mostly conserved in both major and minor receptor groups of rhinoviruses. The interaction of ICAMs with LFA-1 is known to be mediated by a divalent cation bound to the I-(insertion) domain on the alpha chain of LFA-1 and the carboxy group of a conserved glutamic acid residue on ICAMs. Domain D1 has been docked with the known structure of the I-domain. The resultant model is consistent with mutational data and provides a structural framework for the adhesion between these molecules.

  13. Targeting of ICAM-1 on vascular endothelium under static and shear stress conditions using a liposomal Gd-based MRI contrast agent

    NARCIS (Netherlands)

    Paulis, L.E.M.; Jacobs, I.; Akker, N. van de; Geelen, T.; Molin, D.; Starmans, L.W.; Nicolay, K.; Strijkers, G.J.

    2012-01-01

    ABSTRACT: BACKGROUND: The upregulation of intercellular adhesion molecule-1 (ICAM-1) on the endothelium of bloodvessels in response to pro-inflammatory stimuli is of major importance for the regulation oflocal inflammation in cardiovascular diseases such as atherosclerosis, myocardial infarctionand

  14. The Expression of Integrin β3 and Intercellular Adhesion Molecule(ICAM-1)in Decidua and Chorionic Villi during Mifepristone Induced Abortion

    Institute of Scientific and Technical Information of China (English)

    李瑞珍; 王振海; 吴瑞芳

    1999-01-01

    The effects of mifepristone with misoprostol on the expression of the integrin β3 and intercellular adhesion motecule-1 (ICAM-1)in decidua and chorionic villi tissues in early pregnancy in 10 cases were investigated by immuno-ftow cytometry(the eyper-iment group).At the same time,the other 10 cases induced by mechanical vacuum as-piration were collected as the control.The results showed that,the positive rate of inte-grin β3 and ICAM-1 in decidua of the experiment group were 19.1±5. 01% and 20.61±6. 51%;while those in chorionic villi were 21.32±4. 38% and 20. 29±6. 49%,which were significantly lower than those in the control group.These results suggested that integrin β3 and ICAM-1 may take part in the maintenance of early pregnancy.The mechanism of mifepristone induced abortion may be mediated by the down-regulation of the integrin β3 and ICAM-1 expression in decidua and chorionic villi.

  15. Soluble Inter-Cellular Adhesion Molecule-1 in Urban Asian North Indians: Relationships with Anthropometric and Metabolic Covariates

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    Astha Sethi

    2002-01-01

    Full Text Available Background: High prevalence of diabetes, obesity, and dyslipidemias in people belonging to poor socio-economic strata in urban slums of northern India has been recorded recently. To assess whether this population has high levels of soluble intercellular adhesion molecule-1 (sICAM-1, a cytokine involved in the pathogenesis of atherosclerosis, we investigated subjects belonging to poor socio-economic strata in urban slums and compared them to healthy control subjects from non-slum urban areas of New Delhi.

  16. Involvement of MAPKs in ICAM-1 Expression in Glomerular Endothelial Cells in Diabetic Nephropathy

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    Watanabe,Naomi

    2011-08-01

    Full Text Available Inflammatory processes are involved in the pathogenesis of diabetic nephropathy. The aim of this study was to clarify the role of mitogen-activated protein kinase (MAPK pathways for induction of intercellular adhesion molecule-1 (ICAM-1 expression in glomerular endothelial cells under diabetic conditions. We examined the expression of ICAM-1 in the kidneys of experimental diabetic rats. Human glomerular endothelial cells (GE cells were exposed to normal glucose concentration, high glucose concentration (HG, or high mannitol concentration (HM, and then the expression of the ICAM-1 protein and the phosphorylation of the 3 subfamilies of mitogen-activated protein kinase (MAPK were determined using Western blot analysis. Next, to evaluate the involvement of MAPKs in HG- or HM-induced ICAM-1 expression, we preincubated GE cells with the inhibitors for ERK, p38 or JNK 1h prior to the application of glucose or mannitol. Expression of ICAM-1 was increased in the glomeruli of diabetic rats. Both HG and HM induced ICAM-1 expression and phosphorylation of ERK1/2, p38 and JNK in GE cells. Expression of ICAM-1 was significantly attenuated by inhibitors of ERK, p38 and JNK. We conclude that activation of ERK1/2, p38 and JNK cascades may be involved in ICAM-1 expression in glomerular endothelial cells under diabetic conditions.

  17. Serum inter-cellular adhesion molecule 1 is an early marker of diagnosis and prediction of severe acute pancreatitis

    Institute of Scientific and Technical Information of China (English)

    Hai-Hang Zhu; Lin-Lin Jiang

    2012-01-01

    AIM:To determine if serum inter-cellular adhesion molecule 1 (ICAM-1) is an early marker of the diagnosis and prediction of severe acute pancreatitis (SAP)within 24 h of onset of pain,and to compare the sensitivity,specificity and prognostic value of this test with those of acute physiology and chronic health evaluation (APACHE) Ⅱ score and interleukin-6 (IL-6).METHODS:Patients with acute pancreatitis (AP) were divided into two groups according to the Ranson's criteria:mild acute pancreatitis (MAP) group and SAP group.Serum ICAM-1,APACHE Ⅱ and IL-6 levels were detected in all the patients.The sensitivity,specificity and prognostic value of the ICAM-1,APACHE Ⅱ score and IL-6 were evaluated.RESULTS:The ICAM-1 level in 36 patients with SAP within 24 h of onset of pain was increased and was significantly higher than that in the 50 patients with MAP and the 15 healthy volunteers (P < 0.01).The ICAM-1 level (25 ng/mL) was chosen as the optimum cutoff to distinguish SAP from MAP,and the sensitivity,specificity,positive predictive value,negative predictive value (NPV),positive likelihood ratio and negative likelihood ratio were 61.11%,71.42%,0.6111,0.7142,2.1382 and 0.5445,respectively.The area under the curve demonstrated that the prognostic accuracy of ICAM-1 (0.712) was similar to the APACHE-Ⅱ scoring system (0.770) and superior to IL-6 (0.508) in distinguishing SAP from MAP.CONCLUSION:ICAM-1 test is a simple,rapid and reliable method in clinical practice.It is an early marker of diagnosis and prediction of SAP within the first 24 h after onset of pain or on admission.As it has a relatively low NPV and does not allow it to be a stand-alone test for the diagnosis of AP,other conventional diagnostic tests are required.

  18. Tumor necrosis factor beta and ultraviolet radiation are potent regulators of human keratinocyte ICAM-1 expression

    Energy Technology Data Exchange (ETDEWEB)

    Krutmann, J.; Koeck, A.S.; Schauer, E.; Parlow, F.; Moeller, A.K.; Kapp, A.; Foerster, E.S.; Schoepf, E.L.; Luger, T.A. (Univ. of Freiburg (Germany, F.R.))

    1990-08-01

    Intercellular adhesion molecule-1 (ICAM-1) functions as a ligand of leukocyte function-associated antigen-1 (LFA-1), as well as a receptor for human picorna virus, and its regulation thus affects various immunologic and inflammatory reactions. The weak, constitutive ICAM-1 expression on human keratinocytes (KC) can be up-regulated by cytokines such as interferon-gamma (IFN gamma) and tumor necrosis factor alpha (TNF alpha). In order to further examine the regulation of KC ICAM-1 expression, normal human KC or epidermoid carcinoma cells (KB) were incubated with different cytokines and/or exposed to ultraviolet (UV) radiation. Subsequently, ICAM-1 expression was monitored cytofluorometrically using a monoclonal anti-ICAM-1 antibody. Stimulation of cells with recombinant human (rh) interleukin (IL) 1 alpha, rhIL-4, rhIL-5, rhIL-6, rh granulocyte/macrophage colony-stimulating factor (GM-CSF), rh interferon alpha (rhIFN alpha), and rh transforming growth factor beta (TGF beta) did not increase ICAM-1 surface expression. In contrast, rhTNF beta significantly up-regulated ICAM-1 expression in a time- and dose-dependent manner. Moreover, the combination of rhTNF beta with rhIFN gamma increased the percentage of ICAM-1-positive KC synergistically. This stimulatory effect of rhTNF beta was further confirmed by the demonstration that rhTNF beta was capable of markedly enhancing ICAM-1 mRNA expression in KC. Finally, exposure of KC in vitro to sublethal doses of UV radiation (0-100 J/m2) prior to cytokine (rhIFN tau, rhTNF alpha, rhTNF beta) stimulation inhibited ICAM-1 up-regulation in a dose-dependent fashion. These studies identify TNF beta and UV light as potent regulators of KC ICAM-1 expression, which may influence both attachment and detachment of leukocytes and possibly viruses to KC.

  19. Changes in the vascular cell adhesion molecule-1, intercellular adhesion molecule-1 and c-reactive protein following administration of aqueous extract of piper sarmentosum on experimental rabbits fed with cholesterol diet

    Directory of Open Access Journals (Sweden)

    Al-Mekhlafi Hesham M

    2011-01-01

    Full Text Available Abstract Background Inflammation process plays an important role in the development of atherosclerosis. Hypercholesterolemia is one of the major risk factors for atherosclerosis. The present study aimed to evaluate the effect of aqueous extract of Piper sarmentosum (P.s on inflammatory markers like vascular cell adhesion molecule-1 (VCAM-1, intercellular adhesion molecule-1 (ICAM-1, and C-reactive protein (CRP. Methods Forty two male New Zealand white rabbits were divided equally into seven groups; (i C- control group fed normal rabbit chow (ii CH- cholesterol diet (1%cholesterol (iii X1- 1% cholesterol with water extract of P.s (62.5 mg/kg (iv X2- 1% cholesterol with water extract of P.s (125 mg/kg (v X3- 1% cholesterol with water extract of P.s (250 mg/kg (vi X4- 1% cholesterol with water extract of P.s (500 mg/kg and (vii SMV group fed with 1% cholesterol supplemented with simvistatin drug (1.2 mg/kg. All animals were treated for 10 weeks. Blood serum was taken for observing the inflammatory markers at the beginning and end of the experiment. Results Rabbits fed with 1% cholesterol diet (CH showed significant increase in the level of VCAM-1, ICAM-1 and CRP compared to the C group. The levels of VCAM-1, ICAM-1 and CRP in the 1% cholesterol group and supplemented with P.s (500 mg/kg were significantly reduced compared to the cholesterol group. Similar results were also reported with simvistatin group. Conclusion These results suggest that the supplementation of Piper sarmentosum extract could inhibit inflammatory markers which in turn could prevent atherosclerosis.

  20. ICAM-1 is necessary for epithelial recruitment of gammadelta T cells and efficient corneal wound healing.

    Science.gov (United States)

    Wound healing and inflammation are both significantly reduced in mice that lack gammadelta T cells. Here, the role of epithelial intercellular adhesion molecule-1 (ICAM-1) in gammadelta T cell migration in corneal wound healing was assessed. Wild-type mice had an approximate fivefold increase in epi...

  1. Ursolic acid, a natural pentacyclic triterpenoid, inhibits intracellular trafficking of proteins and induces accumulation of intercellular adhesion molecule-1 linked to high-mannose-type glycans in the endoplasmic reticulum

    Directory of Open Access Journals (Sweden)

    Satoshi Mitsuda

    2014-01-01

    Full Text Available Ursolic acid (3β-hydroxy-urs-12-en-28-oic acid is a natural pentacyclic triterpenoid that is present in many plants, including medicinal herbs, and foods. Ursolic acid was initially identified as an inhibitor of the expression of intercellular adhesion molecule-1 (ICAM-1 in response to interleukin-1α (IL-1α. We report here a novel biological activity: ursolic acid inhibits intracellular trafficking of proteins. Ursolic acid markedly inhibited the IL-1α-induced cell-surface ICAM-1 expression in human cancer cell lines and human umbilical vein endothelial cells. By contrast, ursolic acid exerted weak inhibitory effects on the IL-1α-induced ICAM-1 expression at the protein level. Surprisingly, we found that ursolic acid decreased the apparent molecular weight of ICAM-1 and altered the structures of N-linked oligosaccharides bound to ICAM-1. Ursolic acid induced the accumulation of ICAM-1 in the endoplasmic reticulum, which was linked mainly to high-mannose-type glycans. Moreover, in ursolic-acid-treated cells, the Golgi apparatus was fragmented into pieces and distributed over the cells. Thus, our results reveal that ursolic acid inhibits intracellular trafficking of proteins and induces the accumulation of ICAM-1 linked to high-mannose-type glycans in the endoplasmic reticulum.

  2. Polymorphism K469E of intercellular adhesion molecule-1 gene and restenosis after coronary stenting in Chinese patients

    Institute of Scientific and Technical Information of China (English)

    刘兆平; 霍勇; 李建平; 张岩; 薛琳; 赵春玉; 洪秀梅; 黄爱群; 高炜

    2004-01-01

    Background Inflammation is a major cause of restenosis after coronary stenting. Intercellular adhesion molecule-1 ( ICAM-1 ) is an important adhesion molecule that plays a key role in the tight adhesion between leukocytes and vascular endothelium. The object of this study was to investigate the association between the K469E polymorphism of the ICAM-1 gene and restenosis after coronary stenting in North Chinese population.Methods The ICAM-1 K469E polymorphism was genotyped using polymerase chain reaction- restriction fragment length polymorphism method in 124 patients who had undergone coronary stenting and coronary angiography at least 3 months earlier. Information on clinical risk factors and procedure- related data were also collected. Results Of 124 enrolled patients in total, there were 72 cases of in-stent restenosis. The restenosis rate in this population was 58. 1%. The frequencies of the three possible genotypes of the ICAM-1 K469E polymorphism were: KK genotype 50.8%, EE genotype 41.9%, and EK genotype 41.9%.Among restenosis patients, the frequency of the KK genotype was 58. 3% and the frequency of E allele carriers was 41.7%. Among non-restenosis patients, the frequency of the KK genotype was 40.4%, and the frequency of E allele carriers was 59. 6%. The distribution of these two genotype groups between restenosis and non-restenosis patients was significantly different (P=0.049). Using multivariate logistic regression, the difference between the two groups was more apparent. The odds ratio of KK homozygotes vs E allele carriers was 2.6, with 95% confidence interval 1.2 -5.8 (P =0. 018). After grading of risk factors, we found that the KK genotype was a stronger predictor of in- stent restenosis in obesity or hyperlipemia patients, with an odds ratio of 9.3 and 3.7, respectively (P<0.05).Conclusion In our study population, KK homozygotes of the ICAM-1 codon 469 mutation had a higher risk of restenosis after coronary stenting, especially in the case of obese

  3. Activated endothelial interleukin-1beta, -6, and -8 concentrations and intercellular adhesion molecule-1 expression are attenuated by lidocaine.

    LENUS (Irish Health Repository)

    Lan, Wei

    2012-02-03

    Endothelial cells play a key role in ischemia reperfusion injury. We investigated the effects of lidocaine on activated human umbilical vein endothelial cell (HUVEC) interleukin (IL)-1beta, IL-6, and IL-8 concentrations and intercellular adhesion molecule-1 (ICAM-1) expression. HUVECs were pretreated with different concentrations of lidocaine (0 to 0.5 mg\\/mL) for 60 min, thereafter tumor necrosis factor-alpha was added at a concentration of 2.5 ng\\/mL and the cells incubated for 4 h. Supernatants were harvested, and cytokine concentrations were analyzed by enzyme-linked immunosorbent assay. Endothelial ICAM-1 expression was analyzed by using flow cytometry. Differences were assessed using analysis of variance and post hoc unpaired Student\\'s t-test where appropriate. Lidocaine (0.5 mg\\/mL) decreased IL-1beta (1.89 +\\/- 0.11 versus 4.16 +\\/- 1.27 pg\\/mL; P = 0.009), IL-6 (65.5 +\\/- 5.14 versus 162 +\\/- 11.5 pg\\/mL; P < 0.001), and IL-8 (3869 +\\/- 785 versus 14,961 +\\/- 406 pg\\/mL; P < 0.001) concentrations compared with the control. IL-1beta, IL-6, and IL-8 concentrations in HUVECs treated with clinically relevant plasma concentrations of lidocaine (0.005 mg\\/mL) were similar to control. ICAM-1 expression on lidocaine-treated (0.05 mg\\/mL) HUVECs was less than on controls (198 +\\/- 52.7 versus 298 +\\/- 50.3; Mean Channel Fluorescence; P < 0.001). Activated endothelial IL-1beta, IL-6, and IL-8 concentrations and ICAM-1 expression are attenuated only by lidocaine at concentrations larger than clinically relevant concentrations.

  4. The Crystal Structure of Coxsackievirus A21 and Its Interaction with ICAM-1

    Energy Technology Data Exchange (ETDEWEB)

    Xiao, Chuan; Bator-Kelly, Carol M.; Rieder, Elizabeth; Chipman, Paul R.; Craig, Alister; Kuhn, Richard J.; Wimmer, Eckard; Rossmann, Michael G. (Liverpool); (SBU); (Purdue)

    2010-11-30

    CVA21 and polioviruses both belong to the Enterovirus genus in the family of Picornaviridae, whereas rhinoviruses form a distinct picornavirus genus. Nevertheless, CVA21 and the major group of human rhinoviruses recognize intercellular adhesion molecule-1 (ICAM-1) as their cellular receptor, whereas polioviruses use poliovirus receptor. The crystal structure of CVA21 has been determined to 3.2 {angstrom} resolution. Its structure has greater similarity to poliovirus structures than to other known picornavirus structures. Cryo-electron microscopy (cryo-EM) was used to determine an 8.0 {angstrom} resolution structure of CVA21 complexed with an ICAM-1 variant, ICAM-1{sup Kilifi}. The cryo-EM map was fitted with the crystal structures of ICAM-1 and CVA21. Significant differences in the structure of CVA21 with respect to the poliovirus structures account for the inability of ICAM-1 to bind polioviruses. The interface between CVA21 and ICAM-1 has shape and electrostatic complementarity with many residues being conserved among those CVAs that bind ICAM-1.

  5. There is no association between K469E ICAM-1 gene polymorphism and biliary atresia

    Institute of Scientific and Technical Information of China (English)

    Paisarn Vejchapipat; Naruemol Jirapanakom; Nutchanart Thawornsuk; Apiradee Theamboonlers; Voranush Chongsrisawat; Soottiporn Chittmittrapap; Yong Poovorawan

    2005-01-01

    AIM: To determine whether there was an association between inter-cellular adhesion molecule-1 (ICAM-1) gene polymorphism and biliary atresia (BA), and to investigate the relationship between serum soluble ICAM-1 (sICAM-1)and clinical outcome in BA patients after surgical treatment.METHODS: Eighty-three BA patients and 115 normal controls were genotyped. K469EICAM-1 polymorphism was analyzed using PCR assay. Serum sICAM-1 was determined using ELISA method from 72 BA patients. In order to evaluate the association between these variables and their clinical outcome, the patients were categorized into two groups:patients without jaundice and those with persistent jaundice.RESULTS: There were no significant differences between BA patients and controls in terms of gender, K469E ICAM-1genotypes, and alleles. The proportion of patients having serum sICAM-1 ≥3 500 ng/mL in persistent jaundice group was significantly higher than that in the other group. In addition, there was no association between K469EICAM-1polymorphism and the status of jaundice in BA patients after Kasai operation.CONCLUSION: ICAM-1 possibly plays an important and active role in the disease progression. However, the process is not associated with genetic variation of K469EICAM-1 polymorphism.

  6. ICAM1 Is a Potential Cancer Stem Cell Marker of Esophageal Squamous Cell Carcinoma.

    Directory of Open Access Journals (Sweden)

    Sheng-Ta Tsai

    Full Text Available Esophageal squamous cell carcinoma (ESCC accounts for about 90% of esophageal cancer diagnosed in Asian countries, with its incidence on the rise. Cancer stem cell (CSC; also known as tumor-initiating cells, TIC is inherently resistant to cytotoxic chemotherapy and radiation and associates with poor prognosis and therapy failure. Targeting therapy against cancer stem cell has emerged as a potential therapeutic approach to develop effective regimens. However, the suitable CSC marker of ESCC for identification and targeting is still limited. In this study, we screened the novel CSC membrane protein markers using two distinct stemness characteristics of cancer cell lines by a comparative approach. After the validation of RT-PCR, qPCR and western blot analyses, intercellular adhesion molecule 1 (ICAM1 was identified as a potential CSC marker of ESCC. ICAM1 promotes cancer cell migration, invasion as well as increasing mesenchymal marker expression and attenuating epithelial marker expression. In addition, ICAM1 contributes to CSC properties, including sphere formation, drug resistance, and tumorigenesis in mouse xenotransplantation model. Based on the analysis of ICAM1-regulated proteins, we speculated that ICAM1 regulates CSC properties partly through an ICAM1-PTTG1IP-p53-DNMT1 pathway. Moreover, we observed that ICAM1 and CD44 could have a compensation effect on maintaining the stemness characteristics of ESCC, suggesting that the combination of multi-targeting therapies should be under serious consideration to acquire a more potent therapeutic effect on CSC of ESCC.

  7. Role of ICAM-1 polymorphisms (G241R, K469E) in mediating its single-molecule binding ability: Atomic force microscopy measurements on living cells

    Energy Technology Data Exchange (ETDEWEB)

    Bai, Rui [Chinese (301) General Hospital, 28 Fuxing Road, Haidian District, Beijing 100853 (China); Yi, Shaoqiong [Beijing Institute of Biotechnology, 20 Dongdajie, Fengtai, Beijing 100071 (China); Zhang, Xuejie [Beijing National Laboratory for Molecular Sciences, Key Laboratory of Molecular Nanostructure and Nanotechnology, Institute of Chemistry Chinese Academy of Sciences, 2 Zhongguancun North 1st Street, Beijing 100190 (China); Liu, Huiliang, E-mail: lhl518@vip.sina.com [Department of Cardiology, The General Hospital of Chinese People’s Armed Police Forces, Beijing 100039 (China); Fang, Xiaohong, E-mail: xfang@iccas.ac.cn [Beijing National Laboratory for Molecular Sciences, Key Laboratory of Molecular Nanostructure and Nanotechnology, Institute of Chemistry Chinese Academy of Sciences, 2 Zhongguancun North 1st Street, Beijing 100190 (China)

    2014-06-13

    Highlights: • We evaluated both single molecule binding ability and expression level of 4 ICAM-1 mutations. • AFM was used to measure single-molecule binding ability on living cells. • The SNP of ICAM-1 may induce changes in expressions rather than single-molecule binding ability. - Abstract: Atherosclerosis (As) is characterized by chronic inflammation and is a major cause of human mortality. ICAM-1-mediated adhesion of leukocytes in vessel walls plays an important role in the pathogenesis of atherosclerosis. Two single nucleotide polymorphisms (SNPs) of human intercellular adhesion molecule-1 (ICAM-1), G241R and K469E, are associated with a number of inflammatory diseases. SNP induced changes in ICAM-1 function rely not only on the expression level but also on the single-molecule binding ability which may be affected by single molecule conformation variations such as protein splicing and folding. Previous studies have shown associations between G241R/K469E polymorphisms and ICAM-1 gene expression. Nevertheless, few studies have been done that focus on the single-molecule forces of the above SNPs and their ligands. In the current study, we evaluated both single molecule binding ability and expression level of 4 ICAM-1 mutations – GK (G241/K469), GE (G241/E469), RK (R241/K469) and RE (R241/E469). No difference in adhesion ability was observed via cell adhesion assay or atomic force microscopy (AFM) measurement when comparing the GK, GE, RK, or RE genotypes of ICAM-1 to each other. On the other hand, flow cytometry suggested that there was significantly higher expression of GE genotype of ICAM-1 on transfected CHO cells. Thus, we concluded that genetic susceptibility to diseases related to ICAM-1 polymorphisms, G241R or K469E, might be due to the different expressions of ICAM-1 variants rather than to the single-molecule binding ability of ICAM-1.

  8. 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.

  9. An anti-human ICAM-1 antibody inhibits rhinovirus-induced exacerbations of lung inflammation.

    Directory of Open Access Journals (Sweden)

    Stephanie Traub

    Full Text Available Human rhinoviruses (HRV cause the majority of common colds and acute exacerbations of asthma and chronic obstructive pulmonary disease (COPD. Effective therapies are urgently needed, but no licensed treatments or vaccines currently exist. Of the 100 identified serotypes, ∼90% bind domain 1 of human intercellular adhesion molecule-1 (ICAM-1 as their cellular receptor, making this an attractive target for development of therapies; however, ICAM-1 domain 1 is also required for host defence and regulation of cell trafficking, principally via its major ligand LFA-1. Using a mouse anti-human ICAM-1 antibody (14C11 that specifically binds domain 1 of human ICAM-1, we show that 14C11 administered topically or systemically prevented entry of two major groups of rhinoviruses, HRV16 and HRV14, and reduced cellular inflammation, pro-inflammatory cytokine induction and virus load in vivo. 14C11 also reduced cellular inflammation and Th2 cytokine/chemokine production in a model of major group HRV-induced asthma exacerbation. Interestingly, 14C11 did not prevent cell adhesion via human ICAM-1/LFA-1 interactions in vitro, suggesting the epitope targeted by 14C11 was specific for viral entry. Thus a human ICAM-1 domain-1-specific antibody can prevent major group HRV entry and induction of airway inflammation in vivo.

  10. Polymorphisms and linkage analysis for ICAM-1 and the selectin gene cluster

    Energy Technology Data Exchange (ETDEWEB)

    Vora, D.K.; Rosenbloom, C.L.; Cottingham, R.W. [Baylor College of Medicine, Houston, TX (United States)] [and others

    1994-06-01

    Genetic polymorphisms in leukocyte and endothelial cell adhesion molecules may be important variables with regard to susceptibility to multifactorial disease processes that include an inflammatory component. For this reason, polymorphisms were sought for intercellular adhesion molecule-1 (ICAM-1; gene symbol ICAM1) and for the three genes in the selectin cluster, P-selectin, L-selectin, and E-selectin (gene symbols SELP, SELL, and SELE, respectively). Two amino acid polymorphisms were identified for ICAM-1; Gly or Arg at codon 241 and Lys or Glu at codon 469. Dinucleotide repeat polymorphisms were identified in the 3{prime}-untranslated region for ICAM-1 and in intron 9 for P-selectin. Restriction fragment length polymorphisms were found using cDNAs for each of the three selectin genes as probes; E-selectin with BglII, P-selectin with ScaI, and L-selectin with HincII. Linkage analysis was performed for the selectin gene cluster and for ICAM-1 using the CEPH families; ICAM-1 is very tightly linked to the LDL receptor on chromosome 19, and the selectin cluster is linked to markers at chromosome 1q23. 41 refs., 2 tabs.

  11. Disruption of Nrf2 Enhances Upregulation of Nuclear Factor-κB Activity, Proinflammatory Cytokines, and Intercellular Adhesion Molecule-1 in the Brain after Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Wei Jin

    2008-01-01

    Full Text Available Inflammatory response plays an important role in the pathogenesis of secondary brain injury after traumatic brain injury (TBI. Nuclear factor erythroid 2-related factor 2 (Nrf2 is a key transcription factor that plays a crucial role in cytoprotection against inflammation. The present study investigated the role of Nrf2 in the cerebral upregulation of NF-κB activity, proinflammatory cytokine, and ICAM-1 after TBI. Wild-type Nrf2 (+/+ and Nrf2 (−/−-deficient mice were subjected to a moderately severe weight-drop impact head injury. Electrophoretic mobility shift assays (EMSAs were performed to analyze the activation of nuclear factor kappa B (NF-κB. Enzyme-linked immunosorbent assays were performed to quantify the production of tumor necrosis factor-α (TNF-α, interleukin-1β (IL-1β, and interleukin-6 (IL-6. Immunohistochemistry staining experiments were performed to detect the expression of intercellular adhesion molecule-1 (ICAM-1. Nrf2 (−/− mice were shown to have more NF-κB activation, inflammatory cytokines TNF-α, IL-1β and IL-6 production, and ICAM-1 expression in brain after TBI compared with their wild-type Nrf2 (+/+ counterparts. The results suggest that Nrf2 plays an important protective role in limiting the cerebral upregulation of NF-κB activity, proinflammatory cytokine, and ICAM-1 after TBI.

  12. Changes of pulmonary intercellular adhesion molecule-1 and CD11b/CD18 in peripheral polymorphonuclear neutrophils and their significance at the early stage of burns

    Institute of Scientific and Technical Information of China (English)

    金榕兵; 朱佩芳; 王正国; 刘大维; 周继红

    2003-01-01

    Objective: To investigate the role of intercellular adhesion molecule-1 (ICAM-1) in the accumulation of polymorphonuclear neutrophils (PMN) in the lungs at the early stage of burns. Methods: Myeloperoxidase content in lung tissues and bronchoalveolar lavage fluid (BALF) were detected. ICAM-1 and its mRNA expression in lung tissues were determined by immunohistochemical method and in situ hybridization. CD11b/CD18 expression on the peripheral PMNs was measured by flowcytometry. Results: The levels of myeloperoxidase in lung tissues and BALF after burn injury were markedly higher than those of control. Expression of ICAM-1 and its mRNA in the lung tissues and CD11b/CD18 on peripheral PMNs surface was significantly increased at 2, 6, 12, 24 h after burns. Conclusions: PMNs accumulation in the lungs is related to increased ICAM-1 expression on pulmonary microvascular endothelial cells and CD11b/CD18 expression on PMN at the early stage of burn injury.

  13. Elevation of soluble intercellular adhesion molecule-1 levels, but not angiopoietin 2, in the plasma of human immunodeficiency virus-infected African women with clinical Kaposi sarcoma.

    Science.gov (United States)

    Graham, Susan M; Rajwans, Nimerta; Richardson, Barbra A; Jaoko, Walter; McClelland, R Scott; Overbaugh, Julie; Liles, W Conrad

    2014-10-01

    Circulating levels of endothelial activation biomarkers are elevated in during infection with human immunodeficiency virus 1 (HIV-1) and may also be increased in Kaposi sarcoma (KS). We compared 23 HIV-1-seropositive women with clinically diagnosed KS with 46 randomly selected controls matched for visit year, CD4 count, and antiretroviral therapy status. Conditional logistic regression was used to identify differences between cases and controls. The odds of clinical KS increased with increasing plasma viral load and with intercellular adhesion molecule 1 (ICAM-1) levels above or equal to the median. There was a borderline association between increasing plasma angiopoietin 2 levels and KS. In multivariable modeling including plasma viral load, angiopoietin 2, and ICAM-1, plasma ICAM-1 levels above or equal to the median remained associated with clinical KS (odds ratio = 14.2, 95% confidence interval = 2.3-87.7). Circulating ICAM-1 levels should be evaluated as a potential biomarker for disease progression and treatment response among HIV-infected KS patients.

  14. HIV-1Nef调节内皮细胞黏附分子ICAM-1的表达%HIV-1Nef up-regulates the expression of adhesion molecule ICAM-1 on endothelial cells

    Institute of Scientific and Technical Information of China (English)

    杨凡; 刘朝奇; 覃晓琳; 吕佰瑞; 周永芹; 韩钰

    2010-01-01

    目的 研究HIV-1的调节基因Nef对ECV304细胞ICAM-1表达的影响,从而为分析HIV-1感染引起内皮细胞生物学活性的变化,以及为阐明Nef参与HIV-1致病的分子机制奠定基础.方法 应用本实验室已经建立保存的HIV-1Nef基因在内皮细胞的稳定表达细胞株ECV304-Nef和其阴性对照细胞株ECV304 pcDNA 3.1(+),通过RT-PCR、实时定量PCR(real-time PCR)、Western blot、FCM和细胞黏附试验分析ECV304-Nef细胞ICAM-1的表达水平.结果 RT-PCR、real-time PCR结果 显示ECV304-Nef细胞ICAM-1 mRNA表达水平明显升高,为对照组的(4.3±0.2)倍;Western blot结果 示ECV304-Nef细胞Ⅰ-CAM-1蛋白的表达水平高于对照组;FCM分析显示ECV304-Nef细胞和对照组细胞ICAM-1阳性细胞百分率分别为(35.3±2.2)%和(12.5±0.8)%(P<0.01),两组间ICAM-1表达有显著差异.细胞黏附实验观察到ECV304-Nef细胞黏附的Jurkat细胞数明显多于对照组,荧光仪定量分析结果 显示ECV 304-Nef细胞黏附的Jurkat细胞的荧光强度值显著高与对照组(P<0.05).结论 本实验证实了HIV-1 Nef基因可以上调血管内皮细胞细胞黏附分子ICAM-1的表达.

  15. Vascular endothelial growth factor up-regulates the expression of intracellular adhesion molecule-1 in retinal endothelial cells via reactive oxygen species, but not nitric oxide

    Institute of Scientific and Technical Information of China (English)

    ZHANG Xiao-ling; WEN Liang; CHEN Yan-jiong; ZHU Yi

    2009-01-01

    Background The vascular endothelial growth factor (VEGF) is involved in the initiation of retinal vascular leakage and nonperfusion in diabetes. The intracellular adhesion molecule-1 (ICAM-1) is the key mediator of the effect of VEGFs on retinal leukostasis. Although the VEGF is expressed in an early-stage diabetic retina, whether it directly up-regulates ICAM-1 in retinal endothelial cells (ECs) is unknown. In this study, we provided a new mechanism to explain that VEGF does up-regulate the expression of ICAM-1 in retinal ECs.Methods Bovine retinal ECs (BRECs) were isolated and cultured. Immunohistochemical staining was performed to identify BRECs. The cultured cells were divided into corresponding groups. Then, VEGF (100 ng/ml) and other inhibitors were used to treat the cells. Cell lysate and the cultured supernatant were collected, and then, the protein level of ICAM-1 and phosphorylation of the endothelial nitric oxide synthase (eNOS) were detected using Western blotting. Griess reaction was used to detect nitric oxide (NO).Results Western blotting showed that the VEGF up-regulated the expression of ICAM-1 protein and increased phosphorylation of the eNOS in retinal ECs. Neither the block of NO nor protein kinase C (PKC) altered the expression of ICAM-1 or the phosphorylation of eNOS. The result of the Western blotting also showed that inhibition of phosphatidylinositol 3-kinase (PI3K) or reactive oxygen species (ROS) significantly reduced the expression of ICAM-1. Inhibition of PI3K also reduced phosphorylation of eNOS. Griess reaction showed that VEGF significantly increased during NO production. When eNOS was blocked by L-NAME or PI3K was blocked by LY294002, the basal level of NO production and the increment of NO caused by VEGF could be significantly decreased.Conclusion ROS-NO coupling in the retinal endothelium may be a new mechanism that could help to explain why VEGF induces ICAM-1 expression and the resulting leukostasis in diabetic retinopathy.

  16. Growth hormone increases vascular cell adhesion molecule 1 expression

    DEFF Research Database (Denmark)

    Hansen, Troels Krarup; Fisker, Sanne; Dall, Rolf

    2004-01-01

    We investigated the impact of GH administration on endothelial adhesion molecules, vascular cell adhesion molecule-1 (VCAM-1) and E-selectin, in vivo and in vitro. Soluble VCAM-1, E-selectin, and C-reactive protein concentrations were measured before and after treatment in 25 healthy subjects...... and 25 adult GH-deficient (GHD) patients randomized to GH treatment or placebo. Furthermore, we studied the direct effect of GH and IGF-I and serum from GH-treated subjects on basal and TNF alpha-stimulated expression of VCAM-1 and E-selectin on cultured human umbilical vein endothelial cells. Baseline...... levels of VCAM-1, but not E-selectin, were significantly lower in GHD patients than in healthy subjects (362 +/- 15 microg/liter vs. 516 +/- 21 microg/liter, P treatment, compared with placebo [net difference between groups 151.8 microg/liter (95...

  17. Involvement of ICAM-1 in impaired spermatogenesis after busulfan treatment in mice.

    Science.gov (United States)

    Cai, Y; Liu, T; Fang, F; Shen, S; Xiong, C

    2016-02-01

    Expression of adherence proteins, such as P-cadherin, has been identified in the normal testis and changed in impaired testis induced by alkylating agents. Intercellular adhesion molecule-1 (ICAM-1), a member of the immunoglobulin superfamily of cell adhesion molecules, is a constituent component of the blood-testis barrier and a multifunctional molecule in homeostasis of spermatogenesis. However, the distribution of ICAM-1 in the testis of mice and expression changes after busulfan treatment remain unclear. In this study, ICAM-1 immunoreaction was detected in Sertoli and germinal cells, particularly in spermatogonia, and elongating and elongated spermatids of normal testes. Accompanied with degeneration of spermatogenesis (decrease in testicular and epididymal weights, as well as loss of germ cells in histological morphology), ICAM-1 expression declined significantly in the seminiferous tubules during a 4-week experimental period, particularly in the first 2 weeks (40 mg kg(-1) busulfan, single injection). Compared with the control group, busulphan-treated testes showed a significant increase in lipid peroxidation during weeks 1 and 2. Thus, ICAM-1 may play an important role in the homeostasis of spermatogenesis, and busulfan treatment can lead to adhesion disintegration.

  18. Increased plasma concentrations of sICAM-1, sVCAM-1 and sELAM-1 in patients with Plasmodium falciparum or P. vivax malaria and association with disease severity

    DEFF Research Database (Denmark)

    Jakobsen, P H; Morris-Jones, S; Rønn, A;

    1994-01-01

    Increased serum concentrations of soluble intercellular adhesion molecule-1 (sICAM-1), soluble endothelial leucocyte adhesion molecule-1 (sELAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) were detected in Danish malaria patients infected with sequestering Plasmodium falciparum or non......-sequestering P. vivax parasites, as well as in patients with sepsis or meningitis. Levels of soluble adhesion molecules remained elevated in the P. falciparum patients for several weeks after initiation of treatment. Plasma concentrations of sICAM-1, sVCAM-1 and sELAM-1 were higher in Gambian children...

  19. The Serum Changes of Neuron-Specific Enolase and Intercellular Adhesion Molecule-1 in Patients With Diffuse Axonal Injury Following Progesterone Administration: A Randomized Clinical Trial

    Science.gov (United States)

    Shahrokhi, Nader; Soltani, Zahra; Khaksari, Mohammad; Karamouzian, Saeid; Mofid, Behshad; Asadikaram, Gholamreza

    2016-01-01

    Background Improvement of neurologic outcome in progesterone-administered patients with diffuse axonal injury (DAI) has been found in a recent study. Also, there has been interest in the importance of serum parameters as predictors of outcome in traumatic brain injury. Objectives The aim of this study was to examine the effect of progesterone administration on serum levels of neuron-specific enolase (NSE), and intercellular adhesion molecule-1 (ICAM-1) in clinical DAI. Patients and Methods In this study, the serum levels of ICAM-1 and NSE of 32 male DAI patients (18 - 60 years of age, a Glasgow coma scale of 12 or less, and admitted within 4 hours after injury) who were randomized for a controlled phase II trial of progesterone were analyzed. The analysis was performed between the control and progesterone groups at admission time, and 24 hours and six days after DAI, respectively. Results A reduction in the serum level of ICAM-1 was noticed in the progesterone group 24 hours after the injury (P < 0.05). There was no significant difference in the serum level of NSE between the study groups during evaluation. At 24 hours after the injury, the level of ICAM-1 in the control group was higher than that at admission time (P < 0.05). The lowest level of NSE in the two groups was seen six days after DAI (P < 0.01). Conclusions In summary, progesterone administration reduced serum ICAM-1, and whereby may attenuate blood brain barrier disruption, the latter needs further investigation for confirmation. PMID:27800469

  20. Effects of fosinopril and valsartan on expressions of ICAM-1 and NO in human umbilical vein endothelial cells

    Institute of Scientific and Technical Information of China (English)

    管思明; 王斌

    2003-01-01

    ObjectiveTo investigate the effects of fosinopril and valsartan on the expression of intercellular adhesion molecule-1 (ICAM-1) and nitric oxide (NO) induced by oxidizlls. MethodsThe levels of NO, ICAM-1, and nitric oxide synthase (NOS) were determined using the nitrate reductase method, ELISA, immunohistochemical and image analyses.ResultsThe ox-LDL can significantly increase the expression of ICAM-1 and inhibit theexpression of NO and NOS in a dose-dependent manner. Fosinopril and valsartancan significantly inhibit these roles of ox-LDL. The roles of fosinopril and valsartan were not significantly different. ConclusionFosinopril and valsartan inhibit oxidized LDL-induced expression of ICAM-1and increase the expression of NO in human umbilical vein endothelial cells, which is one of the mechanisms of antiatherosclerosis.

  1. Large-scale genomic studies reveal central role of ABO in sP-selectin and sICAM-1 levels

    NARCIS (Netherlands)

    M. Barbalic (maja); J. Dupuis (Josée); A. Dehghan (Abbas); J.C. Bis (Joshua); R.C. Hoogeveen (Ron); R. Schnabel (Renate); V. Nambi (Vijay); M. Bretler (Monique); N.L. Smith (Nicholas); A. Peters (Annette); C. Lu (Chao); R.P. Tracy (Russell); N. Aleksic (Nena); J. Heeriga (Jan); J.F. Keaney (John); K. Rice (Kenneth); G.Y. Lip (Gregory); R.S. Vasan (Ramachandran Srini); N.L. Glazer (Nicole); M.G. Larson (Martin); A.G. Uitterlinden (André); J.F. Yamamoto (Jennifer); P. Durda (Peter); T. Haritunians (Talin); B.M. Psaty (Bruce); E.A. Boerwinkle (Eric); A. Hofman (Albert); W. Koenig (Wolfgang); N.S. Jenny (Nancy); J.C.M. Witteman (Jacqueline); C. Ballantyne (Christie); E.J. Benjamin (Emelia)

    2010-01-01

    textabstractP-selectin and intercellular adhesion molecule-1 (ICAM-1) participate in inflammatory processes by promoting adhesion of leukocytes to vascular wall endothelium. Their soluble levels have been associated with adverse cardiovascular events. To identify loci affecting soluble levels of P-s

  2. A study on the pathogenesis of the radiation pneumonitis. Alterations in pulmonary mRNA encoding adhesion molecules ICAM-1, VCAM-1, and P-selectin following thoracic irradiation in mice

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    Tsujino, Kayoko; Kodama, Akihisa; Kono, Michio [Kobe Univ. (Japan). School of Medicine

    1997-12-01

    To investigate the role of the adhesion molecules in the pathogenesis of the radiation pneumonitis, we quantified the mRNA expression of the adhesion molecules in the lung by Northern blot method following whole thorax irradiation to C57BL/6J mice. After irradiation of 12 Gy to the whole thorax, there were increase of mRNA for ICAM-1 by 42% at 4 hours (p<0.05), 76% at 24 hours (p<0.01) and 51% at 48 hours (p<0.05) compared with controls. And it returned to control level at 1 week. No significant change was observed thereafter until 8 weeks. The expression of VCAM-1 mRNA were also increased by 49% (p<0.01) at 12 hours and were still increased by 25% at 1 week. P-selectin mRNA as transiently increased by 59% at 12 hours. We examined the relationship between the ICAM-1 induction and the radiation dose, and found that ICAM-1 expression was increased by 3 Gy of irradiation and it was increased in radiation dose dependent manner up to 24 Gy. These early inductions of mRNA for ICAM-1, VCAM-1 and P-selectin in mice lungs following thoracic irradiation were transient but significant, and they were one of the most immediate change reported in vivo. It is suggested that these adhesion molecules are possibly related to the pathogenesis of the radiation pneumonitis. (author)

  3. Lipopolysaccharide Binding Protein, Soluble-Intercellular Adhesion Molecule-1, Procalcitonin, and Protein C Activity and Clinical Outcome in Systemic Inflammatory Response Syndrome (SIRS or Sepsis Patients

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    Dewi Muliaty

    2009-04-01

    Full Text Available BACKGROUND: Biochemical markers may be used in diagnosis, prognostic and monitoring treatment and therapy for sepsis patients. In this study we used Lipopolysacharide Binding Protein (LBP, serum-Intercellular Adhesion Molecule-1 (ICAM-1, Procalcitonin (PCT and protein C activity. LBP is related to lipopolysachharide or gram-negative bacterial endotoxin which bound to LBP and induced inflammatory response. ICAM-1 is associated with endothelial dysfunction in response to systemic inflammatory and septic condition. PCT increased in bacterial infection and in severe systemic inflammatory. Role of Protein C is protecting the intravascular system to systemic inflammation, sepsis and the concomitant intravascular coagulopathy. The aim of this study was to examine the associations between levels of serum LBP, sICAM-1, PCT, and protein C activity with the clinical outcome of SIRS or sepsis patients. METHODS: We included 19 post surgery patients with SIRS criteria from intensive care unit (ICU and evaluated the level of LBP serum with Chemiliuminescent Enzyme Immunoassay (Diagnostic Product Co., ICAM-1 with ELISA (R&D System, PCT with immunochromatography (BRAHMS, protein C activity with chromogenic method (Dade Behring. We performed the samples serially at the first admission of patients and after 72 hours. Data were analysed by non-parametric with Wilcoxon test and Mann-Whitney test. Correlation study between biomarkers calculated by Kendall’s tau and Spearman’s rho. RESULTS: Of 19 patients, 9 (47,4% died and 10 (52,6% surviving. The level of LBP serum decreased after 72 hours in surviving-sepsis patients, and increased in nonsurviving sepsis patients with significant different levels at 72 hours examination (p0.05. In all patients were found high level of PCT serum since the first admission examination, decreasing levels were occurred significantly in surviving patients after 72 hours (p0.05 both in surviving and non-surviving patients. CONCLUSIONS

  4. Cerebrospinal fluid and plasma concentration of soluble intercellular adhesion molecule1, vascular cell adhesion molecule1 and endothelial leukocyte adhesion molecule in patients with acute ischemic b

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    Selaković Vesna M.

    2003-01-01

    Full Text Available Background. Leukocyte migration into the ischemic area is a complex process controlled by adhesion molecules (AM in leukocytes and endothelium, by migratory capacity of leukocytes and the presence of hemotaxic agents in the tissue. In this research it was supposed that in the blood and cerebrospinal fluid (CSF of patients in the acute phase of ischemic brain disease (IBD there were relevant changes in the concentration of soluble AM (sICAM-1 sVCAM-1 and sE-selectin, that could have been the indicators of the intensity of damaging processes in central nervous system (CNS. Methods. The study included 45 IBD patients, 15 with transient ischemic attack (TIA 15 with reversible ischemic attack (RIA, and 15 with brain infarction (BI of both sexes, mean age 66±7. Control group consisted of 15 patients with radicular lesions of discal origin, subjected to diagnostic radiculography without the signs of interruption in the passage of CSF. Changes of selected biochemical parameters were determined in all patients in frame 72 hours since the occurence of an ischemic episode. Concentrations of soluble AM were determined in plasma and CSF by ELISA. Total number of leukocytes (TNL in peripheral blood was determined by hematological analyzer. Results. The results showed that during the first 72 hrs of IBD significant increases occured in TNL and that the increase was progressive compared to the severeness of the disease. Significant increase of soluble AM concentration was shown in plasma of IBD patients. The increase was highest in BI somewhat lower in RIA and the lowest in TIA patients compared to the control. In CSF concentrations of sICAM-1, sVCAM-1 and sE-selectin demonstrated similar increasing trend as in plasma. Conclusion. TNL, as well as the soluble AM concentrations in plasma and CSF, were increased during the acute IBD phase and progressive in relation to the severeness of the disease, so that they might have been the indicators of CNS inflammatory

  5. Soluble intercellular adhesion molecule-1, D-lactate and diamine oxidase in patients with inflammatory bowel disease

    Institute of Scientific and Technical Information of China (English)

    Wei-Bing Song; Yong-Hui Lv; Zhen-Shu Zhang; Ya-Nan Li; Li-Ping Xiao; Xin-Pei Yu; Yuan-Yuan Wang; Hong-Li Ji; Li Ma

    2009-01-01

    AIM: To study the levels of serum soluble intercellular adhesion molecule-1 (sICAM-1), plasma D-lactate and diamine oxidase (DAO) in patients with inflammatory bowel disease (IBD), and the potential clinical significance.METHODS: Sixty-nine patients with IBD and 30 healthy controls were included in this study. The concentration of sICAM-1 was detected with enzyme-linked immunosorbent assay, the level of D-lactate and DAO was measured by spectroscopic analysis, and the number of white blood cells (WBC) was determined by routine procedure.RESULTS: The levels of sICAM-l, DAO, and WBC in IBD patients were significantly higher than those in the control group ( P < 0.01). sICAM-l in IBD patients was found to be closely related to the levels of DAO and D-lactate (212.94 ± 69.89 vs 6.35 ± 2.35, P = 0.000),DAO 212.94 ± 69.89 vs 8.65 ± 3.54, P = 0.000) and WBC (212.94 ± 69.89 vs 7.40 ± 2.61, P = 0.000), but no significant difference was observed between patients with ulcerative colitis and patients with Crohn's disease.The post-treatment levels of sICAM-l, D-lactate and WBC were significantly lower than before treatment (sICAM-l 206.57 ± 79.21 vs 146.21 ± 64.43, P = 0.000),(D-lactate 1.46 ± 0.94 vs 0.52 ± 0.32, P = 0.000) and (WBC 7.24 ± 0.2.33 vs 5.21 ± 3.21, P = 0.000).CONCLUSION: sICAM-1, D-lactate and DAO are closely related to the specific conditions of IBD, and thus could be used as a major diagnostic index.

  6. Levels of soluble VCAM-1, soluble ICAM-1, and soluble E-selectin in patients with tuberculous pleuritis

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    A. Hamzaoui

    1996-01-01

    Full Text Available Tuberculosis is characterized by the presence of activated mononuclear cells both in the peripheral circulation and in pleural fluid. Expression and up-regulation of adhesion molecules is the basis of cell-cell adhesion in granuloma formation and in leukocyte migration to the inflammatory site. Soluble isoforms of adhesion molecules have been described, and their expression at high levels indicated an activated state. The purpose of this study was to evaluate levels of soluble adhesion molecules in serum and pleural fluid from patients with tuberculous pleural effusions, compared with non-tuberculous pleural effusions. We analysed levels of soluble vascular cell adhesion molecule-1 (s.VCAM-1, soluble intercellular adhesion molecule-1 (s.ICAM-1, and soluble E-selectin (sE-selectin in serum and pleural fluid from patients with tuberculous pleuritis, by sandwich ELISA. Serum levels of s.ICAM-1 and s.VCAM-1 in patients with tuberculosis were higher than those in healthy controls (p < 0.001. Levels of sE-selectin levels were in the normal range compared with control groups. In pleural fluid, levels of s.VCAM-1 and s.ICAM-1 were increased in pleural effusions. Patients with tuberculous pleural effusion exhibited high levels of s.ICAM-1 compared with patients with neoplastic pleural involvement. Up-regulation of s.VCAM-1 and s.ICAM-1 in serum, along with increased levels of sE-selectin in pleural effusions from tuberculous patients, may result in transmigration of activated inflammatory cells inducing pleural damage, which may contribute to the pathological processes involved.

  7. Expression of pulmonary mRNA encoding ICAM-1, VCAM-1, and P-selectin following thoracic irradiation in mice

    Energy Technology Data Exchange (ETDEWEB)

    Tsujino, Kayoko; Kodama, Akihisa; Nanaoka, Noriyoshi; Maruta, Tsutomu; Kono, Michio [Kobe Univ. (Japan). School of Medicine

    1999-08-01

    Recent studies have revealed that ionizing radiation induces the expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and P-selectin in vitro. The purpose of this study was to investigate the expression of these adhesion molecules in mouse lung following whole thoracic irradiation. C57BL/6J mice were irradiated with a single dose of 12 Gy to the thoraces and sacrificed at 4, 12, 24, and 48 hours and 1, 2, 4, and 8 weeks after irradiation. Expression of total lung mRNA for ICAM-1, VCAM-1, and P-selectin was quantified by the Northern blot method and normalized to {beta}-actin. There were increases in mRNA for ICAM-1 of 42% at 4 hours (p<0.05), 76% at 24 hours (p<0.01), and 51% at 48 hours (p<0.05) compared with the controls. There returned to the control level at 1 week. The expression of VCAM-1 mRNA was also increased by 49% (p<0.01) at 12 hours and was still increased by 25% at 1 week. P-selectin mRNA was transiently increased by 59% at 12 hours. These early inductions of mRNA for ICAM-1, VCAM-1, and P-selectin in mouse lung following thoracic irradiation were transient but significant, and are one of the most immediate changes reported in vivo. (author)

  8. Regional gene expression of LOX-1, VCAM-1, and ICAM-1 in aorta of HIV-1 transgenic rats.

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    Anne Mette Fisker Hag

    Full Text Available BACKGROUND: Increased prevalence of atherosclerotic cardiovascular disease in HIV-infected patients has been observed. The cause of this accelerated atherosclerosis is a matter of controversy. As clinical studies are complicated by a multiplicity of risk-factors and a low incidence of hard endpoints, studies in animal models could be attractive alternatives. METHODOLOGY/PRINCIPAL FINDINGS: We evaluated gene expression of lectin-like oxidized-low-density-lipoprotein receptor-1 (LOX-1, vascular cell adhesion molecule-1 (VCAM-1, and intercellular adhesion molecule-1 (ICAM-1 in HIV-1 transgenic (HIV-1Tg rats; these genes are all thought to play important roles in early atherogenesis. Furthermore, the plasma level of sICAM-1 was measured. We found that gene expressions of LOX-1 and VCAM-1 were higher in the aortic arch of HIV-1Tg rats compared to controls. Also, the level of sICAM-1 was elevated in the HIV-1Tg rats compared to controls, but the ICAM-1 gene expression profile did not show any differences between the groups. CONCLUSIONS/SIGNIFICANCE: HIV-1Tg rats have gene expression patterns indicating endothelial dysfunction and accelerated atherosclerosis in aorta, suggesting that HIV-infection per se may cause atherosclerosis. This transgenic rat model may be a very promising model for further studies of the pathophysiology behind HIV-associated cardiovascular disease.

  9. Comparative immunoexpression of ICAM-1, TGF-β1 and ki-67 in periapical and residual cysts

    Science.gov (United States)

    Armada, Luciana; dos Santos, Teresa-Cristina; Pires, Fabio-Ramoa

    2017-01-01

    Background This study compared the immunohistochemical expression of ki-67, transforming growth factor beta 1 (TGF-β1) and intercellular adhesion molecule-1 (ICAM-1) in inflammatory periapical cysts and residual cysts. Material and Methods The study sample was composed by 25 periapical cysts and 25 residual cysts and immunohistochemical reactions were carried out using antibodies directed against ICAM-1, TGF-β1 and ki-67. Clinical, radiological, gross, histological and immunohistochemical data were tabulated for descriptive and comparative analysis using the SPSS software and differences were considered statistically significant when p<0.05%. Results There were no differences between the expression of ICAM-1 (p=0.239) and TGF-β1 (p=0.258) when comparing both groups. Ki-67 labeling index was higher in residual cysts compared to periapical cysts (p=0.017). Conclusions Results from the present study suggest that some specific inflammatory stimuli on residual cysts would modulate their mechanisms of etiopathogenesis, growing and repair. Key words:Periapical cyst, radicular cyst, residual cyst, transforming growth factor beta 1 (TGF-β1), intercellular adhesion molecule 1 (ICAM-1), ki-67. PMID:27918735

  10. Priming by Chemokines Restricts Lateral Mobility of the Adhesion Receptor LFA-1 and Restores Adhesion to ICAM-1 Nano-Aggregates on Human Mature Dendritic Cells

    NARCIS (Netherlands)

    Borgman, K.J.; Zanten, T.S. van; Manzo, C.; Cabezon, R.; Cambi, A.; Benitez-Ribas, D.; Garcia-Parajo, M.F.

    2014-01-01

    LFA-1 is a leukocyte specific beta2 integrin that plays a major role in regulating adhesion and migration of different immune cells. Recent data suggest that LFA-1 on mature dendritic cells (mDCs) may function as a chemokine-inducible anchor during homing of DCs through the afferent lymphatics into

  11. Priming by Chemokines Restricts Lateral Mobility of the Adhesion Receptor LFA-1 and Restores Adhesion to ICAM-1 Nano-Aggregates on Human Mature Dendritic Cells

    NARCIS (Netherlands)

    Borgman, K.J.; Zanten, van T.S.; Manzo, C.; Cabezon, R.; Cambi, A.; Benitez-Ribas, D.; Garcia Parajo, M.F.

    2014-01-01

    LFA-1 is a leukocyte specific β2 integrin that plays a major role in regulating adhesion and migration of different immune cells. Recent data suggest that LFA-1 on mature dendritic cells (mDCs) may function as a chemokine-inducible anchor during homing of DCs through the afferent lymphatics into the

  12. Serum Interleukin-18, Fetuin-A, Soluble Intercellular Adhesion Molecule-1, and Endothelin-1 in Ankylosing Spondylitis, Psoriatic Arthritis, and SAPHO Syndrome.

    Science.gov (United States)

    Przepiera-Będzak, Hanna; Fischer, Katarzyna; Brzosko, Marek

    2016-08-03

    To examine serum interleukin 18 (IL-18), fetuin-A, soluble intercellular adhesion molecule-1 (sICAM-1), and endothelin-1 (ET-1) levels in ankylosing spondylitis (AS), psoriatic arthritis (PsA), and Synovitis Acne Pustulosis Hyperostosis Osteitis syndrome (SAPHO). We studied 81 AS, 76 PsA, and 34 SAPHO patients. We measured serum IL-18, fetuin-A, sICAM-1, ET-1, IL-6, IL-23, vascular endothelial growth factor (VEGF), and epidermal growth factor (EGF). IL-18 levels were higher in AS (p = 0.001), PsA (p = 0.0003), and SAPHO (p = 0.01) than in controls, and were positively correlated with CRP (p = 0.03), VEGF (p = 0.03), and total cholesterol (TC, p = 0.006) in AS and with IL-6 (p = 0.03) in PsA. Serum fetuin-A levels were lower in AS (p = 0.001) and PsA (p = 0.001) than in controls, and negatively correlated with C-reactive protein (CRP) in AS (p = 0.04) and SAPHO (p = 0.03). sICAM-1 positively correlated with CRP (p = 0.01), erythrocyte sedimentation rate (ESR, p = 0.01), and IL-6 (p = 0.008) in AS, and with IL-6 (p = 0.001) in SAPHO. Serum ET-1 levels were lower in AS (p = 0.0005) than in controls. ET-1 positively correlated with ESR (p = 0.04) and Disease Activity Score 28 (DAS28, p = 0.003) in PsA. In spondyloarthritis, markers of endothelial function correlated with disease activity and TC.

  13. Serum Interleukin-18, Fetuin-A, Soluble Intercellular Adhesion Molecule-1, and Endothelin-1 in Ankylosing Spondylitis, Psoriatic Arthritis, and SAPHO Syndrome

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    Hanna Przepiera-Będzak

    2016-08-01

    Full Text Available To examine serum interleukin 18 (IL-18, fetuin-A, soluble intercellular adhesion molecule-1 (sICAM-1, and endothelin-1 (ET-1 levels in ankylosing spondylitis (AS, psoriatic arthritis (PsA, and Synovitis Acne Pustulosis Hyperostosis Osteitis syndrome (SAPHO. We studied 81 AS, 76 PsA, and 34 SAPHO patients. We measured serum IL-18, fetuin-A, sICAM-1, ET-1, IL-6, IL-23, vascular endothelial growth factor (VEGF, and epidermal growth factor (EGF. IL-18 levels were higher in AS (p = 0.001, PsA (p = 0.0003, and SAPHO (p = 0.01 than in controls, and were positively correlated with CRP (p = 0.03, VEGF (p = 0.03, and total cholesterol (TC, p = 0.006 in AS and with IL-6 (p = 0.03 in PsA. Serum fetuin-A levels were lower in AS (p = 0.001 and PsA (p = 0.001 than in controls, and negatively correlated with C-reactive protein (CRP in AS (p = 0.04 and SAPHO (p = 0.03. sICAM-1 positively correlated with CRP (p = 0.01, erythrocyte sedimentation rate (ESR, p = 0.01, and IL-6 (p = 0.008 in AS, and with IL-6 (p = 0.001 in SAPHO. Serum ET-1 levels were lower in AS (p = 0.0005 than in controls. ET-1 positively correlated with ESR (p = 0.04 and Disease Activity Score 28 (DAS28, p = 0.003 in PsA. In spondyloarthritis, markers of endothelial function correlated with disease activity and TC.

  14. Effects of nitrogen dioxide on the expression of intercellular adhesion molecule-1, neutrophil adhesion, and cytotoxicity: studies in human bronchial epithelial cells.

    Science.gov (United States)

    Ayyagari, Vijayalakshmi N; Januszkiewicz, Adolph; Nath, Jayasree

    2007-02-01

    Nitrogen Dioxide (NO2) is a product of high-temperature combustion and an environmental oxidant of concern. We have recently reported that early changes in NO2-exposed human bronchial epithelial cells are causally linked to increased generation of proinflammatory mediators, such as nitric oxide/nitrite and cytokines like interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha and IL-8. The objective of the present in vitro study was to further delineate the cellular mechanisms of NO2-mediated toxicity, and to define the nature of cell death that ensues upon exposure of normal human bronchial epithelial (NHBE) cells to a brief high dose of NO2. Our results demonstrate that the NHBE cells undergo apoptotic cell death during the early post-NO2 period, but this is independent of any significant increase in caspase-3 activity. However, necrotic cell death was more prevalent at later time intervals. Interestingly, an increased expression of HO-1, a redox-sensitive stress protein, was observed in NO2-exposed NHBE cells at 24 h. Since neutrophils (PMNs) play an active role in acute lung inflammation and resultant oxidative injury, we also investigated changes in human PMN-NHBE cell interactions. As compared to normal cells, increased adhesion of PMNs to NO2-exposed cells was observed, which resulted in an increased NHBE cell death. The latter was also increased in the presence of IL-8 and TNF-alpha + interferon (IFN)-gamma, which correlated with upregulation of intercellular adhesion molecule-1 (ICAM-1). Our results confirmed an involvement of nitric oxide (NO) in NO2-induced cytotoxicity. By using NO synthase inhibitors such as L-NAME and 3-aminoguanidine (AG), a significant decrease in cell death, PMN adhesion, and ICAM-1 expression was observed. These findings indicate a role for the L-arginine/NO synthase pathway in the observed NO2-mediated toxicity in NHBE cells. Therapeutic strategies aimed at controlling excess generation of NO and/or inflammatory cytokines may

  15. The Relationship between Eating Disorders and ICAM-1, E-selection and Ghrelin Resting Level in Overweight People

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    Gholamreza Sharifi

    2014-11-01

    Full Text Available Introduction There is an agreement that eating disorder is related to psychological characteristics and on the other hand, level of ghrelin hormone, Intercellular adhesion molecule-1 (ICAM-1 and E-selection also change during eating disorders. We aimed to study the relationship between eating disorders and rest levels, ICAM-1, E-selection, and ghrelin hormone in obese people. Materials and Methods  In this quasi-experimental study, 120 obese men (25-30 years old were purposefully selected. Then the data about their eating disorders gathered with eating attitudes test (EAT-26 questionnaire. In the next phase in the rest condition and after overnight fasting, blood samples are collected for measurement of rest levels, ICAM-1, E-selection, and ghrelin hormone. Finally the data were analyzed with appropriate statistical tests in SPSS version 18. Results Mean and deviation of rest levels, ICAM-1, E-selection, and ghrelin hormone were respectively 3064.19, 61.5±19.7, and 2.5±1.5 and there was not any statistical significance relationship between eating disorders ICAM-1, E-selection, and ghrelin hormone in obese men (P

  16. Expression, production, and renaturation of a functional single-chain variable antibody fragment (scFv against human ICAM-1

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    H. Sun

    2014-07-01

    Full Text Available Intercellular adhesion molecule-1 (ICAM-1 is an important factor in the progression of inflammatory responses in vivo. To develop a new anti-inflammatory drug to block the biological activity of ICAM-1, we produced a monoclonal antibody (Ka=4.19×10−8 M against human ICAM-1. The anti-ICAM-1 single-chain variable antibody fragment (scFv was expressed at a high level as inclusion bodies in Escherichia coli. We refolded the scFv (Ka=2.35×10−7 M by ion-exchange chromatography, dialysis, and dilution. The results showed that column chromatography refolding by high-performance Q Sepharose had remarkable advantages over conventional dilution and dialysis methods. Furthermore, the anti-ICAM-1 scFv yield of about 60 mg/L was higher with this method. The purity of the final product was greater than 90%, as shown by denaturing gel electrophoresis. Enzyme-linked immunosorbent assay, cell culture, and animal experiments were used to assess the immunological properties and biological activities of the renatured scFv.

  17. ICAM-1-based rabies virus vaccine shows increased infection and activation of primary murine B cells in vitro and enhanced antibody titers in-vivo.

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    James E Norton

    Full Text Available We have previously shown that live-attenuated rabies virus (RABV-based vaccines infect and directly activate murine and human primary B cells in-vitro, which we propose can be exploited to help develop a single-dose RABV-based vaccine. Here we report on a novel approach to utilize the binding of Intracellular Adhesion Molecule-1 (ICAM-1 to its binding partner, Lymphocyte Function-associated Antigen-1 (LFA-1, on B cells to enhance B cell activation and RABV-specific antibody responses. We used a reverse genetics approach to clone, recover, and characterize a live-attenuated recombinant RABV-based vaccine expressing the murine Icam1 gene (rRABV-mICAM-1. We show that the murine ICAM-1 gene product is incorporated into virus particles, potentially exposing ICAM-1 to extracellular binding partners. While rRABV-mICAM-1 showed 10-100-fold decrease in viral titers on baby hamster kidney cells compared to the parental virus (rRABV, rRABV-mICAM-1 infected and activated primary murine B cells in-vitro more efficiently than rRABV, as indicated by significant upregulation of CD69, CD40, and MHCII on the surface of infected B cells. ICAM-1 expression on the virus surface was responsible for enhanced B cell infection since pre-treating rRABV-mICAM-1 with a neutralizing anti-ICAM-1 antibody reduced B cell infection to levels observed with rRABV alone. Furthermore, 100-fold less rRABV-mICAM-1 was needed to induce antibody titers in immunized mice equivalent to antibody titers observed in rRABV-immunized mice. Of note, only 10(3 focus forming units (ffu/mouse of rRABV-mICAM-1 was needed to induce significant anti-RABV antibody titers as early as five days post-immunization. As both speed and potency of antibody responses are important in controlling human RABV infection in a post-exposure setting, these data show that expression of Icam1 from the RABV genome, which is then incorporated into the virus particle, is a promising strategy for the development of a

  18. Expression of inflammation related factors iNOS and ICAM-1 in endothelial cells induced by C-reactive protein

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    Xu-dong SONG

    2011-08-01

    Full Text Available Objective To investigate the expression of inducible nitric oxide synthase(iNOS and intercellular cell adhesion molecule-1(ICAM-1 in endothelial cells induced by C-reactive protein(CRP and its corresponding mechanisms.Methods Human umbilical cord vein endothelial cells(HUVEC were treated with different concentrations of CRP or with phosphate buffered solution as control,and RT-PCR was used for measurement of the expression of ICAM-1 mRNA induced by CRP in HUVECs.HUVEC were treated with CRP of 1mg/L,5mg/L,20mg/L,or with phosphate buffered solution,and expressions of ICAM-1 and iNOS protein in HUVECs were detected by cellular enzyme linked immunosorbent assay(ELISA.Results In groups of 1mg/L,5mg/L and 10mg/L CRP,no different effects on expression of ICAM-1 mRNA in HUVECs was found when compared with control group,whereas the expression of ICAM-1 mRNA was elevated in the group of 20mg/L CRP by 1.48 folds compared with that in control group.Similarly,in groups of 1mg/L and 5mg/L CRP there was no significant difference in the expressions of ICAM-1 and iNOS in HUVECs compared with that in control group(P > 0.05,whereas the expressions of ICAM-1 and iNOS protein were increased significantly in group of 20mg/L CRP compared with that in other groups(P< 0.01.Conclusions Although CRP may induce the expression of inflammatory factors in endothelial cells,the present experioment showed that CRP had no significant effects on inflammatory factors in endothelial cells at normal physiological level,and it gave inducible effects at higher concentration(20mg/L only.

  19. Aldosterone stimulates nuclear factor-kappa B activity and transcription of intercellular adhesion molecule-1 and connective tissue growth factor in rat mesangial cells via serum- and glucocorticoid-inducible protein kinase-1.

    Science.gov (United States)

    Terada, Yoshio; Ueda, Satoko; Hamada, Kazu; Shimamura, Yoshiko; Ogata, Koji; Inoue, Kosuke; Taniguchi, Yoshinori; Kagawa, Toru; Horino, Taro; Takao, Toshihiro

    2012-02-01

    Several clinical and experimental data support the hypothesis that aldosterone contributes to the progression of renal injury. To determine the signaling pathway of aldosterone in relation to fibrosis and inflammation in mesangial cells, we investigated the effects of aldosterone on expression and activation of serum- and glucocorticoid-inducible protein kinase-1 (SGK1), the activation of nuclear factor-kappa B (NF-κB activation, and the expressions of intercellular adhesion molecule-1 (ICAM-1) and connective tissue growth factor (CTGF). Aldosterone stimulated SGK1 expression, phosphorylation (Ser-256), and kinase activity. The increments of phosphorylation and expression of SGK1 induced by aldosterone were inhibited by mineralocorticoid receptor (MR) inhibitor (eplerenone). Aldosterone stimulated NF-κB activity measured by NF-κB responsive elements, luciferase assay, and the levels of inhibitor of kappa B (IκB) phosphorylation. This aldosterone-induced activation of NF-κB was inhibited by the transfection of dominant-negative SGK1. Furthermore, aldosterone augmented the promoter activities and protein expressions of ICAM-1 and CTGF. The effects of aldosterone on ICAM-1 and CTGF promoter activities and protein expressions were inhibited by the transfection of dominant-negative SGK1 and dominant-negative IκBα. We also found that the MR antagonist significantly ameliorated the glomerular injury and enhancements in SGK1, ICAM-1, and CTGF expressions induced by 1% sodium chloride and aldosterone in vivo. In conclusion, our findings suggest that aldosterone stimulates ICAM-1 and CTGF transcription via activation of SGK1 and NF-κB, which may be involved in the progression of aldosterone-induced mesangial fibrosis and inflammation. MR antagonists may serve as useful therapeutic targets for the treatment of glomerular inflammatory disease.

  20. Inside-out regulation of ICAM-1 dynamics in TNF-alpha-activated endothelium.

    Directory of Open Access Journals (Sweden)

    Jaap D van Buul

    Full Text Available BACKGROUND: During transendothelial migration, leukocytes use adhesion molecules, such as ICAM-1, to adhere to the endothelium. ICAM-1 is a dynamic molecule that is localized in the apical membrane of the endothelium and clusters upon binding to leukocytes. However, not much is known about the regulation of ICAM-1 clustering and whether membrane dynamics are linked to the ability of ICAM-1 to cluster and bind leukocyte integrins. Therefore, we studied the dynamics of endothelial ICAM-1 under non-clustered and clustered conditions. PRINCIPAL FINDINGS: Detailed scanning electron and fluorescent microscopy showed that the apical surface of endothelial cells constitutively forms small filopodia-like protrusions that are positive for ICAM-1 and freely move within the lateral plane of the membrane. Clustering of ICAM-1, using anti-ICAM-1 antibody-coated beads, efficiently and rapidly recruits ICAM-1. Using fluorescence recovery after photo-bleaching (FRAP, we found that clustering increased the immobile fraction of ICAM-1, compared to non-clustered ICAM-1. This shift required the intracellular portion of ICAM-1. Moreover, biochemical assays showed that ICAM-1 clustering recruited beta-actin and filamin. Cytochalasin B, which interferes with actin polymerization, delayed the clustering of ICAM-1. In addition, we could show that cytochalasin B decreased the immobile fraction of clustered ICAM-1-GFP, but had no effect on non-clustered ICAM-1. Also, the motor protein myosin-II is recruited to ICAM-1 adhesion sites and its inhibition increased the immobile fraction of both non-clustered and clustered ICAM-1. Finally, blocking Rac1 activation, the formation of lipid rafts, myosin-II activity or actin polymerization, but not Src, reduced the adhesive function of ICAM-1, tested under physiological flow conditions. CONCLUSIONS: Together, these findings indicate that ICAM-1 clustering is regulated in an inside-out fashion through the actin cytoskeleton. Overall

  1. Tanshinone IIA inhibits TNF-α-mediated induction of VCAM-1 but not ICAM-1 through the regulation of GATA-6 and IRF-1.

    Science.gov (United States)

    Nizamutdinova, Irina Tsoy; Kim, Young Min; Jin, Hana; Son, Kun Ho; Lee, Jae Heun; Chang, Ki Churl; Kim, Hye Jung

    2012-12-01

    The goal of this study was to investigate the differential effect of tanshinone IIA on the induction of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) by TNF-α and the possible molecular mechanisms by which it regulates ICAM-1 and VCAM-1 expression differentially. Stimulation of human umbilical vein endothelial cells (HUVEC) with TNF-α increased ICAM-1 and VCAM-1 expressions, and the pretreatment with tanshinone IIA concentration dependently inhibited VCAM-1 expression but not ICAM-1 expression. In previous study, PI3K/Akt, PKC and Jak/STAT-3 pathways were involved in the TNF-α-mediated induction of VCAM-1 but not ICAM-1. Thus, we examined the effect of tanshinone IIA on TNF-α-mediated activations of PI3K/Akt, PKC and Jak/STAT-3 pathways. Tanshinone IIA efficiently inhibited the phosphorylations of Akt, PKC and STAT-3 by TNF-α. Moreover, we determined the effect of tanshinone IIA on IRF-1 or GATAs induction and binding activity to VCAM-1 promoter since the upstream promoter region of VCAM-1 but not ICAM-1 contains IRF-1 and GATA binding motifs. Western blot analysis and ChIP assay showed that tanshinone IIA efficiently inhibited TNF-α-increased nuclear level of IRF-1 and GATA-6 and their binding affinity to VCAM-1 promoter region. Taken together, tanshinone IIA selectively inhibits TNF-α-mediated expression of VCAM-1 but not ICAM-1 through modulation of PI3/Akt, PKC and Jak/STAT-3 pathway as well as IRF-1 and GATA-6 binding activity.

  2. Polymorphisms of ICAM-1 are associated with gastric cancer risk and prognosis

    Institute of Scientific and Technical Information of China (English)

    Meng-Meng Tian; Yu Sun; Zhong-Wu Li; Ying Wu; Ai-Lian Zhao; Ji-You Li

    2012-01-01

    AIM: To investigate the association between single nucleotide polymorphisms (SNPs) in intercellular adhesion molecule-1 (ICAM-1) and the risk, biological behavior and prognosis of gastric cancer (GC) in Chinese population. METHODS: The study group consisted of 332 GC patients and 380 healthy controls. Genotyping was performed using polymerase chain reaction and the results were confirmed by sequencing. The association of ICAM-1 K469E polymorphisms and the risk of GC were studied, and the correlation of ICAM-1 K469E polymorphisms with the clinicopathological parameters and prognosis of the patients with complete clinical and follow-up data was analyzed.RESULTS: Carriers of AA genotype had a significantly increased risk of GC compared with carriers of AG and GG genotypes [odds ratios: 1.36; 95% confidence interval (CI): 1.01-1.84; P = 0.041]. GC patients with AA genotype were more prone to distant metastasis than those carrying AG and GG genotypes (18.9% vs 7.0%, respectively; P = 0.002). In addition, patients at stage Ⅳ had significantly more carriers of AA genotype than those of AG and GG genotype (27.4% vs 16.9%, respectively; P = 0.046). Follow-up study showed that the overall cumulative survival rate was 23.7% in AA genotype group and 42.9% in AG and GG genotypes group. In univariate analysis, AA genotype was correlated with the overall cumulative survival (P = 0.034). But in multivariate analysis, ICAM-1 polymorphism was not an independent prognostic factor for the overall survival (relative risk, 1.145; 95% CI: 0.851-1.540; P = 0.370). CONCLUSION: Polymorphisms of ICAM-1 K469E can be a useful biomarker for identifying individuals with higher risk of GC, predicting disease progression, and guiding individualized treatment.

  3. Expression of ICAM-1 and acute inflammatory cell infiltration in the early phase of radiation colitis in rats

    Energy Technology Data Exchange (ETDEWEB)

    Ikeda, Yuji; Ito, Masahiro; Matsuu, Mutsumi; Shichijo, Kazuko; Fukuda, Eiichiro; Nakayama, Toshiyuki; Nakashima, Masahiro; Naito, Shinji; Sekine, Ichiro [Nagasaki Univ. (Japan). Atomic Bomb Disease Inst.

    2000-09-01

    Inflammatory cell infiltration of the colon is observed at an early stage of radiation-induced colitis. The emigration of inflammatory cells from the circulation requires interactions between cell adhesion molecules on the vascular endothelium and molecules on the surface of leukocytes. To elucidate this process, the present work analyzes the kinetics of the expression of intercellular adhesion molecule-1 (ICAM-1) and the accumulation of inflammatory myeloperoxidase (MPO)-positive cells in relation to the appearance of acute radiation colitis prior to an overt radiation-induced ulcer. Colon tissues were obtained from Wistar Kyoto rats at various times after 22.5 Gy irradiation to the rectum. Histologically, crypt depletion and numerous inflammatory cells were observed 4 days after irradiation, and mucosal ulcer 6 days after irradiation. ICAM-1 immunopositivity was present in the endothelial cells of small vessels in the mucosa of both control and irradiated rats. ICAM-1 mRNA expression was detected in normal colon and irradiated colon by reverse transcription-PCR. In Northern blotting, ICAM-1 mRNA levels were found to increase markedly in the irradiated colon compared to the normal colon. In Western blotting, ICAM-1 protein expression also increased with a peak one day after irradiation, and remained elevated up to 6 days thereafter. The number of MPO-positive cells in lamina propria mucosa increased in a time-dependent fashion from 6 h to 6 days after irradiation. These data suggest that up-regulation of ICAM-1 in endothelial cells and accumulation of MPO positive cells play important roles in the development of radiation-induced colonic ulcer. (author)

  4. Psychological stress increases expression of aortic plaque intercellular adhesion molecule-1 and serum inflammatory cytokines in atherosclerotic rabbit model

    Institute of Scientific and Technical Information of China (English)

    Muwei Li; Xianpei Wang; Lei Yang; Chuanyu Gao; Yexin Ma

    2008-01-01

    Plaque rupture,platelet aggregation,and thrombogenesis are the main mechanisms of acute coronary syndrome (ACS),and inflammation factors play key roles in plaque unstability.Psychological stress promotes acute inflammatory response,leading to increased circulating levels of C-reactive protein (CRP),IL-6,and serum intercellular adhesion molecule (sICAM)-1.But it is not clear that whether psychological stress has a direct effect on atherosclerotic plaque stability.The purpose of this study was to investigate effects of chronic psychological stress on inflammatory marker (ICAM-1 ) in atherosclerotic plaque,and inflammatory markers in peripheral blood.Materials and methods Sixty male rabbits were randomized into 2 groups:the control group (n =10) and the atherosclerotic group (n =50).The latter were fed on high fatty diet and were given a large dose of vitamin D3 (3 600 000IU/kg) via intraperitoneal injection.After 8 weeks,the atherosclerotic model was estaslished.Then the 50 atherosclerotic model rabbits were divided into 3 subgroups:no-stress subgroup (n = 16),physiological stress subgroup (n = 16) and psychological stress subgroup (n =18).In physiological stress subgroup and psychological stress subgroup,drinking was cut from twice a day to once a day.At the same time,psychological stress subgroup was given empty bottle stress,and this process lasted for 2 weeks.One hour after the last stress,the blood samples were collected and the serum levels of CRP,IL-6 amd ICAM-1 were tested by radioimmunoassay or enzyme linked immunosorbent assay.The aorta and heart were extracted for pathology examination,and the express of ICAM-1 was tested by immunohistochemical examination.Results (1) After effective atherosclerotic animal model construction,the expression of ICAM-1 in aorta was higher in atherosclerotic group than that in control group (P<0.01),and was notably higher in psychological stress subgroup than that in no-stress subgroup or in physiological stress subgroup (2

  5. The structure of the two amino-terminal domains of human ICAM-1 suggests how it functions as a rhinovirus receptor and as an LFA-1 integrin ligand.

    Science.gov (United States)

    Bella, J; Kolatkar, P R; Marlor, C W; Greve, J M; Rossmann, M G

    1998-04-14

    The normal function of human intercellular adhesion molecule-1 (ICAM-1) is to provide adhesion between endothelial cells and leukocytes after injury or stress. ICAM-1 binds to leukocyte function-associated antigen (LFA-1) or macrophage-1 antigen (Mac-1). However, ICAM-1 is also used as a receptor by the major group of human rhinoviruses and is a catalyst for the subsequent viral uncoating during cell entry. The three-dimensional atomic structure of the two amino-terminal domains (D1 and D2) of ICAM-1 has been determined to 2.2-A resolution and fitted into a cryoelectron microscopy reconstruction of a rhinovirus-ICAM-1 complex. Rhinovirus attachment is confined to the BC, CD, DE, and FG loops of the amino-terminal Ig-like domain (D1) at the end distal to the cellular membrane. The loops are considerably different in structure to those of human ICAM-2 or murine ICAM-1, which do not bind rhinoviruses. There are extensive charge interactions between ICAM-1 and human rhinoviruses, which are mostly conserved in both major and minor receptor groups of rhinoviruses. The interaction of ICAMs with LFA-1 is known to be mediated by a divalent cation bound to the insertion (I)-domain on the alpha chain of LFA-1 and the carboxyl group of a conserved glutamic acid residue on ICAMs. Domain D1 has been docked with the known structure of the I-domain. The resultant model is consistent with mutational data and provides a structural framework for the adhesion between these molecules.

  6. Large-scale genomic studies reveal central role of ABO in sP-selectin and sICAM-1 levels

    Science.gov (United States)

    Barbalic, Maja; Dupuis, Josée; Dehghan, Abbas; Bis, Joshua C.; Hoogeveen, Ron C.; Schnabel, Renate B.; Nambi, Vijay; Bretler, Monique; Smith, Nicholas L.; Peters, Annette; Lu, Chen; Tracy, Russell P.; Aleksic, Nena; Heeriga, Jan; Keaney, John F.; Rice, Kenneth; Lip, Gregory Y.H.; Vasan, Ramachandran S.; Glazer, Nicole L.; Larson, Martin G.; Uitterlinden, Andre G.; Yamamoto, Jennifer; Durda, Peter; Haritunians, Talin; Psaty, Bruce M.; Boerwinkle, Eric; Hofman, Albert; Koenig, Wolfgang; Jenny, Nancy S.; Witteman, Jacqueline C.; Ballantyne, Christie; Benjamin, Emelia J.

    2010-01-01

    P-selectin and intercellular adhesion molecule-1 (ICAM-1) participate in inflammatory processes by promoting adhesion of leukocytes to vascular wall endothelium. Their soluble levels have been associated with adverse cardiovascular events. To identify loci affecting soluble levels of P-selectin (sP-selectin) and ICAM-1 (sICAM-1), we performed a genome-wide association study in a sample of 4115 (sP-selectin) and 9813 (sICAM-1) individuals of European ancestry as a part of The Cohorts for Heart and Aging Research in Genome Epidemiology consortium. The most significant SNP association for sP-selectin was within the SELP gene (rs6136, P = 4.05 × 10−61) and for sICAM-1 levels within the ICAM-1 gene (rs3093030, P = 3.53 × 10−23). Both sP-selectin and sICAM-1 were associated with ABO gene variants (rs579459, P = 1.86 × 10−41 and rs649129, P = 1.22 × 10−15, respectively) and in both cases the observed associations could be accounted for by the A1 allele of the ABO blood group. The absence of an association between ABO blood group and platelet-bound P-selectin levels in an independent subsample (N = 1088) from the ARIC study, suggests that the ABO blood group may influence cleavage of the P-selectin protein from the cell surface or clearance from the circulation, rather than its production and cellular presentation. These results provide new insights into adhesion molecule biology. PMID:20167578

  7. The experimental study of inhibitory effect on the rejection of rat cardiac allo graft and the expression of intercellular adhesion molecule-1 by mycophenolate mofetil%大鼠心脏移植排斥反应时细胞间粘附分子-1的表达及霉酚酸酯对其的抑制作用

    Institute of Scientific and Technical Information of China (English)

    龙刚; 王西墨; 陈实; 陈刚

    2001-01-01

    Objectives To investigate the expression of intercellular adhesion molecule-1 (ICAM-1) in heart tissues during the course of the rejection and the inhibitory effects of mycophenolate mofetil (MMF) on the rejection of cardiac allograft as well as the expression of ICAM-1.Methods The rat model of heterotopic cardiac allograft was developed. The rats were divided into following groups: control group of car diac isograft of Wistar to Wistar rats, group of cardiac allograft of SD to Wist ar rats and MMF-treated group of cardiac allograft. The grafts were collected t o receive immunohistochemical and histopathological examinations. Quantitative m easurement of ICAM-1 expression in the grafts was done with multimedia patholog y imaging analysis system.Results Faint ICAM-1 expression was observed both in the control group and MMF-treated groups. Also in the latter, rare infiltration of lymphocytes was found. Controv ersially, in the allotransplantation groups, capillary endothelial cells of the grafts strongly expressed ICAM-1 during the episode of rejection, which occurred two or three days earlier than the ordinary histological study. Conclusions The expression level of ICAM-1 was related t o the occurrence and development of rejection. MMF could reduce the expressi on of intercellular adhesion molecule and the infiltration of lymphocytes in the grafts obviously and prolong grafts survival greatly.%目的探讨大鼠同种异位心脏移植排斥反应期间移植心组织细胞间粘附分子-1(ICAM-1)的表达及霉酚酸酯(MMF)对移植心ICAM-1表达和排斥反应的抑制作用。方法建立大鼠心脏腹腔移植模型,设Wistar到Wistar大鼠的同系心脏移植对照组、SD大鼠到Wi s tar大鼠的同种移植组和同种移植MMF治疗组。采集移植心组织标本行免疫组织化学和组织病理学检查,应用多媒体彩色图文分析系统对移植心组织ICAM-1的表达进行定量检测。

  8. The in vitro effect of desflurane preconditioning on endothelial adhesion molecules and mRNA expression.

    Science.gov (United States)

    Biao, Zhu; Zhanggang, Xue; Hao, Jiang; Changhong, Miao; Jing, Cang

    2005-04-01

    Lower expression of intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), and E-selectin may be responsible for attenuated ischemic-reperfusion neutrophil adhesion to vascular endothelium. Desflurane reduces ischemia-reperfusion injury. Therefore, we assessed whether desflurane affects the protein expression of ICAM-1 and E-selectin and mRNA expression of ICAM-1 and VCAM-1 of human umbilical venous endothelial cells (HUVEC) stimulated with tumor necrosis factor-alpha (TNF-alpha). HUVEC were preconditioned for 60 min with 1 minimum alveolar concentration desflurane before stimulating with TNF-alpha. Protein expression of adhesion molecules ICAM-1 and E-selectin of HUVEC were evaluated via immunocytochemical techniques combined with image cytometry. ICAM-1 and VCAM-1 mRNA expression of HUVEC were determined via reverse transcription-polymerase chain reaction. Desflurane not only reduced the protein expression of ICAM-1 and E-selectin but also ICAM-1 and VCAM-1 mRNA expression of the HUVEC. The adhesion rate of neutrophils with desflurane-treated HUVEC was slower. The decreased neutrophil adhesion on the desflurane-treated HUVEC correlated well with the decrease in adhesion molecule expression. These results show that desflurane affects the expression of adhesion molecules involved in the multistep process of neutrophil recruitment. Desflurane related ischemia-reperfusion injury reduction correlates well with expression inhibition of ICAM-1, VCAM-1, and E-selectin that mediates neutrophil rotation and firm adhesion on the vascular endothelium.

  9. Novel association of ABO histo-blood group antigen with soluble ICAM-1: results of a genome-wide association study of 6,578 women.

    Directory of Open Access Journals (Sweden)

    Guillaume Paré

    2008-07-01

    Full Text Available While circulating levels of soluble Intercellular Adhesion Molecule 1 (sICAM-1 have been associated with diverse conditions including myocardial infarction, stroke, malaria, and diabetes, comprehensive analysis of the common genetic determinants of sICAM-1 is not available. In a genome-wide association study conducted among 6,578 participants in the Women's Genome Health Study, we find that three SNPs at the ICAM1 (19p13.2 locus (rs1799969, rs5498 and rs281437 are non-redundantly associated with plasma sICAM-1 concentrations at a genome-wide significance level (P<5x10(-8, thus extending prior results from linkage and candidate gene studies. We also find that a single SNP (rs507666, P = 5.1x10(-29 at the ABO (9q34.2 locus is highly correlated with sICAM-1 concentrations. The novel association at the ABO locus provides evidence for a previously unknown regulatory role of histo-blood group antigens in inflammatory adhesion processes.

  10. Relationship between the expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 on lymphocytes and cardiac function in elderly patients with chronic heart failure%老年慢性心力衰竭患者淋巴细胞细胞间黏附分子-1、血管细胞间黏附分子-1的表达及与心功能的关系探讨

    Institute of Scientific and Technical Information of China (English)

    孟松艳; 于卫刚; 张一娜; 杨奕; 裴丽春

    2015-01-01

    目的:探讨老年慢性心力衰竭(简称心衰)患者淋巴细胞细胞间黏附分子-1(ICAM-1)、血管细胞间黏附分子-1(VCAM-1)水平与血红蛋白(Hb)的关系及与心室重构、心功能的关系。方法对入选的76例老年慢性心衰患者(心衰组)行实验室和超声心动图检查,按 Hb水平又分为贫血组(27例)和非贫血组(49例);并进行心功能分级。同时选择25例同期健康体检老年人为对照组,比较各组间淋巴细胞 ICAM-1、VCAM-1、Hb 、左室射血分数(LVEF)、左心室质量指数(LVMI)和平均室壁应力(MWS)。结果与对照组比较,心衰组患者 ICAM-1、VCAM-1和LVMI、MWS 明显升高,Hb 和 LVEF 降低(P <0.01),随着心功能恶化,淋巴细胞 ICAM-1和 VCAM-1的水平以及 LVMI 和 MWS 逐渐升高,而 Hb 水平则逐渐降低;心衰贫血组患者淋巴细胞 ICAM-1和VCAM-1的水平以及 LVMI 和 MWS 明显高于非贫血组(P <0.05);心衰患者淋巴细胞 ICAM-1和VCAM-1的水平与 LVMI 和 MWS 均呈正相关(P <0.01)。结论心衰患者淋巴细胞 ICAM-1和VCAM-1水平升高和 Hb 水平的降低参与了心功能不全、心室重构发生发展的病理生理过程。%Objective To study the change of intercellular adhesion molecule-1 (ICAM-1)and vascular cell adhesion molecule-1(VCAM-1)and the possible association between ICAM-1,VCAM-1 and hemoglobin(Hb),and their effects on left ventricular mass index(LVMI),mean wall stress(MWS)and cardiac function in elderly patients with chronic heart failure (CHF).Methods 76 inpatients with chronic cardiac failure were selected in the study.The patients were classified with NYHA-class,and were divided into anemia group and non-anemia group according to hemoglobin (Hb)level.25 healthy old persons were selected as control group.Levels of ICAM-1,VCAM-1,and Hb were measured.Left ventricu-lar ejection fraction(LVEF)was determined by echocardiography

  11. CXCL1-Triggered Interaction of LFA1 and ICAM1 Control Glucose-Induced Leukocyte Recruitment during Inflammation In Vivo

    Directory of Open Access Journals (Sweden)

    Kirsten Buschmann

    2012-01-01

    Full Text Available It is well acknowledged that proinflammatory stimulation during acute hyperglycemia is able to aggravate inflammatory diseases. However, the mechanisms of proinflammatory effects of glucose are controversially discussed. We investigated leukocyte recruitment after intravenous injection of glucose in different inflammatory models using intravital microscopy. Flow chamber experiments, expression analysis, functional depletion, and knockout of key adhesion molecules gave mechanistic insight in involved pathways. We demonstrated that a single injection of glucose rapidly increased blood glucose levels in a dose-dependent manner. Notably, during tumor necrosis factor (TNF α-induced inflammation leukocyte recruitment was not further enhanced by glucose administration, whereas glucose injection profoundly augmented leukocyte adhesion and transmigration into inflamed tissue in the trauma model, indicating that proinflammatory properties of glucose are stimulus dependent. Experiments with functional or genetic inhibition of the chemokine receptor CXCR2, intercellular adhesion molecule 1 (ICAM1, and lymphocyte function antigen 1 (LFA1 suggest that keratino-derived-chemokine CXCL1-triggered interactions of ICAM1 and LFA1 are crucially involved in the trauma model of inflammation. The lacking effect of glucose on β2 integrin expression and on leukocyte adhesion in dynamic flow chamber experiments argues against leukocyte-driven underlying mechanisms and favours an endothelial pathway since endothelial ICAM1 expression was significantly upregulated in response to glucose.

  12. Astragalus polysaccharides suppress ICAM-1 and VCAM-1 expression in TNF-α-treated human vascular endothelial cells by blocking NF-KB activation

    Institute of Scientific and Technical Information of China (English)

    Yu-ping ZHU; Tao SHEN; Ya-jun LIN; Bei-dong CHEN; Yang RUAN; Yuan CAO; Yue QIAO

    2013-01-01

    Aim:To investigate the effects ofAstragalus polysaccharides (APS) on tumor necrosis factor (TNF)-α-induced inflammatory reactions in human umbilical vein endothelial cells (HUVECs) and to elucidate the underlying mechanisms.Methods:HUVECs were treated with TNF-α for 24 h.The amounts of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1(VCAM-1) were determined with Western blotting.HUVEC viability and apoptosis were detected using cell viability assay and Hoechst staining,respectively.Reactive oxygen species (ROS) production was measured by DHE staining.Monocyte and HUVEC adhesion assay was used to detect endothelial cell adhesive function.NF-KB activation was detected with immunofluorescence.Results:TNF-α (1-80 ng/mL) caused dose-and time-dependent increases of ICAM-1 and VCAM-1 expression in HUVECs,accompanied by significant augmentation of IKB phosphorylation and NF-KB translocation into the nuclei.Pretreatment with APS (10 and 50 μg/mL)significantly attenuated TNFα-induced upregulation of ICAM-1,VCAM-1,and NF-KB translocation.Moreover,APS significantly reduced apoptosis,ROS generation and adhesion function damage in TNF-α-treated HUVECs.Conclusion:APS suppresses TNFα-induced adhesion molecule expression by blocking NF-KB signaling and inhibiting ROS generation in HUVECs.The results suggest that APS may be used to treat and prevent endothelial cell injury-related diseases.

  13. Characterization of rat lung ICAM-1

    DEFF Research Database (Denmark)

    Beck-Schimmer, B; Schimmer, R C; Schmal, H;

    1998-01-01

    OBJECTIVE AND DESIGN: We expressed soluble rat ICAM-1, generated a polyclonal anti-ICAM-1 antibody, and studied ICAM-1 upregulation in lung inflammatory conditions. Bacterial and baculovirus expression systems were employed. MATERIAL: 250 g adult, male Long Evans rats were used. For in vitro stud...

  14. Squamosamide derivative FLZ inhibits TNF-α-induced ICAM-1 expression via down-regulation of the NF-κB signaling pathway in ARPE-19 cells.

    Science.gov (United States)

    Feng, Ting-Ting; Liang, Ze-Yu; Chen, Song

    2015-01-01

    Dysfunction of the retinal pigment epithelium (RPE) resulting from chronic inflammation is implicated in the pathogenesis of age-related macular degeneration (AMD). It has been reported that tumor necrosis factor-α (TNF-α) could induce intercellular adhesion molecule-1 (ICAM-1) expression in RPE cells. FLZ, a novel synthetic squamosamide derivative from a Chinese herb, Annona glabra, has displayed significant anti-inflammatory activity. However, the effects of FLZ on TNF-α-induced ICAM-1 expression in RPE cells remain unknown. Therefore, in the present study, we evaluated the effects of FLZ on TNF-α-induced ICAM-1 expression in RPE cells. We found that FLZ prevented TNF-α-induced ICAM-1 expression and the ability of monocytes to adhere to ARPE-19 cells induced by TNF-α. Furthermore, FLZ inhibited TNF-α-induced NF-κB p65 expression, as well as phosphorylation of IκBα in ARPE-19 cells. Taken together, these results suggest that FLZ inhibited TNF-α-induced ICAM-1 expression through blocking NF-κB signaling pathway in ARPE-19 cells. Thus, FLZ could be used for designing novel therapeutic agents against AMD.

  15. Fumaric Acid Esters Do Not Reduce Inflammatory NF-κB/p65 Nuclear Translocation, ICAM-1 Expression and T-Cell Adhesiveness of Human Brain Microvascular Endothelial Cells.

    Science.gov (United States)

    Haarmann, Axel; Nehen, Mathias; Deiß, Annika; Buttmann, Mathias

    2015-08-13

    Dimethyl fumarate (DMF) is approved for disease-modifying treatment of patients with relapsing-remitting multiple sclerosis. Animal experiments suggested that part of its therapeutic effect is due to a reduction of T-cell infiltration of the central nervous system (CNS) by uncertain mechanisms. Here we evaluated whether DMF and its primary metabolite monomethyl fumarate (MMF) modulate pro-inflammatory intracellular signaling and T-cell adhesiveness of nonimmortalized single donor human brain microvascular endothelial cells at low passages. Neither DMF nor MMF at concentrations of 10 or 50 µM blocked the IL-1β-induced nuclear translocation of NF-κB/p65, whereas the higher concentration of DMF inhibited the nuclear entry of p65 in human umbilical vein endothelium cultured in parallel. DMF and MMF also did not alter the IL-1β-stimulated activation of p38 MAPK in brain endothelium. Furthermore, neither DMF nor MMF reduced the basal or IL-1β-inducible expression of ICAM-1. In accordance, both fumaric acid esters did not reduce the adhesion of activated Jurkat T cells to brain endothelium under basal or inflammatory conditions. Therefore, brain endothelial cells probably do not directly mediate a potential blocking effect of fumaric acid esters on the inflammatory infiltration of the CNS by T cells.

  16. Fumaric Acid Esters Do Not Reduce Inflammatory NF-κB/p65 Nuclear Translocation, ICAM-1 Expression and T-Cell Adhesiveness of Human Brain Microvascular Endothelial Cells

    Directory of Open Access Journals (Sweden)

    Axel Haarmann

    2015-08-01

    Full Text Available Dimethyl fumarate (DMF is approved for disease-modifying treatment of patients with relapsing-remitting multiple sclerosis. Animal experiments suggested that part of its therapeutic effect is due to a reduction of T-cell infiltration of the central nervous system (CNS by uncertain mechanisms. Here we evaluated whether DMF and its primary metabolite monomethyl fumarate (MMF modulate pro-inflammatory intracellular signaling and T-cell adhesiveness of nonimmortalized single donor human brain microvascular endothelial cells at low passages. Neither DMF nor MMF at concentrations of 10 or 50 µM blocked the IL-1β-induced nuclear translocation of NF-κB/p65, whereas the higher concentration of DMF inhibited the nuclear entry of p65 in human umbilical vein endothelium cultured in parallel. DMF and MMF also did not alter the IL-1β-stimulated activation of p38 MAPK in brain endothelium. Furthermore, neither DMF nor MMF reduced the basal or IL-1β-inducible expression of ICAM-1. In accordance, both fumaric acid esters did not reduce the adhesion of activated Jurkat T cells to brain endothelium under basal or inflammatory conditions. Therefore, brain endothelial cells probably do not directly mediate a potential blocking effect of fumaric acid esters on the inflammatory infiltration of the CNS by T cells.

  17. VCAM1 and ICAM1 expression in oral lichen planus.

    Science.gov (United States)

    Seyedmajidi, Maryam; Shafaee, Shahryar; Bijani, Ali; Bagheri, Soodabeh

    2013-01-01

    Oral lichen planus is a chronic inflammatory immune-mediated disease. ICAM-1 and VCAM-1 are vascular adhesion molecules that their receptors are located on endothelial cells and leukocytes. The aim of this study is the immunohistochemical evaluation of VCAM1 and ICAM1 in oral lichen planus and to compare these two markers with normal mucosa for evaluation of angiogenesis. This descriptive-analytical study was performed on 70 paraffined blocks of oral lichen planus and 30 normal mucosa samples taken from around the lesions. Samples were stained with H & E and then with Immunohistochemistry using monoclonal mouse anti human VCAM1 (CD106), & monoclonal mouse anti human ICAM1(CD54) for confirmation of diagnosis. Slides were evaluated under light microscope and VCAM1 and ICAM1 positive cells (endothelial cells and leukocytes) were counted. Data were analyzed with Mann-Whitney test, Wilcoxon and Chi-Square and plichen planus according to the percentage of stained cells (p=0.000& p=0.000, Mann-Whitney test). Thirty cases of oral normal mucosa associated with lichen planus showed that the VCAM1 has increased significantly in comparison to normal mucosa (plichen planus and normal mucosa, showed a significantly difference (plichen planus was not observed (p>0.05). Regarding the results, it seems that high expression of VCAM1 and ICAM1 is related to oral lichen planus.

  18. Inside-Out Regulation of ICAM-1 Dynamics in TNF-alpha-Activated Endothelium

    NARCIS (Netherlands)

    van Buul, J.D.; van Rijssel, J.; van Alphen, F.P.J.; Hoogenboezem, M.; Tol, S.; Hoeben, K.A.; van Marle, J.; Mul, E.P.J.; Hordijk, P.L.

    2010-01-01

    Background: During transendothelial migration, leukocytes use adhesion molecules, such as ICAM-1, to adhere to the endothelium. ICAM-1 is a dynamic molecule that is localized in the apical membrane of the endothelium and clusters upon binding to leukocytes. However, not much is known about the regul

  19. 粘附分子sICAM-1,sVCAM-1,sCD44在高白细胞急性髓系白血病中的表达%Clinical Significance of Cell Adhesion Molecules sICAM-1, sVCAM-1 and sCD44 Expressions in Hyperleukocytic AML

    Institute of Scientific and Technical Information of China (English)

    杨琦; 郑雪晨; 黄涛生; 臧婷婷; 王占聚

    2014-01-01

    目的探讨高白细胞急性髓系白血病(hyperleukocytic acute myeloid leukemia,HAML)患者治疗前后血清可溶性细胞间粘附分子-1(sICAM-1)、可溶性血管细胞粘附分子(sVCAM-1)和可溶性CD44分子(sCD44)的表达水平及其临床意义。方法采用酶联免疫吸附实验(ELISA),对15例初诊高白细胞急性髓系白血病(WBC>100×109/L)和40例非高白细胞急性髓系白血病(non-hyperleukocytic acute myeloid leukemia,NHAML)(WBC100í109/L) and 40 patients with non-hyperleukocytic acute myeloid leukemia (NHAML, WBC<100í109/L) before and after treatment the serum sICAM-1, sVCAM-1 and sCD44 levels, and compared with the normal people. Results ①Before chemotherapy, NAML and NHAML patient serum sICAM-1, sVCAM-1 and sCD44 levels were significantly higher than those in the control group, the difference has statistical significance. After chemotherapy, in the two groups to achieve remission of bone marrow sICAM-1, sVCAM-1 and sCD44 levels decreased, compared with before treatment was statistical y significant; Compared with the control group, no significant difference. ②Before chemotherapy, HAML patients serum sICAM-1, sVCAM-1 and sCD44 levels were significantly higher than those in NHAML patients with serum sICAM-1, sVCAM-1 and sCD44 level ( <0. 05), HAML patients remission rate (40%) was lower than NHAML patients remission rate (72.5%)( <0.05). Conclusion For patients with HAML, detection of serum sICAM-1, sVCAM-1 and sCD44 levels, help to guide the clinical treatment, provides valuable clinical indicators for monitoring, curative effect observation and prognosis.

  20. Association of serum soluble intercellular cell adhesion molecule-1, soluble vascular cell adhesion molecule-1 and hypersensitivity-CRP levels with peripheral vascular disease of lower limbs in patients with type 2 diabetes mellitus%2型糖尿病患者血清可溶性细胞间和血管细胞黏附分子1及CRP与下肢血管病变的关系

    Institute of Scientific and Technical Information of China (English)

    谭擎缨; 王静; 阮芸; 阮勇; 王秀景; 姚佳琦; 姚乐燕

    2013-01-01

    Objective To investigate the association of serum levels of soluble intercellular cell adhesion molecule-1 (sICAM-1),soluble vascular cell adhesion molecule-1 (sVCAM-1) and high sensitivity C-reactive protein (hs-CRP) with peripheral vascular disease of lower limbs in patients with type 2 diabetes mellitus (T2DM).Methods One hundred and thirty T2DM patients admitted from October 2011 to October 2012,and 30 age/sex-matched healthy subjects were enrolled in the study.The serum levels of sICAM-1,sVCAM-1,hs-CRP and other clinical parameters were measured; the peripheral blood vessels of lower limbs were examined with color Doppler ultrasonography.Based on the extent of angiopathy of lower limbs T2DM patients were classified as normal vascular group (n =26),mild angiopathy group (n =45),moderate/severe angiopathy group (n =59).Results The serum levels of sICAM-1 and sVCAM-1 in moderate/ severe angiopathy group of T2DM patients were higher than those in mild angiopathy group,normal vascular group and healthy controls (t:4.15-8.93,all P <0.05) ; the serum levels of hs-CRP in moderate/severe angiopathy group were higher than those in mild angiopathy group,normal vascular group and healthy controls (t:2.18-4.27,all P < 0.05).The serum sICAM-1 level was positively correlated with total cholesterol (TC),low density lipoprotein cholesterol (LDL-C) and sVCAM-1.The serum sVCAM-1 level was positively correlated with course of disease,systolic blood pressure and CRP.Conclusions Serum levels of sICAM-1,sVCAM-1 and hs-CRP are correlated with the extent of angiopathy of lower limbs in T2DM patients,and the elevated sICAM-1 ; sVCAM-1 and hs-CRP levels are also associated with hyper blood pressure,dislipidemia and chronic inflammation.%目的 探讨2型糖尿病患者血清可溶性细胞间黏附分子1(sICAM-1)、血管细胞黏附分子1(sVCAM-1)及高敏CRP(hsCRP)水平与下肢大血管病变程度的关系.方法 对130例2型糖尿病患者(糖尿病组)与30例年龄匹配

  1. Platelet Endothelial Cell Adhesion Molecule 1 (PECAM-1/CD31): A Multifunctional Vascular Cell Adhesion Molecule.

    Science.gov (United States)

    Delisser, H M; Baldwin, H S; Albelda, S M

    1997-08-01

    PECAM-1/CD31 is a member of the immunoglobulin gene superfamily found on platelets, leukocytes, and endothelial cells, where it concentrates at cell-cell borders. It has been shown to both mediate cell-cell adhesion through homophilic and heterophilic interactions and to transduce intracellular signals that upregulate the function of integrins on leukocytes. Its cellular distribution and ability to mediate adhesive and signaling phenomena suggested that PECAM-1 was a multifunctional vascular cell adhesion molecule involved in leukocyte-endothelial and endothelial-endothelial interactions. These initial suggestions have been largely confirmed as recent studies have implicated PECAM-1 in the inflammatory process and in the formation of blood vessels. As our understanding of the molecular and functional properties of PECAM-1 grows, new insights will be gained that may have therapeutic implications for cardiovascular development and disease. (Trends Cardiovasc Med 1997;7:203-210). © 1997, Elsevier Science Inc.

  2. Cell adhesion molecules and hyaluronic acid as markers of inflammation, fibrosis and response to antiviral therapy in chronic hepatitis C patients

    Directory of Open Access Journals (Sweden)

    Esther Granot

    2001-01-01

    Full Text Available Objective: Cell adhesion molecules (intracellular adhesion molecule-1 (ICAM-1, vascular cell adhesion molecule-1 (VCAM-1 and hyaluronic acid, markers of inflammation and fibrosis were monitored in hepatitis C patients to determine whether changes in plasma levels, during antiviral treatment, can predict long-term response to therapy.

  3. Variation in the ICAM1 gene is not associated with severe malaria phenotypes

    OpenAIRE

    Fry, Andrew E.; Auburn, Sarah; Diakite, Mahamadou; Green, Angela; Richardson, Anna; Wilson, Jonathan; Jallow, Muminatou; Sisay-Joof, Fatou; Pinder, Margaret; Griffiths, Michael J.; Peshu, Norbert; Williams, Thomas N.; Marsh, Kevin; Malcolm E Molyneux; Taylor, Terrie E.

    2008-01-01

    Evidence from autopsy, mouse-model and in vitro binding studies suggests that adhesion of erythrocytes infected with Plasmodium falciparum to the human host intercellular adhesion molecule (ICAM)-1 receptor is important in the pathogenesis of severe malaria. Previous association studies between polymorphisms around the ICAM1 gene and susceptibility to severe malarial phenotypes have been inconclusive and often contradictory. We performed genetic association studies with 15 single-nucleotide-p...

  4. Antidiabetic Rosiglitazone Reduces Soluble Intercellular Adhesion Molecule-1 Level in Type 2 Diabetic Patients with Coronary Artery Disease

    Directory of Open Access Journals (Sweden)

    Guang Wang

    2008-01-01

    Full Text Available Background. We investigated the level of soluble adhesion molecules in diabetic patients and the effect of the peroxisome proliferator-activated receptor-γ (PPAR-γ agonist rosiglitazone on plasma levels of adhesion molecules and an inflammation marker in type 2 diabetic patients with coronary artery disease (CAD after percutaneous coronary intervention (PCI. Methods. A total of 116 diabetic patients with CAD who had undergone PCI were randomized to receive rosiglitazone (4 mg/d or not for 6 months. Plasma levels of soluble intercellular adhesion molecules (sICAM-1 and P-selectin (sP-selectin were measured on ELISA. Results. After 6-month rosiglitazone treatment, plasma levels of sICAM-1 were lower than baseline and control group levels (370.4 (332.4–421.9 pg/mL versus 423.5 (327.4–500.3 pg/mL and 404.6 (345.2–483.4 pg/mL, P<.001. In addition, plasma levels of C-reactive protein were significantly reduced from baseline levels. However, plasma level of sP-selectin was not significantly lowered with rosiglitazone treatment than with control treatment after 6-month follow-up. Conclusions. Rosiglitazone reduces chronic inflammatory responses and improves levels of markers of endothelial dysfunction in patients with diabetes and CAD. PPAR-γ agonist may have a beneficial effect on the vascular endothelium through its anti-inflammatory mechanism and may be useful as therapy in patients undergoing PCI.

  5. Tumour Necrosis Factor α Enhances CCL2 and ICAM-1 Expression in Peripheral Nerve Microvascular Endoneurial Endothelial Cells

    Directory of Open Access Journals (Sweden)

    Kelly A. Langert

    2013-01-01

    Full Text Available Recruitment and trafficking of autoreactive leucocytes across the BNB (blood–nerve barrier is an early pathological insult in GBS (Guillain-Barré syndrome, an aggressive autoimmune disorder of the PNS (peripheral nervous system. Whereas the aetiology and pathogenesis of GBS remain unclear, pro-inflammatory cytokines, including TNFα (tumour necrosis factor α, are reported to be elevated early in the course of GBS and may initiate nerve injury by activating the BNB. Previously, we reported that disrupting leucocyte trafficking in vivo therapeutically attenuates the course of an established animal model of GBS. Here, PNMECs (peripheral nerve microvascular endothelial cells that form the BNB were harvested from rat sciatic nerves, immortalized by SV40 (simian virus 40 large T antigen transduction and subsequently challenged with TNFα. Relative changes in CCL2 (chemokine ligand 2 and ICAM-1 (intercellular adhesion molecule 1 expression were determined. We report that TNFα elicits marked dose- and time-dependent increases in CCL2 and ICAM-1 mRNA and protein content and promotes secretion of functional CCL2 from immortalized and primary PNMEC cultures. TNFα-mediated secretion of CCL2 promotes, in vitro, the transendothelial migration of CCR2-expressing THP-1 monocytes. Increased CCL2 and ICAM-1 expression in response to TNFα may facilitate recruitment and trafficking of autoreactive leucocytes across the BNB in autoimmune disorders, including GBS.

  6. Aluminum excytotoxicity and neuroautotoimmunity: the role of the brain expression of CD32+ (FcγRIIa), ICAM-1+ and CD3ξ in aging.

    Science.gov (United States)

    Jovanova-Nesic, Katica; Shoenfeld, Yehuda; Spector, Novera Herbert

    2012-12-01

    In the central nervous system (CNS) microglia are crucial for the defense of the brain against invading microorganisms, formation of tumors, and damage following trauma. However, uncontrolled activation of these cells may have deleterious outcomes through activation of Fcγ and the complement 3 receptors and the induction of an adaptive immune reaction. Proteins contributing to this reaction are the intercellular adhesion molecule-1 (ICAM-1) and CD3 molecules, among others. Both can be expressed on the glia cells before cytokine release and may facilitate an autoimmune inflammatory reaction in the brain. Round microglial cells among the pyramidal cells of the hippocampus with increased expression of CD32+ (FcγIIa) and near the site of injection of aluminum were detected immunohistochemically and indicate microglial activation at the site of aluminum injury. ICAM-1+ immunoreactivity significantly increased in the hippocampus and in the choroids plexus, indicating increased inflammation in the brain as well as increased CD3ξ+ expression in the hippocampus and non-MHC-restricted T cytotoxicity after aluminum injection. The pattern of expression of CD32+ (FcγIIa receptor) near the site of aluminum injection indicates that microglia may play a phagocytic role at the site of aluminum-induced excitotoxicity in the brain. Significant expression of ICAM-1+ and CD3ξ+ immunoreactive cells with the clusters of ICAM-1+ in the choroid plexus suggests a consequently neurotoxic autoimmune reaction induced by microglial hyperactivation in the injured brain.

  7. Association between functional variants of the ICAM1 and CRP genes and metabolic syndrome in Taiwanese subjects.

    Science.gov (United States)

    Hsu, Lung-An; Chang, Chi-Jen; Wu, Semon; Teng, Ming-Sheng; Chou, Hsin-Hua; Chang, Hsien-Hsun; Chang, Pi-Yueh; Ko, Yu-Lin

    2010-12-01

    Although inflammation has been shown to play an important role in metabolic syndrome (MetS), the association between inflammatory marker gene polymorphisms and the risk of MetS has not been fully elucidated. This study was initiated to investigate the association between functional variants of inflammatory marker genes and the risk of MetS in Taiwanese adults. The sample population comprised 615 unrelated subjects, of which 22% had MetS. The single nucleotide polymorphisms rs5491 on the intercellular adhesive molecule 1 (ICAM1) gene and rs3091244 on C-reactive protein (CRP) were genotyped. The ICAM1 rs5491 polymorphism was significantly associated with the level of soluble intercellular adhesive molecule 1 (P gene polymorphisms play an important role in modulating the risk of insulin resistance and MetS for subjects with central obesity. These findings will contribute toward a better understanding of the mechanism of association between inflammatory markers and the risk of developing atherosclerotic disease.

  8. Testicular cell adhesion molecule 1 (TCAM1) is not essential for fertility

    Science.gov (United States)

    Nalam, Roopa L.; Lin, Yi-Nan; Matzuk, Martin M.

    2009-01-01

    Testicular cell adhesion molecule 1 (Tcam1) is a testis-expressed gene that is evolutionarily conserved in most mammalian species. The putative location of TCAM1 on the cell surface makes it an attractive contraceptive target to study. We found that Tcam1 transcription is enriched in the adult testis, and in situ hybridization revealed that Tcam1 is expressed in pachytene to secondary spermatocytes. Immunofluorescence for TCAM1 protein showed strong expression along cell membranes of spermatocytes and weak localization to round spermatids. In light of this evidence, we hypothesized that TCAM1 interacts with an unknown receptor on the surface of Sertoli cells and that this interaction is important for germ cell-Sertoli cell interactions. However, Tcam1 knockout mice that we generated are fertile, and testis weights and sperm counts were not significantly altered. Therefore, we conclude that TCAM1 is not essential for male fertility or germ cell function in Mus musculus. PMID:19766163

  9. Ba-Wei-Di-Huang-Wan through its active ingredient loganin counteracts substance P-enhanced NF-κB/ICAM-1 signaling in rats with bladder hyperactivity.

    Science.gov (United States)

    Tsai, Wen-Hsin; Wu, Chung-Hsin; Cheng, Chen-Hung; Chien, Chiang-Ting

    2016-09-01

    Overt bladder afferent activation may exacerbate endogenous substance P (SP) release to induce intercellular adhesion molecule-1 (ICAM-1)-mediated inflammation and reactive oxygen species (ROS) production leading to hyperactive bladder. Ba-Wei-Die-Huang-Wan (BWDHW), a traditional Chinese medicine, has been used to treat lower urinary tract symptoms in patients by undefined mechanisms. We explored the possible mechanisms and the active components of BWDHW on exogenous SP-induced bladder hyperactivity. BWDHW contained six major components: loganin, paeoniflorin, 5-hydroxymethylfurfural, cinnamic acid, cinnamaldehyde, and paeonol by high-performance liquid chromatography. In urethane-anesthetized female Wistar rats, we evaluated transcystometrogram, pelvic afferent nerve activity by electrophysiologic recording techniques, ICAM-1 expression by Western blot and immunohistochemistry, ROS amount by an ultrasensitive chemiluminescence method and possible ROS sources from the different leukocytes by specific stains in SP-treated bladder. BWDHW and its major component loganin dose-dependently inhibited H2 O2 and HOCl activity in vitro. Intragastrical BWDHW (250 mg/kg) and loganin (5 mg/kg) twice daily for 2 weeks did not affect the baseline micturition parameters. Intra-arterial SP (20 µg/rat) through neurokinin-1 receptor activation increased voiding frequency (shortened intercontraction intervals), pelvic afferent nerve activity, bladder NF-κB/ICAM-1 expression, bladder ROS amount, neutrophils adhesion to venous endothelium, CD68 (monocyte/macrophage), and mast cell infiltration in the inflamed bladder. BWDHW and loganin pretreatment significantly depressed SP-enhanced pelvic afferent nerve activity, bladder NF-κB/ICAM-1 expression, leukocyte infiltration, and ROS amount, and subsequently improved bladder hyperactivity. In conclusion, our results suggest that BWDHW and its active component loganin improves bladder hyperactivity via inhibiting SP/neurokinin-1

  10. Upregulation of Intercellular Adhesion Molecule 1 and Proinflammatory Cytokines by the Major Surface Proteins of Treponema maltophilum and Treponema lecithinolyticum, the Phylogenetic Group IV Oral Spirochetes Associated with Periodontitis and Endodontic Infections

    Science.gov (United States)

    Lee, Sung-Hoon; Kim, Kack-Kyun; Choi, Bong-Kyu

    2005-01-01

    Treponema maltophilum and Treponema lecithinolyticum belong to the group IV oral spirochetes and are associated with endodontic infections, as well as periodontitis. Recently, the genes encoding the major surface proteins (Msps) of these bacteria (MspA and MspTL, respectively) were cloned and sequenced. The amino acid sequences of these proteins showed significant similarity. In this study we analyzed the functional role of these homologous proteins in human monocytic THP-1 cells and primary cultured periodontal ligament (PDL) cells using recombinant proteins. The complete genes encoding MspA and MspTL without the signal sequence were cloned into Escherichia coli by using the expression vector pQE-30. Fusion proteins tagged with N-terminal hexahistidine (recombinant MspA [rMspA] and rMspTL) were obtained, and any possible contamination of the recombinant proteins with E. coli endotoxin was removed by using polymyxin B-agarose. Flow cytometry showed that rMspA and rMspTL upregulated the expression of intercellular adhesion molecule 1 (ICAM-1) in both THP-1 and PDL cells. Expression of proinflammatory cytokines, such as interleukin-6 (IL-6) and IL-8, was also induced significantly in both cell types by the Msps, as determined by reverse transcription-PCR and an enzyme-linked immunosorbent assay, whereas IL-1β synthesis could be detected only in the THP-1 cells. The upregulation of ICAM-1, IL-6, and IL-8 was completely inhibited by pretreating the cells with an NF-κB activation inhibitor, l-1-tosylamido-2-phenylethyl chloromethyl ketone. This suggests involvement of NF-κB activation. The increased ICAM-1 and IL-8 expression in the THP-1 cells obtained with rMsps was not inhibited in the presence of the IL-1 receptor antagonist (IL-1ra), a natural inhibitor of IL-1. Our results show that the Msps of the group IV oral spirochetes may play an important role in amplifying the local immune response by continuous inflammatory cell recruitment and retention at an

  11. SIRT1在内皮细胞中抑制PMA和ionomycin诱导的ICAM-1的表达

    Institute of Scientific and Technical Information of China (English)

    贾玉艳; 高鹏; 陈厚早; 万言珍; 张然; 张祝琴; 杨瑞锋; 王旭; 徐静; 刘德培

    2013-01-01

    白细胞在内皮中的富集能够引起炎症并触发动脉粥样硬化,intercellular adhesion molecule-1ICAM-1)在该过程中发挥了重要作用.本实验室先前研究显示,内皮特异过表达Ⅲ类组蛋白去乙酰化酶SIRT1能够抑制动脉粥样硬化.因此,提出这样的假设:SIRT1能够抑制内皮细胞中ICAM-1的表达.实验发现,PMA和ionomycin(PMA/Io)能够在人脐静脉内皮细胞(HUVECs)中明显诱导SIRT1和ICAM-1的表达.而且,腺病毒介导的SIRT1过表达在HUVECs中能显著抑制PMA/Io诱导的ICAM-1的表达,而敲低SIRT1的表达则导致ICAM-1表达上调.双荧光素酶报告基因分析表明,过表达SIRT1抑制基础水平和PMA/Io诱导下的ICAM-1的启动子活性.进一步通过染色质免疫共沉淀(ChIP)实验发现,SIRT1参与转录复合物结合在ICAM-1启动子区,而且SIRT1的干扰能够提高NF-κB的亚基p65结合到ICAM-1启动子区的能力.总之,这些数据提示,SIRT1在内皮细胞中抑制ICAM-1表达的作用可能有助于其对抗动脉粥样硬化的发生.

  12. Effect of Cell Adhesion Molecule 1 Expression on Intracellular Granule Movement in Pancreatic α Cells.

    Science.gov (United States)

    Yokawa, Satoru; Furuno, Tadahide; Suzuki, Takahiro; Inoh, Yoshikazu; Suzuki, Ryo; Hirashima, Naohide

    2016-09-01

    Although glucagon secreted from pancreatic α cells plays a role in increasing glucose concentrations in serum, the mechanism regulating glucagon secretion from α cells remains unclear. Cell adhesion molecule 1 (CADM1), identified as an adhesion molecule in α cells, has been reported not only to communicate among α cells and between nerve fibers, but also to prevent excessive glucagon secretion from α cells. Here, we investigated the effect of CADM1 expression on the movement of intracellular secretory granules in α cells because the granule transport is an important step in secretion. Spinning disk microscopic analysis showed that granules moved at a mean velocity of 0.236 ± 0.010 μm/s in the mouse α cell line αTC6 that expressed CADM1 endogenously. The mean velocity was significantly decreased in CADM1-knockdown (KD) cells (mean velocity: 0.190 ± 0.016 μm/s). The velocity of granule movement decreased greatly in αTC6 cells treated with the microtubule-depolymerizing reagent nocodazole, but not in αTC6 cells treated with the actin-depolymerizing reagent cytochalasin D. No difference in the mean velocity was observed between αTC6 and CADM1-KD cells treated with nocodazole. These results suggest that intracellular granules in pancreatic α cells move along the microtubule network, and that CADM1 influences their velocity.

  13. Edge restenosis: impact of low dose irradiation on cell proliferation and ICAM-1 expression

    Directory of Open Access Journals (Sweden)

    Hannekum Andreas

    2006-07-01

    Full Text Available Abstract Background Low dose irradiation (LDI of uninjured segments is the consequence of the suggestion of many authors to extend the irradiation area in vascular brachytherapy to minimize the edge effect. Atherosclerosis is a general disease and the uninjured segment close to the intervention area is often atherosclerotic as well, consisting of neointimal smooth muscle cells (SMC and quiescent monocytes (MC. The current study imitates this complex situation in vitro and investigates the effect of LDI on proliferation of SMC and expression of intercellular adhesion molecule-1 (ICAM-1 in MC. Methods Plaque tissue from advanced primary stenosing lesions of human coronary arteries (9 patients, age: 61 ± 7 years was extracted by local or extensive thrombendarterectomy. SMC were isolated and identified by positive reaction with smooth muscle α-actin. MC were isolated from buffy coat leukocytes using the MACS cell isolation kit. For identification of MC flow-cytometry analysis of FITC-conjugated CD68 and CD14 (FACScan was applied. SMC and MC were irradiated using megavoltage photon irradiation (CLINAC2300 C/D, VARIAN, USA of 6 mV at a focus-surface distance of 100 cm and a dose rate of 6 Gy min-1 with single doses of 1 Gy, 4 Gy, and 10 Gy. The effect on proliferation of SMC was analysed at day 10, 15, and 20. Secondly, total RNA of MC was isolated 1 h, 2 h, 3 h, and 4 h after irradiation and 5 μg of RNA was used in standard Northern blot analysis with ICAM-1 cDNA-probes. Results Both inhibitory and stimulatory effects were detected after irradiation of SMC with a dose of 1 Gy. At day 10 and 15 a significant antiproliferative effect was found; at day 20 after irradiation cell proliferation was significantly stimulated. Irradiation with 4 Gy and 10 Gy caused dose dependent inhibitory effects at day 10, 15, and 20. Expression of ICAM-1 in human MC was neihter inhibited nor stimulated by LDI. Conclusion Thus, the stimulatory effect of LDI on SMC

  14. Clinical significance of serum vascular cell adhesion molecule-1 levels in patients with hepatocellular carcinoma

    Institute of Scientific and Technical Information of China (English)

    Joanna W. Ho; Ronnie T. Poon; Cindy S. Tong; Sheung Tat Fan

    2004-01-01

    AIM: To evaluate the correlation between serum vascular cellular adhesion molecule-1 (VCAM-1) levels and clinicopathological features in patients with hepatocellular carcinoma (HCC).METHODS: Ninety-six patients who underwent HCC resection were recruited in the study. Preoperative serum levels of soluble VCAM-1 were measured by enzyme-linked immunosorbent assay.RESULTS: Serum VCAM-1 level in HCC patients was inversely correlated with platelet count (r=-0.431, P<0.001)and serum albumin level (r=-0.279, P<0.001), and positively correlated with serum bilirubin level (r=0.379, P<0.001).Serum VCAM-1 level was not associated with tumor characteristics such as tumor size, venous invasion,presence of microsatellite nodules, tumor grade and tumor stage. Serum VCAM-1 level was significantly higher in HCC patients with cirrhosis compared with those without cirrhosis (median 704 vs 546 ng/mL, P<0.001). Furthermore, a significantly better disease-free survival was observed in HCC patients with low VCAM-1 level (P=0.019).CONCLUSION: Serum VCAM-1 level appears to reflect the severity of underlying chronic liver disease rather than the tumor status in HCC patients, and low preoperative serum VCAM-1 level is predictive of better disease-free survival after surgery.

  15. Matrine Attenuates COX-2 and ICAM-1 Expressions in Human Lung Epithelial Cells and Prevents Acute Lung Injury in LPS-Induced Mice

    Directory of Open Access Journals (Sweden)

    Chian-Jiun Liou

    2016-01-01

    Full Text Available Matrine is isolated from Sophora flavescens and shows anti-inflammatory effects in macrophages. Here we evaluated matrine’s suppressive effects on cyclooxygenase 2 (COX-2 and intercellular adhesion molecule-1 (ICAM-1 expressions in lipopolysaccharide- (LPS- stimulated human lung epithelial A549 cells. Additionally, BALB/c mice were given various matrine doses by intraperitoneal injection, and then lung injury was induced via intratracheal instillation of LPS. In LPS-stimulated A549 cells, matrine inhibited the productions of interleukin-8 (IL-8, monocyte chemotactic protein-1, and IL-6 and decreased COX-2 expression. Matrine treatment also decreased ICAM-1 protein expression and suppressed the adhesion of neutrophil-like cells to inflammatory A549 cells. In vitro results demonstrated that matrine significantly inhibited mitogen-activated protein kinase phosphorylation and decreased nuclear transcription factor kappa-B subunit p65 protein translocation into the nucleus. In vivo data indicated that matrine significantly inhibited neutrophil infiltration and suppressed productions of tumor necrosis factor-α and IL-6 in mouse bronchoalveolar lavage fluid and serum. Analysis of lung tissue showed that matrine decreased the gene expression of proinflammatory cytokines, chemokines, COX-2, and ICAM-1. Our findings suggest that matrine improved lung injury in mice and decreased the inflammatory response in human lung epithelial cells.

  16. Matrine Attenuates COX-2 and ICAM-1 Expressions in Human Lung Epithelial Cells and Prevents Acute Lung Injury in LPS-Induced Mice.

    Science.gov (United States)

    Liou, Chian-Jiun; Lai, You-Rong; Chen, Ya-Ling; Chang, Yi-Hsien; Li, Zih-Ying; Huang, Wen-Chung

    2016-01-01

    Matrine is isolated from Sophora flavescens and shows anti-inflammatory effects in macrophages. Here we evaluated matrine's suppressive effects on cyclooxygenase 2 (COX-2) and intercellular adhesion molecule-1 (ICAM-1) expressions in lipopolysaccharide- (LPS-) stimulated human lung epithelial A549 cells. Additionally, BALB/c mice were given various matrine doses by intraperitoneal injection, and then lung injury was induced via intratracheal instillation of LPS. In LPS-stimulated A549 cells, matrine inhibited the productions of interleukin-8 (IL-8), monocyte chemotactic protein-1, and IL-6 and decreased COX-2 expression. Matrine treatment also decreased ICAM-1 protein expression and suppressed the adhesion of neutrophil-like cells to inflammatory A549 cells. In vitro results demonstrated that matrine significantly inhibited mitogen-activated protein kinase phosphorylation and decreased nuclear transcription factor kappa-B subunit p65 protein translocation into the nucleus. In vivo data indicated that matrine significantly inhibited neutrophil infiltration and suppressed productions of tumor necrosis factor-α and IL-6 in mouse bronchoalveolar lavage fluid and serum. Analysis of lung tissue showed that matrine decreased the gene expression of proinflammatory cytokines, chemokines, COX-2, and ICAM-1. Our findings suggest that matrine improved lung injury in mice and decreased the inflammatory response in human lung epithelial cells.

  17. Interactions between rs5498 polymorphism in the ICAM1 gene and traditional risk factors influence susceptibility to coronary artery disease.

    Science.gov (United States)

    Sarecka-Hujar, Beata; Zak, Iwona; Krauze, Jolanta

    2009-06-01

    Coronary artery disease (CAD) depends on multiple genetic and environmental factors. Adhesion molecules are markers of endothelium dysfunction. Intercellular adhesion molecule-1 (ICAM-1) interacts with leukocyte integrins and promotes atherosclerotic process at the surface of endothelial cells. The aim of the study was to assess the association between ICAM1 rs5498 polymorphism and CAD and to establish whether there are any interactions between this polymorphism and traditional risk factors in determining the risk of CAD. We studied 191 cases with angiographically documented CAD and 203 controls with no signs of cardiovascular diseases. The ICAM1 polymorphism was genotyped using PCR-RFLP method. Data were analyzed with the STATISTICA 7.1 and EpiInfo 6 softwares. We did not observe significant differences in the distribution of genotypes and alleles of rs5498 between cases and controls. We only found a tendency to a higher prevalence of G allele carriers (AG + GG) in patients compared to controls (68 vs. 64%, P = 0.399). A synergistic effect of G allele carrier-state and smoking that had influenced the risk of CAD [synergy index multiplicative (SIM = 2.09)] was observed. Smoking carriers of G allele compared to non-smoking AA were more prevalent in CAD group (39.8%) than among controls (13.3%, P < 0.0001, OR 4.81). Moreover, there was also a synergistic effect between G allele carrier-state and an elevated level of triacylglycerols (TG) (SIM = 1.28) increasing the risk of CAD. There is a synergistic interaction between rs5498 genotype and smoking that increases the risk of CAD.

  18. EXPRESSION OF ICAM-1 AND LFA-1 MOLECULES IN RELATION TO RENAL ALLOGRAFT REJECTION IN RATSA

    Institute of Scientific and Technical Information of China (English)

    黄孝伦; 沈文律; 李幼平; 周泽清; 谭建三

    1999-01-01

    Objective. The purpose of this study was to assess the renal graft expression of ICAM-I (intercellular adhesion moleculeq) and LFA l(lymphocyte function-aa.soziated antigen-1)molecule with relation to graft rejection. Methods. Rat kidney traansplantation was performed according to the procedure of Kamada with some modification. Experimental rats were dividod into 5 groups. The survival time of recipient rats and function of grafts after renal transplantation were observed. The sections of renal graft were mined forantibody ICAM-1 and LFA-1, and then quantification of ICAM-1 and LFA-1 expression was accomplished by computer image analysis. Results. ICAM-1 and LFA-1 increased significantly in the renal allograft rejection group as compared with the non-rejection groups(P<0. 05). Conclustion. Both biopsy of renal graft and monitoring of ICAM-1 and LFA-1 are useful tools in diagnosing and treating acute rejection.

  19. Variation in the ICAM1 gene is not associated with severe malaria phenotypes

    Science.gov (United States)

    Fry, Andrew E.; Auburn, Sarah; Diakite, Mahamadou; Green, Angela; Richardson, Anna; Wilson, Jonathan; Jallow, Muminatou; Sisay-Joof, Fatou; Pinder, Margaret; Griffiths, Michael J.; Peshu, Norbert; Williams, Thomas N.; Marsh, Kevin; Molyneux, Malcolm E.; Taylor, Terrie E.; Rockett, Kirk A.; Kwiatkowski, Dominic P.

    2009-01-01

    Evidence from autopsy, mouse-model and in vitro binding studies suggests that adhesion of erythrocytes infected with Plasmodium falciparum to the human host intercellular adhesion molecule (ICAM)-1 receptor is important in the pathogenesis of severe malaria. Previous association studies between polymorphisms around the ICAM1 gene and susceptibility to severe malarial phenotypes have been inconclusive and often contradictory. We performed genetic association studies with 15 single-nucleotide-polymorphisms (SNPs) around the ICAM1 locus. All SNPs were screened in a family study of 1071 trios from Gambia, Malawi and Kenya. Two key non-synonymous SNPs with previously reported associations, rs5491 (K56M or ‘ICAM-1Kilifi’) and rs5498 (K469E), were tested in an additional 708 Gambian trios and a case-control study of 4058 individuals. None of the polymorphisms were associated with severe malaria phenotypes. Pooled results across our studies for ICAM-1Kilifi were, in severe malaria, odds ratio (OR) 1.02, 95% confidence interval (CI) 0.96 – 1.09, P=0.54, and cerebral malaria OR 1.07, CI 0.97 – 1.17, P=0.17. We assess the available epidemiological, population genetic and functional evidence which links ICAM-1Kilifi to severe malaria susceptibility. PMID:18528404

  20. Tetraspanins CD81 and CD82 facilitate α4β1-mediated adhesion of human erythroblasts to vascular cell adhesion molecule-1.

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    Frances A Spring

    Full Text Available The proliferation and terminal differentiation of erythroid progenitors occurs in human bone marrow within erythroblastic islands, specialised structures consisting of a central macrophage surrounded by developing erythroid cells. Many cell-cell and cell-matrix adhesive interactions maintain and regulate the co-ordinated daily production of reticulocytes. Erythroid cells express only one integrin, α4β1, throughout differentiation, and its interactions with both macrophage Vascular Cell Adhesion Molecule-1 and with extracellular matrix fibronectin are critical for erythropoiesis. We observed that proerythroblasts expressed a broad tetraspanin phenotype, and investigated whether any tetraspanin could modulate integrin function. A specific association between α4β1 and CD81, CD82 and CD151 was demonstrated by confocal microscopy and co-immune precipitation. We observed that antibodies to CD81 and CD82 augmented adhesion of proerythroblasts to Vascular Cell Adhesion Molecule-1 but not to the fibronectin spliceoforms FnIII12-IIICS-15 and FnIII12-15. In contrast, different anti-CD151 antibodies augmented or inhibited adhesion of proerythroblasts to Vascular Cell Adhesion Molecule-1 and the fibronectin spliceoform FnIII12-IIICS-15 but not to FnIII12-15. These results strongly suggest that tetraspanins have a functional role in terminal erythropoiesis by modulating interactions of erythroblast α4β1 with both macrophages and extracellular matrix.

  1. Comparative Study on the Effects of Serf-made Liver Preservation Solution on Secretion of ICAM-1 and NO in Rats

    Institute of Scientific and Technical Information of China (English)

    Shiming WANG; Peng DAI; Jun XU; Zheng YANG

    2008-01-01

    In order to study the effect of self-made liver preservation solution on liver preservation by comparing with UW solution and HC-A solution, the self-made liver preservation solution (SM) and perfusion solution were prepared under the aseptic conditions. The isolated non-circulated perfu-sion rat liver model was established. According to the different preservation solutions, the rats were randomly divided into UW group, SM group and HC-A group. The three groups were divided into 6subgroups according to the preservation duration (n=6 in each group). The transferase in liver perfu-sion solution and intercellular adhesion molecule-1 (ICAM-1) and nitric oxide (NO) in liver tissues were determined at 2, 8 and 24 h respectively. The results showed that the levels of alanine aml- notransferase (ALT) and aspartate aminotransferase (AST) had no significant difference between SM group and UW group, but significantly lower than in HC-A group. The levels of ICAM-1 and NO were increased simultaneously in SM group and UW group (P>0.05), but there was significant dif-ference as compared with HC-A group (P<0.05). At the same time point, the level of ICAM-1 was higher in SM group than in UW group, but NO was lower. The preservation effect of SM solution is the same as UW solution, but better than HC-A solution.

  2. Largazole, a class I histone deacetylase inhibitor, enhances TNF-α-induced ICAM-1 and VCAM-1 expression in rheumatoid arthritis synovial fibroblasts

    Energy Technology Data Exchange (ETDEWEB)

    Ahmed, Salahuddin, E-mail: Salah.Ahmed@utoledo.edu [Department of Pharmacology, College of Pharmacy and Pharmaceutical Sciences, The University of Toledo, OH (United States); Riegsecker, Sharayah; Beamer, Maria; Rahman, Ayesha; Bellini, Joseph V. [Department of Pharmacology, College of Pharmacy and Pharmaceutical Sciences, The University of Toledo, OH (United States); Bhansali, Pravin; Tillekeratne, L.M. Viranga [Department of Medicinal and Biological Chemistry, College of Pharmacy and Pharmaceutical Sciences, The University of Toledo, OH (United States)

    2013-07-15

    In the present study, we evaluated the effect of largazole (LAR), a marine-derived class I HDAC inhibitor, on tumor necrosis factor-α (TNF-α)-induced expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), and matrix metalloproteinase-2 (MMP-2) activity. LAR (1–5 μM) had no adverse effect on the viability of RA synovial fibroblasts. Among the different class I HDACs screened, LAR (0.5–5 μM) inhibited the constitutive expression of HDAC1 (0–30%). Surprisingly, LAR increased class II HDAC [HDAC6] by ∼ 220% with a concomitant decrease in HDAC5 [30–58%] expression in RA synovial fibroblasts. SAHA (5 μM), a pan-HDAC inhibitor, also induced HDAC6 expression in RA synovial fibroblasts. Pretreatment of RA synovial fibroblasts with LAR further enhanced TNF-α-induced ICAM-1 and VCAM-1 expression. However, LAR inhibited TNF-α-induced MMP-2 activity in RA synovial fibroblasts by 35% when compared to the TNF-α-treated group. Further, the addition of HDAC6 specific inhibitor Tubastatin A with LAR suppressed TNF-α + LAR-induced ICAM-1 and VCAM-1 expression and completely blocked MMP-2 activity, suggesting a role of HDAC6 in LAR-induced ICAM-1 and VCAM-1 expression. LAR also enhanced TNF-α-induced phospho-p38 and phospho-AKT expression, but inhibited the expression of phospho-JNK and nuclear translocation of NF-κBp65 in RA synovial fibroblasts. These results suggest that LAR activates p38 and Akt pathways and influences class II HDACs, in particular HDAC6, to enhance some of the detrimental effects of TNF-α in RA synovial fibroblasts. Understanding the exact role of different HDAC isoenzymes in RA pathogenesis is extremely important in order to develop highly effective HDAC inhibitors for the treatment of RA. - Highlights: • Largazole enhances TNF-α-induced ICAM-1 and VCAM-1. • Largazole upregulates class II HDAC (HDAC6) in RA synovial fibroblasts. • Largazole also induces the expression of phospho-p38

  3. Crawling phagocytes recruited in the brain vasculature after pertussis toxin exposure through IL6, ICAM1 and ITGαM.

    Science.gov (United States)

    Richard, Jean-François; Roy, Monica; Audoy-Rémus, Julie; Tremblay, Pierrot; Vallières, Luc

    2011-11-01

    The cerebral vasculature is constantly patrolled by rod-shaped leukocytes crawling on the luminal endothelial surface. These cells are recruited in greater numbers after exposure to bacterial lipopolysaccharide (LPS) by a mechanism involving tumor necrosis factor (TNF), interleukin-1β (IL1β) and angiopoietin-2 (Angpt2). Here, we report that the population of crawling leukocytes, consisting mainly of granulocytes, is also increased in the brains of mice suffering from experimental autoimmune encephalomyelitis (EAE) or injected with pertussis toxin (PTX), which is commonly used to induce EAE. However, this recruitment occurs through an alternative mechanism, independent of Angpt2. In a series of experiments using DNA microarrays, knockout mice and neutralizing antibodies, we found that PTX acts indirectly on the endothelium in part through IL6, which is essential for the post-transcriptional upregulation of intercellular adhesion molecule 1 (ICAM1) in response to PTX but not to LPS. We also found that phagocytes adhere to brain capillaries through the interaction of integrin αM (ITGαM) with ICAM1 and an unidentified ligand. In conclusion, this study supports the concept that PTX promotes EAE, at least in part, by inducing vascular changes necessary for the recruitment of patrolling leukocytes.

  4. KE and EE Genotypes of ICAM-1 Gene K469E Polymorphism Is Associated with Severe Preeclampsia

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    Ehsan Tabatabai

    2014-01-01

    Full Text Available Background. Preeclampsia (PE is one of the most important complications of pregnancy that is associated with significant mortality and morbidity in mother and fetus. Since the etiologic factors in its development are still unclear, we aimed to examine the intercellular adhesion molecule-1 (ICAM-1 gene K469E polymorphism in preeclamptic and control healthy women. Materials and Methods. Genetic polymorphism was analyzed in 192 PE and 186 healthy control women. PCR-RFLP method was used to identify K469E polymorphism. Results. The frequency of KK, KE, and EE genotypes of ICAM-1 gene was not different between PE patients and healthy pregnant women. Whereas, the frequency of KE and EE genotypes was significantly higher in severe PE than mild PE women and control group, and the risk of severe PE was 2.4-fold higher in subjects with KE genotype (OR, 2.4 [95% CI, 1 to 5.9]; P=0.03 and 3.3-fold higher in subjects with EE genotype (OR, 3.3 [95% CI, 1.2 to 9]; P=0.015 compared to individuals with KK genotype. Conclusion. We concluded that KE and EE genotypes of K469E polymorphism could increase risk of severe PE.

  5. Human rhinovirus 14 enters rhabdomyosarcoma cells expressing icam-1 by a clathrin-, caveolin-, and flotillin-independent pathway.

    Science.gov (United States)

    Khan, Abdul Ghafoor; Pickl-Herk, Angela; Gajdzik, Leszek; Marlovits, Thomas C; Fuchs, Renate; Blaas, Dieter

    2010-04-01

    Intercellular adhesion molecule 1 (ICAM-1) mediates binding and entry of major group human rhinoviruses (HRVs). Whereas the entry pathway of minor group HRVs has been studied in detail and is comparatively well understood, the pathway taken by major group HRVs is largely unknown. Use of immunofluorescence microscopy, colocalization with specific endocytic markers, dominant negative mutants, and pharmacological inhibitors allowed us to demonstrate that the major group virus HRV14 enters rhabdomyosarcoma cells transfected to express human ICAM-1 in a clathrin-, caveolin-, and flotillin-independent manner. Electron microscopy revealed that many virions accumulated in long tubular structures, easily distinguishable from clathrin-coated pits and caveolae. Virus entry was strongly sensitive to the Na(+)/H(+) ion exchange inhibitor amiloride and moderately sensitive to cytochalasin D. Thus, cellular uptake of HRV14 occurs via a pathway exhibiting some, but not all, characteristics of macropinocytosis and is similar to that recently described for adenovirus 3 entry via alpha(v) integrin/CD46 in HeLa cells.

  6. Human Rhinovirus 14 Enters Rhabdomyosarcoma Cells Expressing ICAM-1 by a Clathrin-, Caveolin-, and Flotillin-Independent Pathway ▿

    Science.gov (United States)

    Khan, Abdul Ghafoor; Pickl-Herk, Angela; Gajdzik, Leszek; Marlovits, Thomas C.; Fuchs, Renate; Blaas, Dieter

    2010-01-01

    Intercellular adhesion molecule 1 (ICAM-1) mediates binding and entry of major group human rhinoviruses (HRVs). Whereas the entry pathway of minor group HRVs has been studied in detail and is comparatively well understood, the pathway taken by major group HRVs is largely unknown. Use of immunofluorescence microscopy, colocalization with specific endocytic markers, dominant negative mutants, and pharmacological inhibitors allowed us to demonstrate that the major group virus HRV14 enters rhabdomyosarcoma cells transfected to express human ICAM-1 in a clathrin-, caveolin-, and flotillin-independent manner. Electron microscopy revealed that many virions accumulated in long tubular structures, easily distinguishable from clathrin-coated pits and caveolae. Virus entry was strongly sensitive to the Na+/H+ ion exchange inhibitor amiloride and moderately sensitive to cytochalasin D. Thus, cellular uptake of HRV14 occurs via a pathway exhibiting some, but not all, characteristics of macropinocytosis and is similar to that recently described for adenovirus 3 entry via αv integrin/CD46 in HeLa cells. PMID:20130060

  7. Evaluation of Liver Ischemia-Reperfusion Injury in Rabbits Using a Nanoscale Ultrasound Contrast Agent Targeting ICAM-1.

    Directory of Open Access Journals (Sweden)

    Fang Xie

    Full Text Available To assess the feasibility of ultrasound molecular imaging in the early diagnosis of liver ischemia-reperfusion injury (IRI using a nanoscale contrast agent targeting anti-intracellular adhesion molecule-1 (anti-ICAM-1.The targeted nanobubbles containing anti-ICAM-1 antibody were prepared using the avidin-biotin binding method. Human hepatic sinusoidal endothelial cells (HHSECs were cultured at the circumstances of hypoxia/reoxygenation (H/R and low temperature. The rabbit liver IRI model (I/R group was established using the Pringle's maneuver. The time-intensity curve of the liver contrast ultrasonographic images was plotted and the peak intensity, time to peak, and time of duration were calculated.The size of the targeted nanobubbles were 148.15 ± 39.75 nm and the concentration was 3.6-7.4 × 109/ml, and bound well with the H/R HHSECs. Animal contrast enhanced ultrasound images showed that the peak intensity and time of duration of the targeted nanobubbles were significantly higher than that of common nanobubbles in the I/R group, and the peak intensity and time of duration of the targeted nanobubbles in the I/R group were also significantly higher than that in the SO group.The targeted nanobubbles have small particle size, stable characteristic, and good targeting ability, which can assess hepatic ischemia-reperfusion injury specifically, noninvasively, and quantitatively at the molecular level.

  8. Intercellular adhesion molecule-1 expression in the hippocampal CA1 region of hyperlipidemic rats with chronic cerebral ischemia

    Institute of Scientific and Technical Information of China (English)

    Yingying Cheng; Ying Zhang; Hongmei Song; Jiachun Feng

    2012-01-01

    Chronic cerebral ischemia is a pathological process in many cerebrovascular diseases and it is induced by long-term hyperlipidemia, hypertension and diabetes mellitus. After being fed a high-fat diet for 4 weeks, rats were subjected to permanent occlusion of bilateral common carotid arteries to establish rat models of chronic cerebral ischemia with hyperlipidemia. Intercellular adhesion molecule-1 expression in rat hippocampal CA1 region was determined to better understand the mechanism underlying the effects of hyperlipidemia on chronic cerebral ischemia. Water maze test results showed that the cognitive function of rats with hyperlipidemia or chronic cerebral ischemia, particularly in rats with hyperlipidemia combined with chronic cerebral ischemia, gradually decreased between 1 and 4 months after occlusion of the bilateral common carotid arteries. This correlated with pathological changes in the hippocampal CA1 region as detected by hematoxylin-eosin staining. Immunohistochemical staining showed that intercellular adhesion molecule-1 expression in the hippocampal CA1 region was noticeably increased in rats with hyperlipidemia or chronic cerebral ischemia, in particular in rats with hyperlipidemia combined with chronic cerebral ischemia. These findings suggest that hyperlipidemia aggravates chronic cerebral ischemia-induced neurological damage and cognitive impairment in the rat hippocampal CA1 region, which may be mediated, at least in part, by up-regulated expression of intercellular adhesion molecule-1.

  9. Upregulation of ICAM-1 Expression on J774.2 Macrophages by Endotoxin Involves Activation of NF-κB but not Protein Tyrosine Kinase: Comparison to Induction of iNOS

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    Hartmut Ruetten

    1999-01-01

    Full Text Available This study compares the signal transduction pathway which leads to the upregulation of intercellular adhesion molecule-1 (ICAM-1 expression with that of the increase in the expression of inducible nitric oxide synthase (iNOS protein and activity caused by endotoxin in cultured J774.2 macrophages. Treatment of J774.2 cells with lipopolysaccharide E. coli (LPS induced a concentration-dependent increase in the expression of ICAM-1 on the cell surface within 4 h and an increase in iNOS protein and activity at 24 h. The upregulation of ICAM-1 expression on J774.2 macrophages caused by LPS was significantly inhibited by pretreatment of the cells with inhibitors of the activation of the nuclear transcription factor NF-κB, such as L-1-tosylamido-2-phenylethylchloromethyl ketone (TPCK, pyrrolidine dithiocarbamate (PDTC, rotenone or calpain inhibitor I, but not by the tyrosine kinase inhibitors, tyrphostin AG126 or genistein. In contrast, genistein or tyrphostin AG126 also prevented the induction of iNOS protein and activity in J774.2 macrophages elicited by LPS. Thus, the increase in the expression of ICAM-1 on J774.2 macrophages by endotoxin involves the activation of NFκB, but not of protein tyrosine kinase.

  10. sICAM-1 intrathecal synthesis and release during the acute phase in children suffering from Coxsackie A9 and S. pneumoniae meningoencephalitis Sintesis intratecal de sICAM-1 y liberación durante la fase aguda en niños con meningoencefalitis por Coxsackie A9 y S pneumoniae

    Directory of Open Access Journals (Sweden)

    Alberto J. Dorta-Contreras

    2008-09-01

    Full Text Available The intercellular adhesion molecule is a transmembrane glycoprotein belonging to the immunoglobulin superfamily. Serum and cerebrospinal fluid (CSF soluble intercellular adhesion molecule 1 (sICAM-1 from normal control children as well as from children with Guillain-Barré syndrome (GBS, with Coxsackie A9 virus meningoencephalitis and with Streptococcus pneumoniae meningoencephalitis were studied. sICAM-1 was quantified using an immunoenzimatic assay and albumin using the immunodiffusion technique in both biological fluids. Increased sICAM-1 values in CSF in patients with GBS correspond to an increase of the albumin CSF/serum quotient. In contrast, in inflammatory diseases like S. pneumoniae and Coxsackie A9 virus meningoencephalitis an increased brain-derived fraction was observed. In particular cases these values are 60-65% and 70-75% respectively. The results indicate an additional synthesis of sICAM-1 in subarachnoidal space during central nervous system (CNS inflammatory process. An important role of sICAM-1 in the transmigration of different cell types into CSF during CNS inflammation in children with S. pneumoniae and Coxsackie A9 meningoencephalitis may be suggested.La molécula de adhesión intercelular es una glicoproteína que pertenece a la superfamilia de las inmunoglobulinas. Se estudiaron los niveles de molécula de adhesión intercelular tipo 1 soluble (sICAM-1 en suero y líquido cefalorraquídeo (LCR de niños con meningoencefalitis por Streptococcus pneumoniae y por Coxsackie A9 al igual que en niños con sindrome de Guillain-Barré (SGB. sICAM-1 fue cuantificado por ensayo inmunoenzimático y la albúmina por inmunodifusión en ambos líquidos biológicos. Los valores incrementados de sICAM-1 en LCR en los pacientes con GBS corresponden a valores aumentados de razón LCR/suero de albúmina. En contraste, en las enfermedades inflamatorias como las meningoencefalitis por S. pneumoniae y por Coxsackie A9 se observa un incremento

  11. The impact of ICAM1 and VCAM1 gene polymorphisms on chronic allograft nephropathy and transplanted kidney function.

    Science.gov (United States)

    Kłoda, K; Domański, L; Pawlik, A; Wiśniewska, M; Safranow, K; Ciechanowski, K

    2013-01-01

    ICAM-1 and VCAM-1 adhesion molecules play important roles in the immune response and emergence of chronic allograft nephropathy (CAN). The several polymorphisms of ICAM1 and VCAM1 genes are associated with changes in molecular expression therefore affecting allograft function and immune responses after kidney transplantation. The aim of this study was to examine the impact of polymorphisms in ICAM1 and VCAM1 genes on biopsy-proven CAN and renal allograft function. The 270 Caucasian renal transplant recipients (166 men and 104 women) were genotyped for the rs5498 ICAM1 and rs1041163 and rs3170794 VCAM1 gene polymorphisms using real-time polymerase chain reaction. There was no correlation between polymorphisms and CAN. Creatinine concentrations in the first month after transplantation differed between the rs5498 ICAM1 genotypes (P = .095), being higher for GG carriers (AA + AG vs GG, P =.07) albeit not with statistical significance. Creatinine concentrations at 12, 24, and 36 months after transplantation differed significantly among rs5498 ICAM1 genotypes (P = .0046, P =.016, and P = .02) and were higher among GG carriers (AA + AG vs GG, P = .001, P = .004, and P = .006). Rs5498 ICAM1 GG genotype and receipient male gender were independent factors associated with higher creatinine concentrations. These results suggest that the rs5498 ICAM1 GG genotype may be associated with long-term allograft function.

  12. Curcumin nanoparticles ameliorate ICAM-1 expression in TNF-α-treated lung epithelial cells through p47 (phox and MAPKs/AP-1 pathways.

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    Feng-Lin Yen

    Full Text Available Upregulation of intercellular adhesion molecule-1 (ICAM-1 involves adhesions between both circulating and resident leukocytes and the human lung epithelial cells during lung inflammatory reactions. We have previously demonstrated that curcumin-loaded polyvinylpyrrolidone nanoparticles (CURN improve the anti-inflammatory and anti-oxidative properties of curcumin in hepatocytes. In this study, we focused on the effects of CURN on the expression of ICAM-1 in TNF-α-treated lung epithelial cells and compared these to the effects of curcumin water preparation (CURH. TNF-αinduced ICAM-1 expression, ROS production, and cell-cell adhesion were significantly attenuated by the pretreatment with antioxidants (DPI, APO, or NAC and CURN, but not by CURH, as revealed by western blot analysis, RT-PCR, promoter assay, and ROS detection and adhesion assay. In addition, treatment of TNF-α-treated cells with CURN and antioxidants also resulted in an inhibition of activation of p47 (phox and phosphorylation of MAPKs, as compared to that using CURH. Our findings also suggest that phosphorylation of MAPKs may eventually lead to the activation of transcription factors. We also observed that the effects of TNF-α treatment for 30 min, which includes a significant increase in the binding activity of AP-1 and phosphorylation of c-jun and c-fos genes, were reduced by CURN treatment. In vivo studies have revealed that CURN improved the anti-inflammation activities of CURH in the lung epithelial cells of TNF-α-treated mice. Our results indicate that curcumin-loaded polyvinylpyrrolidone nanoparticles may potentially serve as an anti-inflammatory drug for the treatment of respiratory diseases.

  13. 甲状腺疾病患者血清可溶性细胞间黏附分子-1测定的临床意义%Clinical value of soluble intercellular adhesion molecule -1 in patients with thyroid disease

    Institute of Scientific and Technical Information of China (English)

    罗章伟; 廖书鸿; 方文珠

    2010-01-01

    Objective To explore the contents and clinical significance of soluble intracellular adhesion molecule-1 ( sICAM-1 ) in patients with single goitre,Graves'and Hashimoto disease. Methods The contents of sICAM-1 in 100 cases of simple goiter group, Graves disease (GD) group 250 cases, Hashimot group 50 cases and 100 normal control were examined by sICAM-1 Radioimmunoassay(RIA) method,and the results were analyzed. Results There were no significant difference of sICAM-1 contents between ( 170.43 ± 34. 23 ) μg/L in normal control group and ( 182.48 ± 40.05) μg/L in simple goiter group( t = 1. 104, P > 0. 05 ); The contents of slCAM-1 in GD group and HT group [( 279.93 ± 86.69) μg/L、 (250.36 ± 81.56) μg/L] were higher than the control group( t = 2.310,2. 210, all P <0. 05) ;The sICAM-1 contents in 3 species.methods after treatment [( 178.95 ±59.78) μg/L, ( 185.65 ±53.25)μg/L, (259.41 ± 71.46) μg/L)] were significantly lower than before treatment [(316.53 ± 66.13) μg/L, (277.79±64.30)μg/L,(285.71 ±72.14)μg/L](t=2.312,2.278,2.328,all P <0.05);After the Graves'patients were treated and their thyroid function were normal,their serum sICAM-1 levels( 251.92 ± 77.75 )μg/L were lower than that( 329.34 ± 90.47 ) μg/L in relapse Graves'group( t= 2.412 ,P < 0. 05). Conclusion sICAM-1 RIA can be used as a parameter in diagnosing autoimmune thyroid diseases and in evaluating effects of therapy,stopping medicine or the relapse of Graves' disease.%目的 探讨单纯甲状腺肿、格雷夫斯病(GD)和桥本甲状腺炎(HT)患者血清可溶性细胞间黏附分子-1(sICAM-1)的含量及其临床意义.方法 用放射免疫分析法检测单纯性甲状腺肿大100例、GD 250例、HT 50例及健康人对照组100例血清sICAM-1含量,进行比较分析.结果 健康人sICAM-1含量(170.43±34.23)μg/L和单纯性甲肿(182.48±40.05)μg/L差异无统计学意义(t=1.104,P>0.05);GD和HT的sICAM-1含量分别为(279.93±86.69)μg/L,(250.36±81

  14. THE EFFECTS OF NF-KB ON ICAM-1 PROTEIN EXPRESSIONS OF RAT DURA MATER WITH MIGRAINE%NF-κB上调偏头痛大鼠脑膜ICAM-1蛋白表达

    Institute of Scientific and Technical Information of China (English)

    何秋; 王怀良; 章新华; 陈磊

    2007-01-01

    目的:探讨核转录因子-κB(nuclear factor-kappa B,NF-κB)在偏头痛脑膜炎症反应中的作用及细胞间黏附分子-1(intercellular adhesion molecules-1,ICAM-1)表达的调控机制.方法采用静脉注射(iv)硝酸甘油(glyceryl trinitrate,GTN)法建立大鼠偏头痛模型,分为对照组、模型组、溶剂对照组、吡咯烷二硫氨基甲酸(pyrrolidine dithiocarbamate,PDTC)组.各组分别包括0.9%生理盐水或GTN iv后1.5,4h两个实验小组.应用Western印迹法分别观察PDTC对GTN iv后1.5h大鼠脑膜NF-κB蛋白表达水平与GTN iv后4h ICAM-1蛋白表达水平的影响.结果:PDTC 50,100,200 mg.kg-1各剂量组GTN iv后1.5h大鼠脑膜NF-κB蛋白表达量较模型组分别降低30%(P<0.05)、52%(P<0.01)和65%(P<0.01),呈剂量依赖性;PDTC 50,100,200 mg.kg-1各剂量组GTN iv后4h大鼠脑膜ICAM-1蛋白表达量较模型组分别降低36%(P<0.05)、71%(P<0.01)和51%(P<0.01),无剂量依赖关系.结论:NF-κB参与偏头痛时脑膜ICAM-1的蛋白合成调控,在偏头痛的脑膜炎症机制中起着重要作用.

  15. PPARγ ligand ciglitazone inhibits TNFα-induced ICAM-1 in human airway smooth muscle cells

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    Chien-Da Huang

    2014-08-01

    Full Text Available Background: Modification of human airway smooth muscle (ASM function by proinflammatory cytokines has been regarded as a potential mechanism underlying bronchial hyperresponsiveness in asthma. Human ASM cells express intercellular adhesion molecule (ICAM-1 in response to cytokines. Synthetic ligands for peroxisome proliferator-activated receptor (PPARγ reportedly possess anti-inflammatory and immunomodulatory properties. In this study, we examined whether ciglitazone, a synthetic PPARγ ligand, can modulate the basal and tumor necrosis factor (TNFα-induced ICAM1 gene expression in human ASM cells. Methods: Human ASM cells were treated with TNFα. ICAM-1 expression was assessed by flow cytometry and reverse transcriptase-polymerase chain reaction (RT-PCR analysis. PPARγ activity was inhibited by target-specific small interfering (si RNA targeting PPARγ and GW9662, a PPARγ antagonist. Activity of nuclear factor (NF-κB was assessed by using immunoblot analysis, immune-confocal images, and electrophoretic mobility shift assay (EMSA. Results: By flow cytometry, ciglitazone alone had no effect on ICAM-1 expression in ASM cells, but inhibited ICAM-1 expression in response to TNFα (10 ng/ml in a dose-dependent manner (1-10 μM. It also inhibited TNFα-induced ICAM1 gene expression by RT-PCR analysis. Knockdown of PPARγ gene by target-specific siRNA targeting PPARγ enhanced ICAM-1 expression and the inhibitory effect of ciglitazone on TNFα-induced ICAM-1 expression was reversed by PPARγ siRNA and GW9662. SN-50 (10 μg/ml, an inhibitor for nuclear translocation of NF-κB, inhibited TNFα-induced ICAM-1 expression. Ciglitazone did not prevent TNFα-induced degradation of the cytosolic inhibitor of NF-κB (IκB, but inhibited the nuclear translocation of p65 induced by TNFα and suppressed the NF-κB/DNA binding activity. Conclusion: These findings suggest that ciglitazone inhibits TNFα-induced ICAM1 gene expression in human ASM cells through

  16. A single-arm, open-label, phase 2 clinical trial evaluating disease response following treatment with BI-505, a human anti-intercellular adhesion molecule-1 monoclonal antibody, in patients with smoldering multiple myeloma

    Science.gov (United States)

    Wichert, Stina; Juliusson, Gunnar; Johansson, Åsa; Sonesson, Elisabeth; Teige, Ingrid; Wickenberg, Anna Teige; Frendeus, Björn; Korsgren, Magnus; Hansson, Markus

    2017-01-01

    Background Smoldering multiple myeloma (SMM) is an indolent disease stage, considered to represent the transition phase from the premalignant MGUS (Monoclonal Gammopathy of Undetermined Significance) state towards symptomatic multiple myeloma (MM). Even though this diagnosis provides an opportunity for early intervention, few treatment studies have been done and the current standard of care is observation until progression. BI-505, a monoclonal antibody directed against intercellular adhesion molecule 1 (ICAM-1) with promising anti-myeloma activity in preclinical trials, is a possible treatment approach for this patient category with potential to eliminate tumor cells with minimal long-term side effects. BI-505 was well tolerated in an earlier phase 1 trial. Methods and findings In this phase 2 trial the effects of BI-505 in patients with SMM were studied. Four patients were enrolled and three of them completed the first cycle of treatment defined as 5 doses of BI-505, a total of 43 mg/kg BW, over a 7-week period. In the three evaluable patients, BI-505 showed a benign safety profile. None of the patients achieved a response as defined per protocol. EudraCT number: 2012-004884-29. Conclusions The study was conducted to assess the efficacy, safety and pharmacodynamics of BI-505 in patients with SMM. BI-505 showed no clinically relevant efficacy on disease activity in these patients with SMM, even if well tolerated. Trial registration ClinicalTrials.gov Identifier: NCT01838369. PMID:28158311

  17. 不同吸烟量对大鼠气道上皮细胞中细胞问黏附分子1表达的影响%Effects of different smoking quantity on expressions of intercellular adhesion molecule-1 in rat airway endothelial cells

    Institute of Scientific and Technical Information of China (English)

    索耀君; 许建英

    2009-01-01

    Objective To study the relationship between smoking as well as smoke abatement and airway inflammation of chronic obstructive pulmonary disease (COPD) through researching effects of different smoking quantity and different smoking time,smoking and smoke abatement on expression of intercellular adhesion molecule-1 (ICAM-1) in airway endothelial cells in rat model of smoking.Methods Forty Wistar rats were randomly divided into control group,long-term multiplicity smoking group,long-term manipulus smoking group,short-term multiplicity smoking group and smoke abatement group,eight rats in a group.The expressions of ICAM-1 in airway endothelial cells of rats were detected by immunohistochemistry and hybridization in situ.Results The expression of ICAM-1 mRNA and protein level in bronchial endothelial cells of long-term multiplicity smoking group were (6.93±1.44,19.22±0.22),short-term multiplicity smoking group (2.92±0.67,12.91±1.31 ),long-term manipulus smoking group (4.76±0.68, 14.03±2.39) and smoke abatement group (4.84±0.94,14.95±1.82),which were significantly increased compared with those of control group (1.45±0.98,8.83±0.77 ),peaking in the long-term multiplicity smoking group( P<0.05).The expression of ICAM-1 in bronchial endothelial cells of long-term manipulus smoking group,short-term multiplicity smoking group,smoke abatement group and the control group were lower than that of long-term multiplicity smoking group( P<0.05).Conclusions Smoking can result in the high expression of ICAM-1 mRNA and protein level in airway endothelial cells of rat model.The expression of ICAM-1 mRNA and protein level increase with the augmentation of smoking time and quantity and decrease after smoke abatement.It means smoke abatement can relieve airway inflammation but can not eliminate the change.Smoking abatement is an effective measure of preventing COPD.%目的 通过研究不同吸烟量、不同吸烟持续时间吸烟及戒烟对大鼠气道上皮

  18. ICAM-1 expression and organization in human endothelial cells is sensitive to gravity

    Science.gov (United States)

    Zhang, Yu; Sang, Chen; Paulsen, Katrin; Arenz, Andrea; Zhao, Ziyan; Jia, Xiaoling; Ullrich, Oliver; Zhuang, Fengyuan

    2010-11-01

    Transendothelial migration (TEM) of immune cells is a crucial process during a multitude of physiological and pathological conditions such as development, defense against infections and wound healing. Migration within the body tissues and through endothelial barriers is strongly dependent and regulated both by cytoskeletal processes and by expression of surface adhesion molecules such as ICAM-1 and VCAM-1. Space flight experiments have confirmed that TEM will be inhibited and may cause astronauts' immune function decreased and make them easy for infection. We used NASA RCCS to provide a simulated microgravity environment; endothelial cells were cultured on microcarrier beads and activated by TNF-α. Results demonstrate after clinorotation ICAM-1 expression increased, consistent with the notion in parabolic flights. However, VCAM-1 showed no significant change between activated or inactivated cells. Depolymerization of F-actin and clustering of ICAM-1 on cell membrane were also observed in short-term simulated microgravity, and after 24 h clinorotation, actin fiber rearrangement was initiated and clustering of ICAM-1 became stable. ICAM-1 mRNA and VCAM-1 mRNA were up-regulated after 30 min clinorotation, and returned to the same level with controls after 24 h clinorotation.

  19. 青少年肥胖与血清可溶性细胞间黏附分子-1相关性分析%Relationship between obesity and serum soluble intercellular adhesion molecule-1 in adolescents

    Institute of Scientific and Technical Information of China (English)

    马春明; 吴广飞; 韩改玲; 张宏; 陆强; 王术艺; 尹福在; 刘博伟; 娄东辉; 刘晓丽; 王锐

    2009-01-01

    Objective To evaluate the relationship between obesity and serum soluble intercellular adhesion molectde-1 (sICAM-1) in adolescents. Methods Totally, 158 adolescents aged 13-15 years were divided into three groups based on their body mass index (BMI) , 80 in control group, 44 in overweight group and 34 in obesity group. Height, weight, waist circumference (WC) and blood pressure were measured for all of them and sICAM-1 was assayed from fasting venous blood collected. Results BMI, WC and systolic blood pressure were significantly higher in overweight group than those in control group (P < 0. 01). BMI, WC, systolic blood pressure and diastolic blood pressure were significantly higher in obesity group than those in overweight group (P<0. 05). Level of sICAM-1 was significantly higher in obesity group than that in control group (P <0.05). Their sICAM-1 showed positive correlation with BMI (r = 0.168, P=0.035) and WC (r=0. 179, P =0.025). Multiple linear regression analysis using sICAM-1 as a dependent variable showed that WC (β= 0.009, 95% CI 0. 001-0.018, P=0.025) was an independent predictors for sICAM-1 adjusted for age, sex, BMI and blood pressure. Conclusions Results mentioned above suggest that endothelial dysfunction associates with obesity, particularly with abdominal obesity. sICAM-1 can be used as an early marker of atherosclerosis in adolescents.%目的 探讨青少年肥胖与血清可溶性细胞间黏附分子-1(sICAM-1)的关系.方法 根据体重指数(BMI),将158名13~15岁青少年分为对照组(80例)、超重组(44例)和肥胖组(34例),测量身高、体重、腰围及血压,应用酶联免疫吸附法榆测空腹静脉血sICAM-1水平.结果 3组数据均呈逐渐升高趋势,超重组BMI、腰围和收缩压高于对照组(P<0.01),肥胖组BMI、腰围、收缩压和舒张压高于超重组(P<0.05).肥胖组血清sICAM-1水平高于对照组(P<0.05).sICAM-1与BMI(r=0.168,P=0.035)和腰围(r=0.179,P=0.025)存在单变量相关.多元线性回归分析显示以sICAM

  20. Intercellular Adhension Molecule-1 in the Pathogenesis of Heroin-induced Acute Lung Injury in Rats

    Institute of Scientific and Technical Information of China (English)

    周琼; 白明; 邹世清

    2004-01-01

    The expression of intercellular adhesion molecule-1 (ICAM-1) in the pathogenesis of heroin-induced acute lung injury (ALI) in rats was investigated. The model of ALI was established by intravenous injection of heroin into tail vein in rats. Thirty-six rats were randomly divided into heroin-treated groups (1 h, 2 h, 4 h, 6 h and 24 h) and normal control group. Changes in histopathologic morphology and biological markers of ALI were measured. The expression of ICAM-1in lung tissue was detected by using immunohistochemistry and RT-PCR. The results showed that the W/D ratio and protein contents in BALF of the heroin-treated groups were significantly higher than that of the control group (P<0.01). The histopathological changes in the lung tissue were more obvious in heroin-treated groups. The ICAM-1 protein and mRNA expression in the lung tissue of heroin-treated groups were significantly increased as compared with that of the control group (P<0.01), and correlated with the ALI parameters in a time-dependent manner. Increasing of ICAM-1 expression was involved in the formation of heroin-induced lung injury. Furthermore, the level of expression was positively correlated with the severity of lung injury.

  1. Apicobasal Polarity Controls Lymphocyte Adhesion to Hepatic Epithelial Cells

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    Natalia Reglero-Real

    2014-09-01

    Full Text Available Loss of apicobasal polarity is a hallmark of epithelial pathologies. Leukocyte infiltration and crosstalk with dysfunctional epithelial barriers are crucial for the inflammatory response. Here, we show that apicobasal architecture regulates the adhesion between hepatic epithelial cells and lymphocytes. Polarized hepatocytes and epithelium from bile ducts segregate the intercellular adhesion molecule 1 (ICAM-1 adhesion receptor onto their apical, microvilli-rich membranes, which are less accessible by circulating immune cells. Upon cell depolarization, hepatic ICAM-1 becomes exposed and increases lymphocyte binding. Polarized hepatic cells prevent ICAM-1 exposure to lymphocytes by redirecting basolateral ICAM-1 to apical domains. Loss of ICAM-1 polarity occurs in human inflammatory liver diseases and can be induced by the inflammatory cytokine tumor necrosis factor alpha (TNF-α. We propose that adhesion receptor polarization is a parenchymal immune checkpoint that allows functional epithelium to hamper leukocyte binding. This contributes to the haptotactic guidance of leukocytes toward neighboring damaged or chronically inflamed epithelial cells that expose their adhesion machinery.

  2. PRIMING EFFECT OF HOMOCYSTEINE ON INDUCIBLE VASCULAR CELL ADHESION MOLECULE-1 EXPRESSION IN ENDOTHELIAL CELLS

    Science.gov (United States)

    Séguin, Chantal; Abid, Md. Ruhul; Spokes, Katherine C.; Schoots, Ivo G; Brkovic, Alexandre; Sirois, Martin G.; Aird, William C.

    2017-01-01

    Hyperhomocysteinemia is an independent risk factor for the development of atherosclerosis, as well as for arterial and venous thrombosis. However, the mechanisms through which elevated circulating levels of homocysteine cause vascular injury and promote thrombosis remain unclear. Here, we tested the hypothesis that homocysteine (Hcy) sensitizes endothelial cells to the effect of inflammatory mediators. Human umbilical vein endothelial cells (HUVEC) were incubated with Hcy 1.0 mM for varying time points, and then treated in the absence or presence of 1.5 U/ml thrombin or 10 ng/ml lipopolysaccharide (LPS). Hcy alone had no effect on the expression of vascular cell adhesion molecule (VCAM)-1. However, Hcy enhanced thrombin- and LPS-mediated induction of VCAM-1 mRNA and protein levels. Consistent with these results, pretreatment of HUVEC with Hcy resulted in a two-fold increase in LSP-mediated induction of leukocyte adhesion. The latter effect was significantly inhibited by anti-VCAM-1 antibodies. Together, these findings suggest that Hcy sensitizes HUVEC to the effect of inflammatory mediators thrombin and LPS, at least in part through VCAM-1 expression and function. PMID:18406566

  3. Expression of ICAM1 and VCAM1 Serum Levels in Rheumatoid Arthritis Clinical Activity. Association with Genetic Polymorphisms

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    Rosa Elena Navarro-Hernández

    2009-01-01

    Full Text Available To investigate the association of sICAM-1 and sVCAM-1 with ICAM1 721G>A and VCAM1 1238G>C polymorphisms and rheumatoid arthritis (RA clinical activity, sixty RA patients and 60 healthy non-related subjects (HS matched for age and sex were recruited. Soluble adhesion molecules were determined by ELISA technique. Rheumatoid factor (RF, C reactive protein (CRP and the erythrocyte sedimentation rate (ESR were measured by routine methods. Disability and clinical activity was measured with Spanish-HAQ-DI and DAS28 scores, respectively. The ICAM1 and VCAM1 polymorphism were identified using the PCR-RFLP procedure. Inter-group comparison showed increased levels of sICAM-1 and sVCAM-1 in RA patients (284 and 481 ng/mL versus HS (132 and 280 ng/mL; in the RA group, significant correlations between sVCAM-1 and RF (r = 0.402, ESR (r = 0.426, Spanish-HAQ-DI (r = 0.276, and DAS28 (r = 0.342 were found, whereas sICAM-1 only correlated with RF (r = 0.445. In RA patients, a significant association with the 721A allele of ICAM1 polymorphism (p = 0.04, was found. In addition, the allele impact (G/A + A/A of this polymorphism was confirmed, (p = 0.038, OR = 2.3, C.I. 1.1–5.0. sVCAM-1 and sICAM-1 serum levels reflected the clinical status in RA, independently of the ICAM1 and VCAM1 polymorphism. However, the ICAM1 721A allele could be a genetic marker to RA susceptibility.

  4. Effect of ischemic preconditioning on expression of intracellular adhesion molecule-1 in brain tissues following traumatic brain injury in rats%缺血预处理对大鼠创伤性脑损伤后脑组织细胞间黏附分子-1表达的影响

    Institute of Scientific and Technical Information of China (English)

    朱克军; 黄洪; 储辉; 罗志勇; 徐志明; 俞航; 张世明

    2014-01-01

    目的 探讨缺血预处理(ischemic precoudition,IPC)对大鼠创伤性脑损伤(traumatic brain injury,TBI)后脑组织细胞间黏附分子-1(intracellular adhesion molecule-1,ICAM-1)表达的影响. 方法 雄性SD大鼠60只,体重220 ~250 g,按随机数字表法分为假手术组、TBI组和IPC组,每组20只.短暂夹闭双侧颈总动脉制备脑IPC模型,采用Feeney自由落体撞击法制作TBI模型,假手术组仅行右侧顶部开窗而无TBI.分别于TBI后6,72 h处死10只大鼠,取损伤脑组织,计算脑组织湿/干重比(W/D)值,采用免疫组化法测定ICAM-1表达水平,光镜观察病理学结果. 结果 与假手术组比较,TBI组脑组织W/D值升高(6 h:4.2±0.4比2.7±0.4;72 h:5.0±0.1比3.1±0.2,P<0.05),脑组织ICAM-1表达上调(6 h:25.4 ±3.5比8.6±1.3;72 h:36.5 ±5.4比8.4±1.6,P<0.05);与TBI组比较,IPC组脑组织W/D值降低(6 h:3.5±0.6比4.2±0.4;72 h:3.7±0.4比5.0±0.1,P <0.05),脑组织ICAM-1表达下调(6 h:16.5±2.7比25.4 ±3.5;72 h:24.3 ±4.6比36.5 ±5.4,P<0.05).IPC组脑组织损伤程度轻于TBI组. 结论 IPC可以下调脑组织ICAM-1表达,从而减轻大鼠TBI.%Objective To investigate the effect of ischemic preconditioning (IPC) on expression of intracellular adhesion molecule-1 (ICAM-1) in brain tissues following traumatic brain injury (TBI) in rats.Methods Sixty male SD rats weighing 220-250 g were randomly divided into three groups (n =20 for each):sham operation group,TBI group,and IPC group.Cerebral IPC models were induced by transient occlusion of the bilateral common carotid arteries; TBI models were induced by Feeney's freefalling method; rats in sham operation group were only performed exposure of dura of the right parietal lobe.Ten rats were sacrificed respectively at 6 and 72 hours after TBI and injured brain tissues were harvested to estimate wet/dry weight (W/D) ratio for the brain,determine ICAM-1 expression by immunohistochemistry and perform microscopic examination.Results Brain W

  5. Interleukin 3 stimulates proliferation and triggers endothelial-leukocyte adhesion molecule 1 gene activation of human endothelial cells.

    Science.gov (United States)

    Brizzi, M F; Garbarino, G; Rossi, P R; Pagliardi, G L; Arduino, C; Avanzi, G C; Pegoraro, L

    1993-06-01

    Proliferation and functional activation of endothelial cells within a tissue site of inflammation are regulated by humoral factors released by cells, such as T lymphocytes and monocytes, infiltrating the perivascular space. In the present study we investigated the effects of interleukin 3 (IL-3), an activated T lymphocyte-derived cytokine, on cultured human umbilical vein endothelial cells (HUVEC). Proliferative activity, evaluated both by estimation of the fraction of cells in the S phase and by direct cell count demonstrated that IL-3, at the dose of 25 ng/ml, enhances more than threefold both DNA synthesis and cell proliferation above baseline control conditions. Binding studies with radioiodinated ligand demonstrated that HUVEC constitutively express a smaller number of IL-3 binding sites (approximately 99 binding sites per cell, with an apparent Kd of 149 pM). Accordingly, molecular analysis showed the presence of transcripts for both alpha and beta subunits of the IL-3 receptor. Functional activation of endothelial cells was evaluated by the expression of the endothelial-leukocyte adhesion molecule 1 (ELAM-1) transcript and by leukocyte adhesion. The ELAM-1 gene transcript was clearly detectable 4 h after IL-3 addition and started to decrease after 12 h. Moreover, IL-3-induced ELAM-1 transcription was followed by enhanced adhesion of neutrophils and CD4+ T cells to HUVEC. The findings that IL-3 can stimulate both proliferation and functional activation of endothelial cells suggest that this cytokine can be involved in sustaining the process of chronic inflammation.

  6. VCAM-1 and ICAM-1 serum levels as markers of relapse in visceral leishmaniasis

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    Alexandros Makis

    2017-01-01

    Full Text Available Objectives-Methods. Visceral leishmaniasis (VL is characterized by chronicity and relapses despite efficacious treatment. Acute and chronic inflammatory processes and concomitant disturbances in cell adhesion characterize the pathogenesis of the disease. To investigate these processes further we measured adhesion molecules (L-selectin, ICAM-1 and VCAM-1 serum levels in 16 children with VL, as well as in 20 healthy controls. All children were treated with liposomal amphotericin B (3 mg/kg on days 1 to 5, 14, and 21. Measurements were performed at days 0, 15 and 30. Results. All children responded well to treatment in both clinical and laboratory terms. In three cases relapse occurred at 3, 5 and 6 months after treatment had ended. Serum L-selectin levels, both pre-treatment and post-treatment, did not significantly differ between patients and controls. VCAM-1 and ICAM-1 median levels were similar in patients and controls (P>0.05 at day 0 and significantly increased at day 15 (P0.05, but not in the 3 patients who relapsed (P<0.05. Conclusions. Despite the small number of the patients, the changes in VCAM-1 and ICAM-1 levels indicate the anti-parasite activation of the immune system during the course of VL and the effect of treatment. Decline in post-treatment serum VCAM-1 and ICAM-1 levels might be used as a marker of treatment efficacy in childhood VL.

  7. 不同冠心病血清soL-CXCL16,soL-ICAM1及hsCRP水平研究%The level and clinical significance of sol-CXCL16,sol-ICAM1and hsCRP in patients with different coronary heart diseases

    Institute of Scientific and Technical Information of China (English)

    陈阳

    2011-01-01

    目的 探讨不同冠心病血清soL-CXCL16,soL-ICAM1及hsCRP水平及临床意义.方法 选取冠心病患者61例,其中急性冠状动脉综合征(ACS)患者30例(ACS组),稳定型心绞痛(SAP)患者31例(SAP组),另选30例正常志愿者作为正常对照组.所有患者均检测soL-CXCL16,soL-ICAM1及hsCRP水平.并随访6个月的主要不良心血管病事件(MACE).结果 ACS组比SAP组有较高的soL-CXCL16(P<0.05),soL-ICAM1(P<0.01)及hsCRP(P<0.05)水平,且2组均显著性高于正常对照组(P<0.05或P<0.01).CXCL16与hsCRP、TG、CHO、LDL,存在相关性,而与其他指标均无相关性;但在ACS组、soL-CXCL16与soL-ICAM1有相关性,与其他指标无相关性.结论 检测soL-CXCL16、soL-ICAM1及hsCRP水平对冠心病有一定的临床诊断和预测意义.%Objective To explore the serum level and their clinical significance of high-sensitivity C- reactive protein(hs- CRP), soluble CXC chemokine iigand 16 (sol - CXCL16) and soluble vascular cell adhesion molecule - 1 ( sol - VCAM - 1 ) in patients with different coronary heart diseases(CHD). Methods Sixty one patients with CHD are randomized into acute coronary syndrome group(ACS group, 30 cases)and stable angina pectoris group(SAP group, 31 cases), and 30 volunteers are selected as controls. Serum levels of sol - CXCL16, sol - ICAM1 and hsCRP are measured by enzyme - linked immunosorbent assay. Results The Serum levels of sol - CXCL16( P< 0.05 ), sol - ICAM1 ( P < 0.01 ) and hsCRP ( P < 0.05) in ACS group are higher than that in SAP group, which in both groups are higher than that in control(P<0.05 or P<0.01). the level of sol - CXCL16 correlate with the levels of hsCRP, TG, CHO and LDL in all the selected ,while it correlate with the level of sol - ICAM1 only in ACS group. Conclusion To detect the Serum levels of sol - CXCL16, sol - ICAM1 and hsCRP has some clinical diagnosis and prognostic significance to coronary heart disease.

  8. Expression and significance of ICAM-1 and its counter receptors LFA-1 and Mac-1 in experimental acute pancreatitis of rats

    Institute of Scientific and Technical Information of China (English)

    Wei Sun; Yasuhiro Watanabe; Zhong-Qiu Wang

    2006-01-01

    AIM: To investigate the role of intercellular adhesion molecule-1 (ICAM-1) and its counter receptors LFA-1 and Mac-1 in acute pancreatitis (AP).METHODS: SD rats were allocated to AP group and control group randomly (25 rats each). AP was induced by infusion of 5% chenodeoxycholic acid into the pancreatic duct, followed by ligation of pancreatic duct.The rats were sacrificed at 1, 3, 6, 12 and 24 h after induction of pancreatitis. Five rats were sacrificed at one time point in the two groups before the blood and specimens from pancreas and lung were obtained. Serum amylase and ascitic fluid were measured at each time point. Expression of ICAM-1 at different time points was assessed by immunohistochemistry in pancreas and lung,and the expression of LAF-1 and Mac-1 on neutrophils at different time points was detected by flow cytometer.RESULTS: Induction of AP was confirmed by the serum levels of amylase and histological studies. The expression of ICAM-1 in pancreas increased significantly than that in the control group at all time points (P<0.05 or P<0.01),as well as the expression in lung except at 1 h. The expression of LFA-1 and Mac-1 on neutrophil in blood increased significantly in AP group than that in control group at several time points (P<0.05 or P<0.01). The amount of ascitic fluid and serum amylase level of AP group increased significantly than that of control group at all time points (P<0.05 or P<0.01). Parallel to these results, a significant neutrophil infiltration was found in pancreas and lung tissues of AP group rats.CONCLUSION: Our findings suggest the important role for ICAM-1, LFA-1 and Mac-1 in mediating the development of AP from a local disease to a systemic illness. Upregulation of ICAM-1, LFA-1, Mac-1 and subsequent leukocyte infiltration appear to be significant events of pancreatic and pulmonary injuries in AP.

  9. Effects of Sera from Patients with SLE on ICAM - 1 and MCP- 1 Expression in HUVEC and Fluvastatin Intervention%SLE患者血清对人脐静脉内皮细胞ICAM-1和MCP-1表达的影响及氟伐他汀的干预作用

    Institute of Scientific and Technical Information of China (English)

    梁倩; 李霞; 刘伏友; 刘虹; 许向青; 彭佑铭

    2009-01-01

    Objective: To investigate the effect of ANA- positive and anti - dsDNA antibody - positive sera from patients with SLE on intercellular adhesion molecule - 1 ( ICAM - 1 ) and monocyte chemoattractant protein - 1 (MCP-1 ) released from cul-tured human umbilical vein endothdial cells (HUVEC) and whether fluvastatin can attenuate these effect. Methods:Confluent mono-layers of culturad HUVEC with serum samples (diluted 1:5) were from 15 female patients and 5 normal female controls or with both serum samples and solution of fluvastatin for 24 hours. ICAM- 1 and MCP- 1 concentrations in the culture supernatant were mea-sured by EL1SA and intracellular expressions of ICAM- 1 and MCP- 1 were measured by immunocytochemistry. Results: The ex-pression of ICAM - 1 and MCP - 1 incubated with ANA-positive and anti - dsDNA antibody - positive sera from patient with SLE were higher than HUVEC incubated with ANA-negative sera from patients with SLE(P < 0.01 ) and normal controls( P < 0.01 ).Fluvaststin showed significant inhibition of ANA - positive and anti - dsDNA antibody- positive sera induced ICAM- 1 and MCP - 1expression on HUVEC(P<0.01 ,and P<0.05). Conclusion:ANA- pcsitive and anti- dsDNA antibody- positive sera's ability to activate HUVEC is evidenced by induction of ICAM- 1 and MCP- 1 expression in vitro. Fluvastatin can inhibit up- reguhtion of ICAM- 1 and MCP- 1 on HUVEC by ANA- positive and anti- dsDNA antibody- positive sera from patients with SLE in vitro.%目的:观察抗核抗体(ANA)和抗ds-DNA抗体对人脐静脉血管内皮细胞(HUVEC)细胞间黏附分子-1(ICAM-1)、单核细胞趋化因子-1(MCP-1)表达的影响及他汀类药物氟伐他汀(fluvastatin,flu)干预后的变化,以探讨ANA和抗ds-DNA抗体在系统性红斑狼疮(SLE)血管炎中的致病机制和flu对血管内皮保护作用.方法:体外培养HUVEC,收集女性SLE患者血清(以抗核抗体全套为依据,分3组:ANA阴性、ANA滴度1:80、ANA滴度1:80和抗ds-DNA抗

  10. Pre-diagnostic levels of adiponectin and soluble vascular cell adhesion molecule-1 are associated with colorectal cancer risk

    Institute of Scientific and Technical Information of China (English)

    Mathilde Touvier; Pilar Galan; Sébastien Czernichow; Léopold Fezeu; Namanjeet Ahluwalia; Chantal Julia; Nathalie Charnaux; Angela Sutton; Caroline Méjean; Paule Latino-Martel; Serge Hercberg

    2012-01-01

    AIM:To examine the relationships between pre-diag-nostic biomarkers and colorectal cancer risk and assess their relevance in predictive models.METHODS:A nested case-control study was designed to include all first primary incident colorectal cancer cases diagnosed between inclusion in the SUpplementation en VItamines et Minéraux AntioXydants cohort in 1994 and the end of follow-up in 2007.Cases (n =50) were matched with two randomly selected controis (n =100).Conditional logistic regression models were used to investigate the associations between prediagnostic levels of hs-CRP,adiponectin,leptin,soluble vascular cell adhesion molecule-1 (sVCAM-1),soluble intercellular adhesion molecule-1,E-selectin,monocyte chemoattractant protein-1 and colorectal cancer risk.Area under the receiver operating curves (AUC) and relative integrated discrimination improvement (RIDI) statistics were used to assess the discriminatory poten tial of the models.RESULTS:Plasma adiponectin level was associated with decreased colorectal cancer risk (P for linear trend =0.03).Quartiles of sVCAM-1 were associated with increased colorectal cancer risk (P for linear trend =0.02).No association was observed with any of the other biomarkers.Compared to standard models with known risk factors,those including both adiponectin and sVCAM-1 had substantially improved performance for colorectal cancer risk prediction (P for AUC improvement =0.01,RIDI =26.5%).CONCLUSION:These results suggest that pre-diagnostic plasma adiponectin and sVCAM-1 levels are associated with decreased and increased colorectal cancer risk,respectively.These relationships must be confirmed in large validation studies.

  11. Meta- analysis of association between K469E polymorphism of the ICAM-1 gene and retinopathy in type 2 diabetes

    Institute of Scientific and Technical Information of China (English)

    Wen-Ying; Fan; Ning-Pu; Liu

    2015-01-01

    AIM: To collectively evaluate the association of intercellular adhesion molecule-1(ICAM-1) gene K469 E polymorphism(rs5498) with diabetic retinopathy(DR) in patients with type 2 diabetic mellitus(T2DM). METHODS: Overall review of available literatures relating K469 E polymorphism to the risk of DR was conducted on 4 electronic databases. Meta-analysis was performed by Stata 12.0 to calculate pooled odds ratios(ORs). Potential sources of heterogeneity and bias were explored.RESULTS: Seven studies with genotype frequency data including 1120 cases with DR and 956 diabetic controls free of DR were included. Meta-analysis did not show significant association of K469 E polymorphism with DR(P >0.05). A statistically significant association was detected between the K469 E polymorphism and proliferative DR(PDR) in Asians only in dominant model(GG+AG vs AA) with pooled OR of 0.729(95%CI: 0.564-0.942, P=0.016, P heterogeneity=0.143), however, this association was not detected in recessive model(AG +AA vs GG;OR=1.178, 95%CI: 0.898-1.545, P =0.236, P heterogeneity=0.248)or allelic model(G vs A; OR=0.769, 95% CI: 0.576-1.026,P =0.074, P heterogeneity=0.094). No publication bias was found by Funnel plot, Begg’s and Egger’s test. CONCLUSION: This research found no statistically significant association between ICAM-1 gene K469 E polymorphism and DR in patients with T2 DM, but showed significant association of the K469 E polymorphism with PDR in Asian diabetic patients only in dominant model. Further investigation would be required to consolidate the conclusion.

  12. Expression of LFA-1/ICAM-1 in CNS lymphomas: possible mechanism for lymphoma homing into the brain.

    Science.gov (United States)

    Bashir, R; Coakham, H; Hochberg, F

    1992-02-01

    We examined a possible role for the adhesion molecules LFA-1 and ICAM-1 in localizing central nervous system non-Hodgkin's lymphomas (CNS-NHLs) to the brain. Fresh frozen sections from 12 monoclonal CNS NHLs (11 primary, one secondary) were stained with monoclonal antibodies to LFA-1 alpha chain (CD11a), beta chain (CD18) and, ICAM-1 (CD54). Additional staining made use of rat monoclonal antibodies to the human and mouse high endothelial venule antigens HECA 452 and MECA 79 and mouse ICAM-1. The expression of these same molecules was also studied in mice with severe combined immunodeficiency (SCID) mice, bearing intracranial human lymphoblastoid cells. Eleven of the CNS-NHL tumors expressed LFA-1 alpha (one strongly, one intermediate, nine weakly). Nine of the tumors weakly expressed LFA-1 beta.. Nine of twelve tumors weakly expressed ICAM-1. In six of seven tumors definite blood vessels stained for ICAM-1. Non-tumor brain from two patients and non-tumor cerebral blood vessels showed no staining with CD11a, CD18 or CD54 antibodies. Strong expression of LFA-alpha and LFA-beta as well as ICAM-1 was noted in human lymphoblastoid cells (LCLs)/SCID mouse CNS lymphomas. Tumor blood vessels in these mice stained for mouse ICAM-1. Normal SCID mouse brains showed no staining with CD11a, CD18, CD54 or mouse ICAM-1 antibodies. Human, human/mouse CNS lymphomas, normal human, and mouse brains showed no staining with either HECA 452 or MECA 79.(ABSTRACT TRUNCATED AT 250 WORDS)

  13. A Novel Domain Cassette Identifies Plasmodium falciparum PfEMP1 Proteins Binding ICAM-1 and Is a Target of Cross-Reactive, Adhesion-Inhibitory Antibodies

    DEFF Research Database (Denmark)

    Bengtsson, Anja; Jørgensen, Louise; Rask, Thomas Salhøj

    2013-01-01

    Cerebral Plasmodium falciparum malaria is characterized by adhesion of infected erythrocytes (IEs) to the cerebral microvasculature. This has been linked to parasites expressing the structurally related group A subset of the P. falciparum erythrocyte membrane protein 1 (PfEMP1) family of IE...... genes from six genetically distinct P. falciparum parasites. The three domains in the cassette, which we call DC4, had a high level of sequence identity and cluster together phylogenetically. Erythrocytes infected by these parasites and selected in vitro for expression of DC4 adhered specifically...

  14. Hemorrhage and resuscitation alter the expression of ICAM-1 and P-selectin in mice.

    Science.gov (United States)

    Shenkar, R; Cohen, A J; Vestweber, D; Miller, Y E; Tuder, R; Abraham, E

    1995-01-01

    Acute inflammatory lung injury is a common clinical occurrence following blood loss and trauma, and is characterized by massive neutrophil infiltration into the lung. In order to better examine cell trafficking that may contribute to lung injury in this setting, we investigated in vivo mRNA levels and immunohistochemically determined expression of the adhesion molecules P-selectin and the intercellular adhesion molecule (ICAM)-1 in murine lungs over the 3-day period following hemorrhage and resuscitation. Significant increases in P-selectin mRNA levels were present in lungs obtained 3 days after hemorrhage. ICAM-1 mRNA levels were significantly increased 6 and 72 hr after hemorrhage. Immunohistochemical staining for P-selectin was enhanced on pulmonary vascular endothelium in all visible vessels at 6, 24, and 72 hr after hemorrhage. ICAM-1 immunoreactivity was significantly increased on the alveolar epithelium at 6 and 72 hr post-hemorrhage. These results suggest that increased expression of adhesion molecules in the lung at early post-hemorrhage timepoints may contribute to neutrophil infiltration into the lungs and the frequent development of acute lung injury following blood loss and trauma.

  15. Effects of Estrogen Level on the Function of Vascular Endothelial Cells and Expression of Vascular Cell Adhesion Molecule - 1φ

    Institute of Scientific and Technical Information of China (English)

    WU Saizhu(吴赛珠); LIU Jiangguo(刘建国); TAN Jiayu(谭家余); ZHoU Kexiang(周可祥); Gorge D Webb; WEI Heming(隗和明); GUO Zhiguang(郭志刚)

    2002-01-01

    Objectives To ob- serve the effect of different estrogen levels on the se- cretory function of vascular endothelial cells of female rats, and study the effect of modulation of estrogen level on the expression of vascular cell adhesion molecule - 1 and the concentration of estrogen receptorin vascular endothelial cells. Methods Radioim-munology was used to measure the serum concentrationof endothelin and PGI2, and copper-cadmium re-duction was employed to measure the serum content ofnitrogen monoxide. Radioligand binding and flowcy-tometry were used to measure the expression of estrogenreceptor and vascular cell adhesion molecule (VCAM-1 ) of vascular endothelial cells respectively. Re-sults 1. The serum concentration of nitric oxide andPGI2 decreased when the ovaries of female rats wereremoved. In ovariectomized rats, given estrogen, theconcentration rose ( P < 0.05), but the plasma con-centration of endothelin was adverse to it. 2. Theconcentration of estrogen receptor of vascular endothe-lial cells decreased remarkably when the ovaries of fe-male rats were removed. When given estrogen, it in-creased. 3. The percent of expressed VCAM - 1 in-creased siguificantly after interleukin- lβoperated onthe cells, but 17 - βestradiol at 3 × 10-8 ~ 10-6 mol/lall decreased the percent. Conclusions Estrogenlevel can influence the secretion of nitrogen monoxide,PGI2 and endothlin of vascular endothelial cells, andalso influence the concentration of estrogen receptor ofvascular endothelial cells. 17 -β Estradiol at 3 × 10-8~ 10-6 M can decrease the elevation of VCAM - 1 ofvascular endothelial cells induced by interleukin - 1 β.

  16. Early Detection of Junctional Adhesion Molecule-1 (JAM-1) in the Circulation after Experimental and Clinical Polytrauma.

    Science.gov (United States)

    Denk, Stephanie; Wiegner, Rebecca; Hönes, Felix M; Messerer, David A C; Radermacher, Peter; Weiss, Manfred; Kalbitz, Miriam; Ehrnthaller, Christian; Braumüller, Sonja; McCook, Oscar; Gebhard, Florian; Weckbach, Sebastian; Huber-Lang, Markus

    2015-01-01

    Severe tissue trauma-induced systemic inflammation is often accompanied by evident or occult blood-organ barrier dysfunctions, frequently leading to multiple organ dysfunction. However, it is unknown whether specific barrier molecules are shed into the circulation early after trauma as potential indicators of an initial barrier dysfunction. The release of the barrier molecule junctional adhesion molecule-1 (JAM-1) was investigated in plasma of C57BL/6 mice 2 h after experimental mono- and polytrauma as well as in polytrauma patients (ISS ≥ 18) during a 10-day period. Correlation analyses were performed to indicate a linkage between JAM-1 plasma concentrations and organ failure. JAM-1 was systemically detected after experimental trauma in mice with blunt chest trauma as a driving force. Accordingly, JAM-1 was reduced in lung tissue after pulmonary contusion and JAM-1 plasma levels significantly correlated with increased protein levels in the bronchoalveolar lavage as a sign for alveolocapillary barrier dysfunction. Furthermore, JAM-1 was markedly released into the plasma of polytrauma patients as early as 4 h after the trauma insult and significantly correlated with severity of disease and organ dysfunction (APACHE II and SOFA score). The data support an early injury- and time-dependent appearance of the barrier molecule JAM-1 in the circulation indicative of a commencing trauma-induced barrier dysfunction.

  17. Early Detection of Junctional Adhesion Molecule-1 (JAM-1 in the Circulation after Experimental and Clinical Polytrauma

    Directory of Open Access Journals (Sweden)

    Stephanie Denk

    2015-01-01

    Full Text Available Severe tissue trauma-induced systemic inflammation is often accompanied by evident or occult blood-organ barrier dysfunctions, frequently leading to multiple organ dysfunction. However, it is unknown whether specific barrier molecules are shed into the circulation early after trauma as potential indicators of an initial barrier dysfunction. The release of the barrier molecule junctional adhesion molecule-1 (JAM-1 was investigated in plasma of C57BL/6 mice 2 h after experimental mono- and polytrauma as well as in polytrauma patients (ISS ≥ 18 during a 10-day period. Correlation analyses were performed to indicate a linkage between JAM-1 plasma concentrations and organ failure. JAM-1 was systemically detected after experimental trauma in mice with blunt chest trauma as a driving force. Accordingly, JAM-1 was reduced in lung tissue after pulmonary contusion and JAM-1 plasma levels significantly correlated with increased protein levels in the bronchoalveolar lavage as a sign for alveolocapillary barrier dysfunction. Furthermore, JAM-1 was markedly released into the plasma of polytrauma patients as early as 4 h after the trauma insult and significantly correlated with severity of disease and organ dysfunction (APACHE II and SOFA score. The data support an early injury- and time-dependent appearance of the barrier molecule JAM-1 in the circulation indicative of a commencing trauma-induced barrier dysfunction.

  18. Soluble Vascular Cell Adhesion Molecule-1 (VCAM-1) as a Biomarker in the Mouse Model of Experimental Autoimmune Myocarditis (EAM)

    Science.gov (United States)

    Grabmaier, U.; Kania, G.; Kreiner, J.; Grabmeier, J.; Uhl, A.; Huber, B. C.; Lackermair, K.; Herbach, N.; Todica, A.; Eriksson, U.; Weckbach, L. T.; Brunner, S.

    2016-01-01

    Vascular cell adhesion molecule-1 (VCAM-1) is strongly upregulated in hearts of mice with coxsackie virus-induced as well as in patients with viral infection-triggered dilated cardiomyopathy. Nevertheless, the role of its soluble form as a biomarker in inflammatory heart diseases remains unclear. Therefore, we investigated whether plasma levels of soluble VCAM-1 (sVCAM-1) directly correlated with disease activity and progression of cardiac dysfunction in the mouse model of experimental autoimmune myocarditis (EAM). EAM was induced by immunization of BALB/c mice with heart-specific myosin-alpha heavy chain peptide together with complete Freund`s adjuvant. ELISA revealed strong expression of cardiac VCAM-1 (cVCAM-1) throughout the course of EAM in immunized mice compared to control animals. Furthermore, sVCAM-1 was elevated in the plasma of immunized compared to control mice at acute and chronic stages of the disease. sVCAM-1 did not correlate with the degree of acute cardiac inflammation analyzed by histology or cardiac cytokine expression investigated by ELISA. Nevertheless, heart to body weight ratio correlated significantly with sVCAM-1 at chronic stages of EAM. Cardiac systolic dysfunction studied with positron emission tomography indicated a weak relationship with sVCAM-1 at the chronic stage of the disease. Our data provide evidence that plasma levels of sVCAM-1 are elevated throughout all stages of the disease but showed no strong correlation with the severity of EAM. PMID:27501319

  19. The effect of inhaled sodium cromoglycate on cellular infiltration into the bronchial mucosa and the expression of adhesion molecules in asthmatics.

    Science.gov (United States)

    Hoshino, M; Nakamura, Y

    1997-04-01

    There is no direct evidence of the anti-inflammatory effect of inhaled sodium cromoglycate (SCG). To investigate whether inhaled SCG has any effect on cellular infiltration into the bronchial mucosa and the expression of adhesion molecules in patients with asthma, biopsies of the bronchial mucosa were taken from nine patients with atopic bronchial asthma before and after treatment with inhaled SCG (8 mg x day(-1)) from a metered-dose inhaler (MDI). Eosinophils were stained with anti-EG2, neutrophils with anti-NP57, mast cells with anti-AA1, T-lymphocytes with anti-CD4, CD8 and CD3, and macrophages with anti-CD68. Intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), endothelial leucocyte adhesion molecule-1 (ELAM-1) and P-selectin were stained at the same time as adhesion molecules expressed in vascular endothelium. The intensity of ICAM-1 expression in the bronchial epithelium was also evaluated. The numbers of eosinophils, mast cells, T-lymphocytes and macrophages were significantly reduced as a result of SCG administration, and the expression of ICAM-1, VCAM-1 and ELAM-1 was also significantly inhibited. A significant correlation was found between ICAM-1 expression and T-lymphocytes and between VCAM-1 expression and eosinophils. It was concluded that sodium cromoglycate does have an effect on the infiltration of the bronchial mucosa by inflammatory cells and also on the expression of adhesion molecules.

  20. Study of the effect of atorvastatin on the interaction between ICAM-1 and CD11b by live-cell single-molecule force spectroscopy

    Institute of Scientific and Technical Information of China (English)

    2010-01-01

    The interaction between the cell adhesion molecule CD11b and its ligand ICAM-1 plays an important role in inflammatory responses in the disease of atherosclerosis. Atorvastatin is a commonly prescribed statin drug which has been considered as one of the most potent therapeutic agents for atherosclerosis due to its lipid-lowering effect. Recently, there is a growing body of evidence that atorvastatin has anti-inflammatory effect. We have applied the advanced method of live-cell single-molecule force spectroscopy to investigate the effect of atorvastatin on adhesion force between ICAM-1 and CD11b. Our result showed that single-molecule binding force of ICAM-1 and CD11b detected by AFM in the living cells was about 40 pN, and atorvastatin did not affect this force by blocking ICAM-1 or CD11b. This was different from the ICAM-1 monoclonal antibody, which could directly reduce the binding force of ICAM-1 and CD11b. Flow cytometry results revealed that atorvastatin pretreatment decreased the ICAM-1 expression in TNF-α activated HUVECs, which may contribute to its anti-inflammatory effect. The study provides a new approach to study anti-inflammatory mechanism for clinic drugs.

  1. Soluble ICAM-1 activates lung macrophages and enhances lung injury

    DEFF Research Database (Denmark)

    Schmal, H; Czermak, B J; Lentsch, A B

    1998-01-01

    production of TNF-alpha and the CXC chemokine, macrophage inflammatory protein-2 (MIP-2). Alveolar macrophages exhibited cytokine responses to both sICAM-1 and immobilized sICAM-1, while rat PBMCs failed to demonstrate similar responses. Exposure of alveolar macrophages to sICAM-1 resulted in NFkappa...... of TNF-alpha and MIP-2 and increased neutrophil recruitment. Therefore, through engagement of beta2 integrins, sICAM-1 enhances alveolar macrophage production of MIP-2 and TNF-alpha, the result of which is intensified lung injury after intrapulmonary disposition of immune complexes.......B activation (which was blocked by the presence of the aldehyde peptide inhibitor of 28S proteosome and by genistein, a tyrosine kinase inhibitor). As expected, cross-linking of CD18 on macrophages with Ab resulted in generation of TNF-alpha and MIP-2. This response was also inhibited in the presence...

  2. Expression of ICAM-1 in colon epithelial cells

    DEFF Research Database (Denmark)

    Vainer, Ben; Sørensen, Susanne; Seidelin, Jakob;

    2003-01-01

    on monolayers of cancer cells. Conflicting results exist on epithelial ICAM-1 expression, and the aim of this study was to compare the expression in various models of colonic epithelium. MATERIALS AND METHODS: Colonic biopsies from four UC patients and four controls were examined by cryoimmuno......-electron microscopy using ICAM-1-antibodies. In four other controls, the epithelium was isolated from colonic biopsies, embedded in collagen, and evaluated similarly. Isolated crypts and cultured cancer cells were stimulated with interferon-gamma (IFN-gamma) or tumor necrosis factor-alpha (TNF-alpha). RESULTS: ICAM-1......, both colonocytes and HT29 cells were capable of expressing ICAM-1 on their apical membranes in response to supraphysiologic cytokine concentrations. These observations question the justification of extrapolating observations from colon cancer cell lines to in vivo inflammatory conditions....

  3. FMC46, a cell protrusion-associated leukocyte adhesion molecule-1 epitope on human lymphocytes and thymocytes.

    Science.gov (United States)

    Pilarski, L M; Turley, E A; Shaw, A R; Gallatin, W M; Laderoute, M P; Gillitzer, R; Beckman, I G; Zola, H

    1991-07-01

    In this report, we describe a 76-kDa glycoprotein recognized by mAb FMC46 that, by virtue of its concentration on cell protrusions involved in motility, may be important in lymphoid cell locomotion. FMC46 detects an epitope of the leukocyte adhesion molecule-1 (LAM-1), a member of the selecting family (LAM-1, Endothelial Leukocyte Adhesion Molecular-1 (ELAM-1), and Granule Membrane Protein-140 (GMP-140), that is expressed on LAM-1-transfected cell lines, is a glycosylation epitope based on its loss after culture in tunicamycin, and is closely related to the LAM-1.2 epitope. FMC46 is expressed at high density on the majority of CD45RA+ and CD45RO+ peripheral blood T cells (60 to 70%) and on a subset of thymocytes that includes the multinegative CD3- CD4- CD8- progenitor cells (100% FMC46hi) and the CD45R0- presumptive thymic generative lineage (70% FMC46hi). It appears at reduced density and frequency on CD45RA- thymocytes (50% FMC46lo), comprised mainly of death-committed thymocytes. Among thymic subsets defined by expression of CD4 and/or CD8, FMC46 is expressed at high density predominantly on a subset of single-positive cells and not on double-positive cells. These results suggest a fundamental role for LAM-1 in thymic development, with a high density preferentially expressed on cells involved in thymic generative processes and a low density on cells progressing to intrathymic death. A major subset of peripheral blood B cells and thymic B cells also express FMC46. Immunohistochemistry on frozen sections indicated strong staining in splenic follicles and around blood vessels, staining of the thymic medulla and subcapsular areas, and staining of the mantle zone of germinal centers of the lymph node. FMC46+ lymphocytes accumulated along high endothelial venules in the lymph node. On locomoting multinegative thymocytes, FMC46 is concentrated on the leading tip of extended processes, on pseudopods, and on ruffles, unlike the distribution of either CD44 or TQ1 (LAM 1

  4. Inhibitory effects of manassantin A and B isolated from the roots of Saururus chinensis on PMA-induced ICAM-1 expression.

    Science.gov (United States)

    Rho, Mun-Chual; Kwon, Oh Eok; Kim, Koanhoi; Lee, Seung Woong; Chung, Mi Yeon; Kim, Young Ho; Hayashi, Masahiko; Lee, Hyun Sun; Kim, Young-Kook

    2003-12-01

    Cell adhesion inhibitors were isolated from the methanol extract of Saururus chinensis roots by bioactivity-guided fractionation. The active compounds were identified as manassantin A ( 1) and B ( 2), dineolignan compounds. Compounds 1 and 2 inhibited PMA-induced ICAM-1/LFA-1-mediated homotypic aggregation of the HL-60 cells without cytotoxicity with MIC values of 1.0 and 5.5 nM, respectively. Even though 1 and 2 did not affect the adhesion of ICAM-1 to LFA-1, these compounds inhibited PMA-induced ICAM-1 expression in HL-60 cells in a dose-dependent fashion. These results suggest that 1 and 2 inhibit cell aggregation through down-regulation of ICAM-1 expression.

  5. Expression of mucosal addressin cell adhesion molecule 1 on vascular endothelium of gastric mucosa in patients with nodular gastritis

    Institute of Scientific and Technical Information of China (English)

    Hiroshi Ohara; Takehiko Koji; Hiroshi Nagura; Shigeru Kohno; Hajime Isomoto; Chun-Yang Wen; Chieko Ejima; Masahiro Murata; Masanobu Miyazaki; Fuminao Takeshima; Yohei Mizuta; Ikuo Murata

    2003-01-01

    AIM: The interaction of mucosal addressin cell adhesion molecule 1 (MAdCAM-1) with integrin α4β7 mediates lymphocyte recruitment into mucosa-associated lymphoid tissue (MALT). Nodular gastritis is characterized by a unique military pattern on endoscopy representing increased numbers of lymphoid follicles with germinal center, strongly associated with H pylori infection. The purpose of this study was to address the implication of the MAdCAM-1/integrin β7 pathway in NG.METHODS: We studied 17 patients with NG and H pylori infection and 19 H pylori-positive and 14 H pylori-negative controls. A biopsy sample was taken from the antrum and snap-frozen for immunohistochemical analysis of MAdCAM1 and integrin β7. In simultaneous viewing of serial sections,the percentage of MAdCAM-1-positive to von Willebrand factor-positive vessels was calculated. We also performed immunostaining with anti-CD20, CD4, CD8 and CD68 antibodies to determine the lymphocyte subsets coexpressing integrin β7.RESULTS: Vascular endothelial MAdCAM-1 expression was more enhanced in gastric mucosa with than without H pylori infection. Of note, the percentages of MAdCAM-1-positive vessels were significantly higher in the lamina propria of NG patients than in H pylori-positive controls. Strong expression of MAdCAM-1 was identified adjacent to lymphoid follicles and dense lymphoid aggregates. Integrin β7-expressing mononuclear cells, mainly composed of CD20 and CD4 lymphocytes, were associated with vessels lined with MAdCAM-1-expressing endothelium.CONCLUSION: Our results suggest that the MAdCAM-1/integrin α4β7 homing system may participate in gastric inflammation in response to H pylori-infection and contributes to MALT formation, typically leading to the development of NG.

  6. Glycyrrhizin Ameliorates Imiquimod-Induced Psoriasis-like Skin Lesions in BALB/c Mice and Inhibits TNF-a-Induced ICAM-1 Expression via NF-κB/MAPK in HaCaT Cells

    Directory of Open Access Journals (Sweden)

    Hui Xiong

    2015-02-01

    Full Text Available Background/Aim: Glycyrrhizin (GL is an important derivative of certain herbal medicines used in Asian countries. Currently, GL is used to treat hepatitis and allergic disease worldwide because of its anti-viral and anti-allergy effects. In addition to these prominent functions, GL likely regulates cellular functions such as tumor cell growth and cellular immunity. However, how GL affects the keratinocyte inflammation response remains poorly understood. The current paper investigates the effect of GL on psoriasis and explores the mechanisms involved. Methods: We used an in vitro cell model of tumor necrosis factor (TNF-a-induced keratinocyte inflammation and the topical application of imiquimod (IMQ using an animal model (mouse skin of IMQ-induced psoriasis-like inflammation (IPI to investigate the effect of GL on skin inflammation. Cell viability was analyzed using the Cell Counting Kit-8 (CCK8. Carboxyfluorescein succinimidyl ester (CFSE labeling was used to trace monocyte adherence to keratinocytes. A Western blot analysis was used to detect the expression of intercellular adhesion molecule 1 (ICAM-1 and the activation of the nuclear factor (NF-κB/mitogen-activated protein kinase (MAPK signaling pathway. A modified version of the Psoriasis Area Severity Index (PASI was used to monitor disease severity. Hematoxylin and eosin (H&E staining was used to observe pathological changes. An immunohistochemistry (IHC analysis was used to detect ICAM-1 expression in mouse skin. Results: GL treatment significantly reduced the levels of ICAM-1 in TNF-a-stimulated HaCaT cells, inhibited subsequent monocyte adhesion to keratinocytes, and suppressed the nuclear translation and phosphorylation of p65 following the degradation of inhibitor κB (IκB. GL treatment blocked the phosphorylation of extracellular signal-regulated kinase (ERK/p38 MAPK. GL effectively delayed the onset of IPI in mice and ameliorated ongoing IPI, thereby reducing ICAM-1 expression in

  7. 细胞间黏附分子-1靶向微泡超声造影成像评价肾移植后急性排异反应%Ultrasound imaging of acute renal allograft rejection with microbubbles targeted to intercellular adhesion molecule-1

    Institute of Scientific and Technical Information of China (English)

    纪丽景; 王宝平; 罗利红; 吴凤林

    2011-01-01

    目的 探讨靶向超声分子成像评价肾移植后急性排异反应的可行性.方法 采用“亲和素-生物素”桥接法构建携抗细胞间黏附分子-1(ICAM-1)靶向微泡(MBI)和携同型抗体对照微泡(MB).10只SD大鼠行左侧肾异种移植术,术后72 h移植肾随机先后注入MBI和MB(间隔30 min),分别于注入3 min后行移植肾超声造影检查,并测量移植肾声强度(VI),最后进行肾组织病理及免疫组化检测.结果 移植肾在注入靶向超声微泡后可见肾区域明显灌注显影,延迟3 min显像MBI组在移植肾可见显著的超声显影增强.而MB组移植肾仅见轻度的超声显影增强,其显影强度较前者明显减弱.MBI组和MB组移植肾VI值分别为(27.0±7.4)U、(10.2±2.4)U,两者之间差异有统计学意义(F=64.744,P<0.05).结论应用靶向ICAM-1超声微泡和超声造影结合能有效评价大鼠肾移植急性排异.%Objective To assess the feasibility of evaluation of renal allograft acute rejection in rat with contrast-enhanced ultrasound ( CEUS ) and targeted microbubbles.Methods Phospholipid microbubbles targeted to intercellular adhesion molecule -1 (ICAM-1)(MBI) and control microbubbles (MB) were created by conjugating monoclonal antibody against ICAM-1 or isotype control antibody to the lipid capsule via “avidin-biotin” bridging.Ten SD rats with acute renal allograft rejection were injected intravenous of MBI and MB in random order with a 30-min interval.After 3 min of intravenous injection of microbubbles,targeted CEUS imaging was performed in all rats.And then the video intensity (VI) was determined.Results In MBI group,a significant ultrasonic enhancement was observed,but it was not very obvious in MB group.Increment in VI value of transplant kidney in MBI group was great and it amounted to (27.0 ± 7.4)U,however,increment in VI value of in MB group was minor and it was merely (10.2 ± 2.4) U,Difference was evident in transplant kidney between of the two

  8. CRP、ICAM-1与冠心病心功能的关系研究%Relationship between CRP,ICAM-1 and cardiac function in patients with coronary heart disease

    Institute of Scientific and Technical Information of China (English)

    臧金凤

    2016-01-01

    Objective:To study the relationship between the level of serum C reactive protein and intercellular adhesion molecule and the pathogenesis and progression of coronary heart disease.Methods:84 patients with coronary heart disease were selected as the coronary heart disease group,and we selected 80 normal healthy persons as the control group.Then measured CRP levels in the two groups using radioimmunoassay,and using ELISA to detect the level of ICAM-1.Results:The level of serum CRP and ICAM-1 in the CHD group were significantly higher than those in the control group(P<0.05).With the increasing of gensini score in patients with coronary heart disease,the level of CRP and ICAM-1 were significantly raised(P<0.05).Conclusion:CRP and ICAM-1 have closely relationship with the incidence of coronary heart disease and disease progression,so it can be used as indicators to evaluate the prognosis of coronary heart disease.%目的:探讨血清C反应蛋白及胞间黏附分子水平与冠心病发病及病情进展的关系。方法:收治冠心病患者84例为冠心病组,另选取80例正常体检者为对照组,应用放射免疫法测定两组CRP水平,ELISA法测定ICAM-1水平。结果:冠心病组血清 CRP、ICAM-1水平高于对照组(P<0.05),随着冠心病患者 Gensini 评分的增高,患者CRP、ICAM-1水平升高(P<0.05)。结论:CRP、ICAM-1与冠心病发病及病情进展有密切的关系,CRP、ICAM-1水平可作为评价冠心病预后的指标。

  9. Evaluation of C-Reactive Protein, Endothelin-1, Adhesion Molecule(s, and Lipids as Inflammatory Markers in Type 2 Diabetes Mellitus Patients

    Directory of Open Access Journals (Sweden)

    Hala El-Mesallamy

    2007-01-01

    Full Text Available This study compared lipids, the product of lipid peroxidation malondialdehyde (MDA, the acute phase reactant high sensitive C-reactive protein (hsCRP, endothelin-1 (ET-1, P-selectin, intercellular adhesion molecule-1 (ICAM-1, and vascular cell adhesion molecule-1 (VCAM-1 between healthy controls, subjects with ischemic heart disease (IHD and type 2 diabetes mellitus (DM subjects who did not perform coronary artery bypass graft (CABG surgery as well as type 2 DM subjects who performed CABG. HbA1c, lipids, MDA, hsCRP, ET-1, P-selectin, ICAM-1, and VCAM-1 levels were significantly higher in the diabetic groups than in either healthy controls or IHD subjects. In the diabetic groups, there was a negative association among hsCRP and HDL-C. ET-1, ICAM-1 levels and TAG were positively correlated, as do the association between P-selectin, VCAM-1 and HbA1c%. Also a positive relation was found among hsCRP levels and ICAM-1, as well as MDA and ET-1. P-selectin and ICAM-1 were significantly positively correlated. This study indicates that increased level of oxidative stress marker, proinflammatory markers and their downstream effectors adhesion molecules occurs in type 2 DM.

  10. Molecular imaging of vascular cell adhesion molecule-1 expression in experimental atherosclerotic plaques with radiolabelled B2702-p

    Energy Technology Data Exchange (ETDEWEB)

    Broisat, A.; Riou, L.M.; Ardisson, V.; Fagret, D.; Ghezzi, C. [INSERM, U340, Radiopharmaceutiques Biocliniques, La Tronche (France); Universite de Grenoble, Saint Martin d' Heres (France); Boturyn, D.; Dumy, P. [Universite de Grenoble, Saint Martin d' Heres (France); LEDSS V - Ingenierie Moleculaire, CNRS UMR 5616, Saint Martin d' Heres (France)

    2007-06-15

    VCAM-1 plays a major role in the chronic inflammatory processes present in vulnerable atherosclerotic plaques. The residues 75-84 (B2702-p) and 84-75/75-84 (B2702-rp) of the major histocompatibility complex-1 (MHC-1) molecule B2702 were previously shown to bind specifically to VCAM-1. We hypothesised that radiolabelled B2702-p and B2702-rp might have potential for the molecular imaging of vascular cell adhesion molecule-1 (VCAM-1) expression in atherosclerotic plaques. Preliminary biodistribution studies indicated that {sup 125}I-B2702-rp was unsuitable for in vivo imaging owing to extremely high lung uptake. {sup 123}I- or {sup 99m}Tc-labelled B2702-p was injected intravenously to Watanabe heritable hyperlipidaemic rabbits (WHHL, n = 6) and control animals (n = 6). After 180 min, aortas were harvested for ex vivo autoradiographic imaging, gamma-well counting, VCAM-1 immunohistology and Sudan IV lipid staining. Robust VCAM-1 immunostaining was observed in Sudan IV-positive and to a lesser extent in Sudan IV-negative areas of WHHL animals, whereas no expression was detected in control animals. Significant 2.9-fold and 1.9-fold increases in {sup 123}I-B2702-p and {sup 99m}Tc-B2702-p aortic-to-blood ratios, respectively, were observed between WHHL and control animals (p < 0.05). Tracer uptake on ex vivo images co-localised with atherosclerotic plaques. Image quantification indicated a graded increase in {sup 123}I-B2702-p and {sup 99m}Tc-B2702-p activities from control to Sudan IV-negative and to Sudan IV-positive areas, consistent with the observed pattern of VCAM-1 expression. Sudan IV-positive to control area tracer activity ratios were 17.0 {+-} 9.0 and 5.9 {+-} 1.8 for {sup 123}I-B2702-p and {sup 99m}Tc-B2702-p, respectively. Radiolabelled B2702-p is a potentially useful radiotracer for the molecular imaging of VCAM-1 in atherosclerosis. (orig.)

  11. Complex structure of engineered modular domains defining molecular interaction between ICAM-1 and integrin LFA-1.

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    Sungkwon Kang

    Full Text Available Intermolecular contacts between integrin LFA-1 (α(Lβ(2 and ICAM-1 derive solely from the integrin α(L I domain and the first domain (D1 of ICAM-1. This study presents a crystal structure of the engineered complex of the α(L I domain and ICAM-1 D1. Previously, we engineered the I domain for high affinity by point mutations that were identified by a directed evolution approach. In order to examine α(L I domain allostery between the C-terminal α7-helix (allosteric site and the metal-ion dependent adhesion site (active site, we have chosen a high affinity variant without mutations directly influencing either the position of the α7-helix or the active sites. In our crystal, the α(L I domain was found to have a high affinity conformation to D1 with its α7-helix displaced downward away from the binding interface, recapitulating a current understanding of the allostery in the I domain and its linkage to neighboring domains of integrins in signaling. To enable soluble D1 of ICAM-1 to fold on its own, we also engineered D1 to be functional by mutations, which were found to be those that would convert hydrogen bond networks in the solvent-excluded core into vdW contacts. The backbone structure of the β-sandwich fold and the epitope for I domain binding of the engineered D1 were essentially identical to those of wild-type D1. Most deviations in engineered D1 were found in the loops at the N-terminal region that interacts with human rhinovirus (HRV. Structural deviation found in engineered D1 was overall in agreement with the function of engineered D1 observed previously, i.e., full capacity binding to α(L I domain but reduced interaction with HRV.

  12. 银杏叶提取物对大鼠急性缺血心肌细胞间黏附分子-1和白细胞介素-6表达的影响%Effects of ginkgo biloba extract on intercellular adhesion molecule-1 and interleukin-6 in acute is chemic myocardium of Rats

    Institute of Scientific and Technical Information of China (English)

    黄陆力; 王崇军; 付庆林; 韩培立; 张新中; 刘永强; 王丽娜; 崔勤涛; 周朝元

    2012-01-01

    心肌损伤的程度和冠脉病变范围.(2)大鼠急性心肌梗死中应用银杏叶提取物干预,可下调心肌中ICAM-1和IL-6的表达,减轻大鼠心肌损伤程度,证实银杏叶提取物有较好的心肌保护作用.%Objective To study the expressiou of intercellular adhesion molecule-1 (ICAM-1) and interleukin (IL)-6 in myocardium with acute myocardial infarction in rats and the influence of ginkgo biloba extract on them,and to explore the mechanism of protective effects of ginkgo biloba extract on acute infarcted myocardium.Methods One hundred and nine healthy female SD rats were selected to make acute myocardial infartion model by ligation of the left anterior descending (LAD) coronary artery,and then they were randomly divided into model group ( group A,n =38 ),ginkgo biloba treatment group ( group B,n =39 ),and sham operation group ( group C,n =32).In goup A,the left anterior descending (LAD) coronary artery was ligated solely; in group B,Ginkgo biloba extract (2 mg/kg body weight) was intravenously injected 30 min before ligation of LAD coronary artery; in group C,a loose knol was made around the first descending branch of LAD coronary arterv,witbout ligation.Each group was then randomly divided into 4 subgroups,which were observed 2 h,6 h,48 h,and 7 days after operation,respectively.Blood and heart samples were collected at every time point.Morphological changes were observed by HE staining method under the light microscopy,and ICAM-1 and IL-6 expression was detected by using immunohistochemistry.Results By using HE staining,in group A,the number of myocardial cells was decreased,and myocardial interstitial congestion,edema,myocardial fiber dissolution,flaky necrosis and infiltration of inflammatory cells were observed.Range of myocardial infarction was more than 1/2 of cardiac wall,and large number of viable myocardial cells still could be seen in the other side of cardiac wall; In group B,myocardial injuries were significantly milder than

  13. ICAM-1 and AMPK regulate cell detachment and apoptosis by N-methyl-N Prime -nitro-N-nitrosoguanidine, a widely spread environmental chemical, in human hormone-refractory prostate cancers

    Energy Technology Data Exchange (ETDEWEB)

    Chen, Yi-Cheng; Lu, Pin-Hsuan; Hsu, Jui-Ling; Yu, Chia-Chun; Guh, Jih-Hwa, E-mail: jhguh@ntu.edu.tw

    2011-12-15

    Poly(ADP-ribose) polymerase-1 (PARP-1), a sensor of DNA damage, plays a crucial role in the regulation of DNA repair. PARP-1 hyperactivation causes DNA damage and cell death. The underlying mechanism is complicated and is through diverse pathways. The understanding of responsible signaling pathways may offer implications for effective therapies. After concentration-response determination of N-Methyl-N Prime -Nitro-N-Nitrosoguanidine (MNNG, a PARP-1 activating agent and an environmental mutagen) in human hormone-refractory prostate cancers, the data showed that concentrations below 5 {mu}M did not change cell survival but cause a time-dependent up-regulation of intracellular adhesion molecule-1 (ICAM-1) in mRNA, total protein and cell surface levels. Detection of phosphorylation and degradation of I{kappa}B-{alpha} and nuclear translocation of NF-{kappa}B showed that MNNG induced the activation of NF-{kappa}B that was responsible for the ICAM-1 up-regulation since PDTC (a NF-{kappa}B inhibitor) significantly abolished this effect. However, higher concentrations (e.g., 10 {mu}M) of MNNG induced a 61% detachment of the cells which were apoptosis associated with the activation of AMP-activated protein kinase (AMPK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK). Further identification showed that both AMPK and JNK other than p38 MAPK functionally contributed to cell death. The remaining 39% attached cells were survival associated with high ICAM-1 expression. In conclusion, the data suggest that NF-{kappa}B-dependent up-regulation of ICAM-1 plays a key role on cell attachment and survival; whereas, activation of AMPK and JNK participates in cytotoxic signaling pathways in detached cells caused by PARP-1 activation. Highlights: Black-Right-Pointing-Pointer Low level of DNA damage helps cell attachment and survival via ICAM-1 upregulation. Black-Right-Pointing-Pointer High level of DNA damage causes AMPK- and JNK-involved cell detachment

  14. Mild hypothermia effects on intercellular adhesion molecule-1 and serum interleukin-6 expression in brain tissues of a rat focal ischemia model

    Institute of Scientific and Technical Information of China (English)

    Shengqi Fu; Lei Yang; Shuling Zhang; Shilong Sun; Xingai Mao

    2008-01-01

    BACKGROUND: Previous studies have confirmed the neuroprotective effect of mild hypothermia on ischemic brain injury.OBJECTIVE: To investigate the effects of mild hypothermia on intercellular adhesion molecule-1 expression and serum interleukin-6 levels in ischemic brain tissues of focal brain ischemia rats, and to explore the neuroprotective effects of mild hypothermia on ischemic brain injury.DESIGN, TIME AND SETTING: A randomized, controlled, neurobiological experiment was performed at the Central Laboratory, First Affiliated Hospital, Xinxiang Medical College, China from February to July 2006.MATERIALS: Thirty healthy, adult, Sprague Dawley rats were used to establish middle cerebral artery occlusion models using the suture method. The immunohistochemistry (streptavidin-biotin-peroxidase complex method) kit was purchased from Boster, China. Interleukin-6 radioimmunoassay was supplied by Institute of Radioimmunity, Technology Development Center, General Hospital of Chinese PLA. METHODS: The rats were equally and randomly assigned into mild hypothermia and control groups, and middle cerebral artery occlusion models were established. The rectal temperature was maintained at (37 ± 0.5)℃ in the control group. In the mild hypothermia group, the rectal temperature was maintained at (33±1)℃.MAIN OUTCOME MEASURES: At 12 hours after model establishment, the ischemic brain hemispheres were coronally sliced at the level of the optic chiasm. The number of intercellular adhesion molecule- 1 -positive vessels per high-power field was observed with an optical microscope. Serum interleukin-6 levels were measured by radioimmunoassay.RESULTS: Compared with the control group, intercellular adhesion molecule-I and serum interleukin-6 expressions were significantly decreased in ischemic brain tissues of the mild hypothermia group (P < 0.01).CONCLUSION: Mild hypothermia exhibits a neuroprotective effect by reducing serum interleukin-6 and intercellular adhesion molecule- 1

  15. β2 integrin-mediated crawling on endothelial ICAM-1 and ICAM-2 is a prerequisite for transcellular neutrophil diapedesis across the inflamed blood-brain barrier.

    Science.gov (United States)

    Gorina, Roser; Lyck, Ruth; Vestweber, Dietmar; Engelhardt, Britta

    2014-01-01

    In acute neuroinflammatory states such as meningitis, neutrophils cross the blood-brain barrier (BBB) and contribute to pathological alterations of cerebral function. The mechanisms that govern neutrophil migration across the BBB are ill defined. Using live-cell imaging, we show that LPS-stimulated BBB endothelium supports neutrophil arrest, crawling, and diapedesis under physiological flow in vitro. Investigating the interactions of neutrophils from wild-type, CD11a(-/-), CD11b(-/-), and CD18(null) mice with wild-type, junctional adhesion molecule-A(-/-), ICAM-1(null), ICAM-2(-/-), or ICAM-1(null)/ICAM-2(-/-) primary mouse brain microvascular endothelial cells, we demonstrate that neutrophil arrest, polarization, and crawling required G-protein-coupled receptor-dependent activation of β2 integrins and binding to endothelial ICAM-1. LFA-1 was the prevailing ligand for endothelial ICAM-1 in mediating neutrophil shear resistant arrest, whereas Mac-1 was dominant over LFA-1 in mediating neutrophil polarization on the BBB in vitro. Neutrophil crawling was mediated by endothelial ICAM-1 and ICAM-2 and neutrophil LFA-1 and Mac-1. In the absence of crawling, few neutrophils maintained adhesive interactions with the BBB endothelium by remaining either stationary on endothelial junctions or displaying transient adhesive interactions characterized by a fast displacement on the endothelium along the direction of flow. Diapedesis of stationary neutrophils was unchanged by the lack of endothelial ICAM-1 and ICAM-2 and occurred exclusively via the paracellular pathway. Crawling neutrophils, although preferentially crossing the BBB through the endothelial junctions, could additionally breach the BBB via the transcellular route. Thus, β2 integrin-mediated neutrophil crawling on endothelial ICAM-1 and ICAM-2 is a prerequisite for transcellular neutrophil diapedesis across the inflamed BBB.

  16. 糖基化终产物刺激大鼠骨髓内皮细胞表达细胞间粘附分子-1的机制探讨%The mechanism of intercellular adhesion molecule-1 expression in endothelial cells stimulated by advanced glycosylation end products

    Institute of Scientific and Technical Information of China (English)

    余路; 邱鸿鑫; 王亚平; 司良毅; 吴珊; 祝继华

    2001-01-01

    AIM: To explore the relationship between intercellular adhesionmolecule-1(ICAM-1)expression in endothelial cells(EC) and advanced glycosylation end products(AGEs) stimulation. METHODS: Murine bone marrow derived ECs was stimulated by AGEs after pretreated with anti-AGEs, anti-IL-1β and N-acetylcysteine(NAC),then SOD activity and ICAM-1 concentration and adhesion rate(AR) were evaluated. RESULTS: ECs which expressed ICAM-1[(0.65±0.14) vs (0.11±0.02)] induced by AGEs showed lower SOD activity [(0.69±0.19)×103 U/L vs (1.71±0.42)×103 U/L]. The ICAM-1 expression as well as the increase of AR caused by AGEs stimulation could be suppressed by anti-AGEs(0.12±0.01) and NAC(0.11±0.05). Anti-IL-1β had no influence on these changes. CONCLUSION: AGEs could induce endothelial cells to express ICAM-1 in vitro, most probably due to the formation of free radicals. Besides, AGEs may stimulate other cells to secrete cytokines resulting in ICAM-1 expression in endothelial cells.%目的:探讨糖基化终产物(AGEs)致内皮细胞表达细胞间粘附分子-1(ICAM-1)与自由基产生之间的关系。方法:内皮细胞(EC)用抗AGEs抗体、抗IL-1β多抗、N-乙酰半胱氨酸(NAC)预处理1h后AGEs作用6h,测定IL-1β、超氧化物歧化酶(SOD)、ICAM-1、内皮细胞-中性粒细胞粘附率。结果:AGEs刺激后ICAM-1表达增加[吸光度(A)为0.65±0.14vs0.11±0.02]的内皮细胞SOD活性降低[(0.69±0.19)×103U/Lvs(1.71±0.42)×103U/L]。ICAM-1的增加可被抗AGEs抗体[吸光度(A)为(0.12±0.01)]、NAC[吸光度(A)为(0.11±0.05)]和抗ICAM-1抗体[吸光度(A)为(0.10±0.04)]抑制。外源性IL-1β也可刺激内皮细胞表达ICAM-1[吸光度(A)为(0.72±0.23)]。结论:AGEs刺激内皮细胞表达ICAM-1可能与其导致细胞自由基的产生有关;AGEs还可通过刺激其他细胞产生细胞因子间接作用于EC,参与促进ICAM-1表达。

  17. 地屈孕酮对多囊卵巢综合征妊娠大鼠种植窗期 PR、ICAM-1的影响%Effect of dydrogesterone on progesterone receptor and intercellular adhesion molecule-1 in pregnant rats with polycystic ovarian syndrome in planting window period

    Institute of Scientific and Technical Information of China (English)

    刘音吟; 谈勇; 徐菊芳

    2016-01-01

    pregnant rats);group C(PCOS pregnant rats with dydrogesterone).On the 5th day of pregnancy, the levels of E2, P and TNF-αin each group were determined by ELISA , and the expression levels of progesterone receptor( PR) and intercellular adhesion molecule-1(ICAM-1) in endometrium were detected by immunohistochemistry.Results:In planting window period ,the levels of E2 and TNF-αin group B and C were higher than those in group A ( P0.05).ICAM-1 was positively correlated with P, while TNF-αwas negatively correlated with E2/P. Conclusion: Low rate of implantation in PCOS pregnant rats was probably associated with abnormal sex hormone levels, TNF-αand decreased expression of PR and ICAM-1 .Dydrogesterone can possibly improve the rate of implantation through adjusting P and E2/P, upregulating ICAM-1 and PR expression, and improving ovarian function and the receptivity of endometrium.%目的:探讨多囊卵巢综合征( PCOS)大鼠低着床率的可能原因及地屈孕酮在种植窗期的作用机制。方法:80日龄始正常大鼠以生理盐水(NS)、PCOS模型大鼠以克罗米芬(CC)连续灌胃5 d后分别与雄鼠合笼,选取妊娠大鼠随机分为A组(正常妊娠组)、B组( PCOS妊娠组)、C组( PCOS妊娠加地屈孕酮组)3组。于妊娠第5天各组大鼠以酶联免疫吸附法( ELISA)测定雌二醇( E2)、孕酮( P)、肿瘤坏死因子( TNF-a)表达水平,免疫组化法测定右侧子宫内膜孕激素受体(PR)、细胞间黏附分子(ICAM-1)表达水平。结果:种植窗期E2、TNF-a表达B、C组高于A组(P<0.05,P<0.01),P表达C、A组高于B组(P<0.05,P<0.01),E2/P值3组间差异显著(P<0.05,P<0.01),PR表达B组低于A组(P<0.05),ICAM-1表达B组低于A、C组(P<0.05);PR与E2、P、E2/P值均无相关性(P>0.05),ICAM-1与P呈正相关(P<0.05),TNF-a与E2/P值呈负相关。结

  18. T Cell Migration from Inflamed Skin to Draining Lymph Nodes Requires Intralymphatic Crawling Supported by ICAM-1/LFA-1 Interactions.

    Science.gov (United States)

    Teijeira, Alvaro; Hunter, Morgan C; Russo, Erica; Proulx, Steven T; Frei, Thomas; Debes, Gudrun F; Coles, Marc; Melero, Ignacio; Detmar, Michael; Rouzaut, Ana; Halin, Cornelia

    2017-01-24

    T cells are the most abundant cell type found in afferent lymph, but their migration through lymphatic vessels (LVs) remains poorly understood. Performing intravital microscopy in the murine skin, we imaged T cell migration through afferent LVs in vivo. T cells entered into and actively migrated within lymphatic capillaries but were passively transported in contractile collecting vessels. Intralymphatic T cell number and motility were increased during contact-hypersensitivity-induced inflammation and dependent on ICAM-1/LFA-1 interactions. In vitro, blockade of endothelial cell-expressed ICAM-1 reduced T cell adhesion, crawling, and transmigration across lymphatic endothelium and decreased T cell advancement from capillaries into lymphatic collectors in skin explants. In vivo, T cell migration to draining lymph nodes was significantly reduced upon ICAM-1 or LFA-1 blockade. Our findings indicate that T cell migration through LVs occurs in distinct steps and reveal a key role for ICAM-1/LFA-1 interactions in this process.

  19. ICAM-1 Upregulation in Ethanol-Induced Fatty Murine Livers Promotes Injury and Sinusoidal Leukocyte Adherence after Transplantation

    Directory of Open Access Journals (Sweden)

    Tom P. Theruvath

    2012-01-01

    Full Text Available Background. Transplantation of ethanol-induced steatotic livers causes increased graft injury. We hypothesized that upregulation of hepatic ICAM-1 after ethanol produces increased leukocyte adherence, resulting in increased generation of reactive oxygen species (ROS and injury after liver transplantation (LT. Methods. C57BL/6 wildtype (WT and ICAM-1 knockout (KO mice were gavaged with ethanol (6 g/kg or water. LT was then performed into WT recipients. Necrosis and apoptosis, 4-hydroxynonenal (4-HNE immunostaining, and sinusoidal leukocyte movement by intravital microscopy were assessed. Results. Ethanol gavage of WT mice increased hepatic triglycerides 10-fold compared to water treatment (P<0.05. ICAM-1 also increased, but ALT was normal. At 8 h after LT of WT grafts, ALT increased 2-fold more with ethanol than water treatment (P<0.05. Compared to ethanol-treated WT grafts, ALT from ethanol-treated KO grafts was 78% less (P<0.05. Apoptosis also decreased by 75% (P<0.05, and 4-HNE staining after LT was also decreased in ethanol-treated KO grafts compared to WT. Intravital microscopy demonstrated a 2-fold decrease in leukocyte adhesion in KO grafts compared to WT grafts. Conclusions. Increased ICAM-1 expression in ethanol-treated fatty livers predisposes to leukocyte adherence after LT, which leads to a disturbed microcirculation, oxidative stress and graft injury.

  20. Nanoscale Imaging Reveals a Tetraspanin-CD9 Coordinated Elevation of Endothelial ICAM-1 Clusters.

    Directory of Open Access Journals (Sweden)

    Jonas Franz

    Full Text Available Endothelial barriers have a central role in inflammation as they allow or deny the passage of leukocytes from the vasculature into the tissue. To bind leukocytes, endothelial cells form adhesive clusters containing tetraspanins and ICAM-1, so-called endothelial adhesive platforms (EAPs. Upon leukocyte binding, EAPs evolve into docking structures that emanate from the endothelial surface while engulfing the leukocyte. Here, we show that TNF-α is sufficient to induce apical protrusions in the absence of leukocytes. Using advanced quantitation of atomic force microscopy (AFM recordings, we found these structures to protrude by 160 ± 80 nm above endothelial surface level. Confocal immunofluorescence microscopy proved them positive for ICAM-1, JAM-A, tetraspanin CD9 and f-actin. Microvilli formation was inhibited in the absence of CD9. Our findings indicate that stimulation with TNF-α induces nanoscale changes in endothelial surface architecture and that--via a tetraspanin CD9 depending mechanism--the EAPs rise above the surface to facilitate leukocyte capture.

  1. Cytokine and adhesion molecule expression evolves between the neutrophilic and lymphocytic phases of viral meningitis.

    Science.gov (United States)

    Makis, Alexandros; Shipway, David; Hatzimichael, Eleftheria; Galanakis, Emmanouil; Pshezhetskiy, Dmitry; Chaliasos, Nikolaos; Stebbing, Justin; Siamopoulou, Antigone

    2010-09-01

    Viral meningitis is characterized by cerebrospinal fluid (CSF) lymphocyte pleocytosis, although neutrophils may predominate in the early phase. The T helper 1 (Th1)/Th2 cytokine balance and expression of adhesion molecules seem to be involved in the CSF chemotaxis. We aimed to determine expression of cytokines and adhesion molecules in enteroviral meningitis. We investigated the serum and CSF levels of adhesion molecules (E-selectin, L-selectin, vascular cell adhesion molecule-1 [VCAM-1], and intracellular adhesion molecule-1 [ICAM-1]) and cytokines (interleukin-12 [IL-12] and IL-4) in 105 children during an outbreak of enteroviral meningitis. Diagnosis was confirmed with positive polymerase chain reaction (PCR) and/or serology for echovirus or Coxsackie virus, and matched with control subjects for clinical features but with negative PCR and/or serology. Apart from VCAM-1, the CSF levels of all investigated inflammatory molecules were significantly increased. In serum, sL-selectin and ICAM-1 levels were significantly higher than control subjects. Serum and CSF L-selectin, serum VCAM-1, and CSF IL-12 were all observed to be expressed in significantly higher levels in the neutrophil-dominant subgroup (72% had duration of symptoms 24 h). Serum and CSF ICAM-1 was found at significantly higher levels in the latter group. Evolving expression of adhesion molecules and cytokines indicates a shift from Th1 to Th2 immune responses as infection progresses.

  2. ICAM1 and fibrinogen-γ are increased in uterine epithelial cells at the time of implantation in rats.

    Science.gov (United States)

    Lecce, Laura; Kaneko, Yui; Madawala, Romanthi J; Murphy, Christopher R

    2011-05-01

    Uterine epithelial cells transform into a receptive state to adhere to an implanting blastocyst. Part of this transformation includes the apical concentration of cell adhesion molecules at the time of implantation. This study, for the first time, investigates the expression of ICAM1 and fibrinogen-γ (FGG) in uterine epithelial cells during normal pregnancy, pseudopregnancy and in hormone-treated rats. An increase (P FGG dimerization increased (P FGG in the uterine epithelium at the time of implantation in the rat is similar to that seen in lymphocyte-endothelium adhesion, and we suggest a similar mechanism in embryo-uterine epithelium adhesion is utilized.

  3. TWEAK enhances E-selectin and ICAM-1 expression, and may contribute to the development of cutaneous vasculitis.

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    Tao Chen

    Full Text Available Our previous work indicated that TWEAK is associated with various types of cutaneous vasculitis (CV. Herein, we investigate the effects of TWEAK on vascular injury and adhesion molecule expression in CV mice. We showed that TWEAK priming in mice induced a local CV. Furthermore, TWEAK priming also increased the extravasation of FITC-BSA, myeloperoxidase activity and the expression of E-selectin and ICAM-1. Conversely, TWEAK blockade ameliorated the LPS-induced vascular damage, leukocyte infiltrates and adhesion molecules expression in LPS-induced CV. In addition, TWEAK treatment of HDMECs up-regulated E-selectin and ICAM-1 expression at both mRNA and protein levels. TWEAK also enhanced the adhesion of PMNs to HDMECs. Finally, western blot data revealed that TWEAK can induce phosphorylation of p38, JNK and ERK in HDMECs. These data suggest that TWEAK acted as an inducer of E-selectin and ICAM-1 expression in CV mice and HDMECs, may contribute to the development of CV.

  4. Reduction of atherosclerosis in cholesterol-fed rabbits and decrease of expressions of intracellular adhesion molecule-1 and vascular endothelial growth factor in foam cells by a water-soluble fraction of Polygonum multiflorum.

    Science.gov (United States)

    Yang, Peng-Yuan; Almofti, Mohamad Radwan; Lu, Ling; Kang, Hui; Zhang, Jing; Li, Tie-Jun; Rui, Yao-Cheng; Sun, Lian-Na; Chen, Wan-Sheng

    2005-11-01

    Polygonum multiflorum stilbeneglycoside (PMS) is a water-soluble fraction of Polygonum multiflorum Thunb., one of the most famous tonic traditional Chinese medicines, that has protective effects on the cardiovascular system. The purpose of the present study is to elucidate the effects of PMS on macrophage-derived foam cell functions and the reduction of severity of atherosclerosis in hypercholesterolemic New Zealand White (NZW) rabbits. NZW rabbits were fed for 12 weeks with a normal diet, a high cholesterol diet, or a high cholesterol diet associated with irrigation with different doses of PMS (25, 50, or 100 mg/kg). Treatment of NZW rabbits fed with high cholesterol diet with 100 mg/kg PMS attenuated the increase in plasma cholesterol, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, and plasma triglyceride. Treatment with 50 and 100 mg/kg PMS caused 43% and 60% decrease in atherosclerotic lesioned area ratio to total surface area, respectively. In U937 foam cells, PMS could decrease the high expression of intercellular adhesion molecule (ICAM)-1 protein and the vascular endothelial growth factor (VEGF) protein levels in the medium induced by oxidized lipoprotein when analyzed by flow cytometry. The results proved that PMS is a powerful agent against atherosclerosis and that PMS action could possibly be through the inhibition of the expression of ICAM-1 and VEGF in foam cells.

  5. Omentin inhibits TNF-{alpha}-induced expression of adhesion molecules in endothelial cells via ERK/NF-{kappa}B pathway

    Energy Technology Data Exchange (ETDEWEB)

    Zhong, Xia, E-mail: zhongxia1977@126.com [Department of Emergency, Provincial Hospital Affiliated to Shandong University, Jinan 250021 (China); Li, Xiaonan; Liu, Fuli; Tan, Hui [Department of Emergency, Provincial Hospital Affiliated to Shandong University, Jinan 250021 (China); Shang, Deya, E-mail: wenhuashenghuo1@163.com [Department of Emergency, Provincial Hospital Affiliated to Shandong University, Jinan 250021 (China)

    2012-08-24

    Highlights: Black-Right-Pointing-Pointer Omentin inhibited TNF-{alpha}-induced adhesion of THP-1 cells to HUVECs. Black-Right-Pointing-Pointer Omentin reduces expression of ICAM-1 and VCAM-1 induced by TNF-{alpha} in HUVECs. Black-Right-Pointing-Pointer Omentin inhibits TNF-{alpha}-induced ERK and NF-{kappa}B activation in HUVECs. Black-Right-Pointing-Pointer Omentin supreeses TNF-{alpha}-induced expression of ICAM-1 and VCAM-1 via ERK/NF-{kappa}B pathway. -- Abstract: In the present study, we investigated whether omentin affected the expression of intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in tumor necrosis factor-{alpha} (TNF-{alpha}) induced human umbilical vein endothelial cells (HUVECs). Our data showed that omentin decreased TNF-{alpha}-induced expression of ICAM-1 and VCAM-1 in HUVECs. In addition, omentin inhibited TNF-{alpha}-induced adhesion of THP-1 cells to HUVECs. Further, we found that omentin inhibited TNF-{alpha}-activated signal pathway of nuclear factor-{kappa}B (NF-{kappa}B) by preventing NF-{kappa}B inhibitory protein (I{kappa}B{alpha}) degradation and NF-{kappa}B/DNA binding activity. Omentin pretreatment significantly inhibited TNF-{alpha}-induced ERK activity and ERK phosphorylation in HUVECs. Pretreatment with PD98059 suppressed TNF-{alpha}-induced NF-{kappa}B activity. Omentin, NF-kB inhibitor (BAY11-7082) and ERK inhibitor (PD98059) reduced the up-regulation of ICAM-1 and VCAM-1 induced by TNF-{alpha}. These results suggest that omentin may inhibit TNF-{alpha}-induced expression of adhesion molecules in endothelial cells via blocking ERK/NF-{kappa}B pathway.

  6. Molecular Mechanisms of Curcumin on Diabetes-Induced Endothelial Dysfunctions: Txnip, ICAM-1, and NOX2 Expressions

    Directory of Open Access Journals (Sweden)

    Natchaya Wongeakin

    2014-01-01

    Full Text Available We aim to investigate the effects of curcumin on preventing diabetes-induced vascular inflammation in association with its actions on Txnip, ICAM-1, and NOX2 enzyme expressions. Male Wistar rats were divided into four groups: control (CON, diabetic (DM; streptozotocin (STZ, i.v. 55 mg/kg BW, control-treated with curcumin (CONCUR; 300 mg/kg BW, and diabetes treated with curcumin (DMCUR; 300 mg/kg BW. 12th week after STZ injection, iris blood perfusion, leukocyte adhesion, Txnip, p47phox, and malondialdehyde (MDA levels were determined by using laser Doppler, intravital fluorescent confocal microscopy, Western Blot analysis, and TBAR assay, respectively. The iris blood perfusion of DM and DMCUR was decreased significantly compared to CON and CONCUR (P<0.001. Plasma glucose and HbA1c of DM and DMCUR were increased significantly compared to CON and CONCUR (P<0.001. Leukocyte adhesion, ICAM-1, p47phox expression, and MDA levels in DM were increased significantly compared to CON, CONCUR, and DMCUR (P<0.05. Txnip expression in DM and DMCUR was significantly higher than CON and CONCUR (P<0.05. From Pearson’s analysis, the correlation between the plasma MDA level and the endothelial functions was significant. It suggested that curcumin could ameliorate diabetic vascular inflammation by decreasing ROS overproduction, reducing leukocyte-endothelium interaction, and inhibiting ICAM-1 and NOX2 expression.

  7. ICAM-1 triggers liver regeneration through leukocyte recruitment and Kupffer cell-dependent release of TNF-alpha/IL-6 in mice.

    NARCIS (Netherlands)

    Selzner, N; Selzner, M; Odermatt, B; Tian, Y; Rooijen, van N.; Clavien, PA

    2003-01-01

    AIMS: Tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 mediate hepatocyte proliferation in vivo, suggesting that local and systemic inflammatory reactions may trigger hepatic regeneration after major tissue loss. METHODS: Wild-type, intercellular adhesion molecule (ICAM)-1-/-, and neutropeni

  8. Different effects of antisense RelA p65 and NF-κB1 p50 oligonucleotides on the nuclear factor-κB mediated expression of ICAM-1 in human coronary endothelial and smooth muscle cells

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    Both Anton

    2001-08-01

    Full Text Available Abstract Background Activation of nuclear factor-κB (NF-κB is one of the key events in early atherosclerosis and restenosis. We hypothesized that tumor necrosis factor-α (TNF-α induced and NF-κB mediated expression of intercellular adhesion molecule-1 (ICAM-1 can be inhibited by antisense RelA p65 and NF-κB1 p50 oligonucleotides (RelA p65 and NF-κB1 p50. Results Smooth muscle cells (SMC from human coronary plaque material (HCPSMC, plaque material of 52 patients, SMC from the human coronary media (HCMSMC, human endothelial cells (EC from umbilical veins (HUVEC, and human coronary EC (HCAEC were successfully isolated (HCPSMC, HUVEC, identified and cultured (HCPSMC, HCMSMC, HUVEC, HCAEC. 12 hrs prior to TNF-α stimulus (20 ng/mL, 6 hrs RelA p65 and NF-κB1 p50 (1, 2, 4, 10, 20, and 30 μM and controls were added for a period of 18 hrs. In HUVEC and HCAEC there was a dose dependent inhibition of ICAM-1 expression after adding of both RelA p65 and NF-κB1 p50. No inhibitory effect was seen after incubation of HCMSMC with RelA p65 and NF-κB1 p50. A moderate inhibition of ICAM-1 expression was found after simultaneous addition of RelA p65 and NF-κB1 p50 to HCPSMC, no inhibitory effect was detected after individual addition of RelA p65 and NF-κB1 p50. Conclusions The data point out that differences exist in the NF-κB mediated expression of ICAM-1 between EC and SMC. Experimental antisense strategies directed against RelA p65 and NF-κB1 p50 in early atherosclerosis and restenosis are promising in HCAEC but will be confronted with redundant pathways in HCMSMC and HCPSMC.

  9. The impact of high intensity aerobic interval training (HIIT and flaxseed oil on ICAM-1 gene expression in heart tissue in male Wistar rats

    Directory of Open Access Journals (Sweden)

    Y Khademi

    2016-12-01

    Full Text Available Abstract Background: The prevalence of cardiovascular disease may be due to inflammation and systemic inflammation plays an important role in the development and progression of atherosclerosis. ICAM-1 is one of the important factors in the pathogenesis of atherosclerosis is an inflammatory effect of physical activity and plant protection products on the response it is not well known. Methods  Thirty Wistar rats were selected as sample. Rats were randomly divided into six groups of five, including control, exercise, extracts dose of 10 mg / kg, extract dose 30 mg / kg, a dose of extract practice mg / kg 10, and extracts Practice dose of 30 mg / kg, respectively. Training groups, five sessions per week for 10 weeks, intense interval training involves running on a treadmill with an intensity of 90 to 95 percent of VO2max for rodents, at specified hours during the day. After the rats were sacrificed and the heart tissue, and to measure gene expression of ICAM-1 and LFA-1 were used. Result Data analysis showed that the expression of ICAM-1 has been reduced in training supplement groups The expression of intercellular adhesion molecule receptor (ITG has decreased in the exercise and supplement group. Conclusion: The results of this study show that both exercise and extract significant effect on gene expression of ICAM-1. And decreased expression of ICAM-1 was also flax oil ICAM-1 gene expression was also reduced. The findings of this study showed that the combination of training and flax oil reduces the expression of ICAM-1 compared to the control group. So it is likely that this method can be used as a way to prevent cardiovascular disease.

  10. Th17 Cells Induce Dopaminergic Neuronal Death via LFA-1/ICAM-1 Interaction in a Mouse Model of Parkinson's Disease.

    Science.gov (United States)

    Liu, Zhan; Huang, Yan; Cao, Bei-Bei; Qiu, Yi-Hua; Peng, Yu-Ping

    2016-11-14

    T helper (Th)17 cells, a subset of CD4(+) T lymphocytes, have strong pro-inflammatory property and appear to be essential in the pathogenesis of many inflammatory diseases. However, the involvement of Th17 cells in Parkinson's disease (PD) that is characterized by a progressive degeneration of dopaminergic (DAergic) neurons in the nigrostriatal system is unclear. Here, we aimed to demonstrate that Th17 cells infiltrate into the brain parenchyma and induce neuroinflammation and DAergic neuronal death in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)- or 1-methyl-4-phenylpyridinium (MPP(+))-induced PD models. Blood-brain barrier (BBB) disruption in the substantia nigra (SN) was assessed by the signal of FITC-labeled albumin that was injected into blood circulation via the ascending aorta. Live cell imaging system was used to observe a direct contact of Th17 cells with neurons by staining these cells using the two adhesion molecules, leukocyte function-associated antigen (LFA)-1 and intercellular adhesion molecule (ICAM)-1, respectively. Th17 cells invaded into the SN where BBB was disrupted in MPTP-induced PD mice. Th17 cells exacerbated DAergic neuronal loss and pro-inflammatory/neurotrophic factor disorders in MPP(+)-treated ventral mesencephalic (VM) cell cultures. A direct contact of LFA-1-stained Th17 cells with ICAM-1-stained VM neurons was dynamically captured. Either blocking LFA-1 in Th17 cells or blocking ICAM-1 in VM neurons with neutralizing antibodies abolished Th17-induced DAergic neuronal death. These results establish that Th17 cells infiltrate into the brain parenchyma of PD mice through lesioned BBB and exert neurotoxic property by promoting glial activation and importantly by a direct damage to neurons depending on LFA-1/ICAM-1 interaction.

  11. Amino acid sequences mediating vascular cell adhesion molecule 1 binding to integrin alpha 4: homologous DSP sequence found for JC polyoma VP1 coat protein

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    Michael Andrew Meyer

    2013-07-01

    Full Text Available The JC polyoma viral coat protein VP1 was analyzed for amino acid sequences homologies to the IDSP sequence which mediates binding of VLA-4 (integrin alpha 4 to vascular cell adhesion molecule 1. Although the full sequence was not found, a DSP sequence was located near the critical arginine residue linked to infectivity of the virus and binding to sialic acid containing molecules such as integrins (3. For the JC polyoma virus, a DSP sequence was found at residues 70, 71 and 72 with homology also noted for the mouse polyoma virus and SV40 virus. Three dimensional modeling of the VP1 molecule suggests that the DSP loop has an accessible site for interaction from the external side of the assembled viral capsid pentamer.

  12. Amino Acid Sequences Mediating Vascular Cell Adhesion Molecule 1 Binding to Integrin Alpha 4: Homologous DSP Sequence Found for JC Polyoma VP1 Coat Protein.

    Science.gov (United States)

    Meyer, Michael Andrew

    2013-01-01

    The JC polyoma viral coat protein VP1 was analyzed for amino acid sequences homologies to the IDSP sequence which mediates binding of VLA-4 (integrin alpha 4) to vascular cell adhesion molecule 1. Although the full sequence was not found, a DSP sequence was located near the critical arginine residue linked to infectivity of the virus and binding to sialic acid containing molecules such as integrins (3). For the JC polyoma virus, a DSP sequence was found at residues 70, 71 and 72 with homology also noted for the mouse polyoma virus and SV40 virus. Three dimensional modeling of the VP1 molecule suggests that the DSP loop has an accessible site for interaction from the external side of the assembled viral capsid pentamer.

  13. Detection of IL-32, ICAM-1 and IL-10 in serum of patients with rheumatoid arthritis%类风湿关节炎患者血清白细胞介素-32细胞间黏附分子-1白细胞介素-10的检测及意义

    Institute of Scientific and Technical Information of China (English)

    安新; 高利常; 张英杰; 李秀山; 孙欣

    2014-01-01

    Objective Concentrations of interleukin-32(IL-32) ,intercellular adhesion molecule-1 (ICAM-1) and interleukin-10 (IL-10) in serum of patients with rheumatoid arthritis (RA) were detected ,so to explore the relationships between the upper cytokines and the pathogenesis ,progression and effect on RA .Methods ELISA was used to detect the concentrations of IL-32 ,ICAM-1 and IL-10 in the serum of 115 patients with RA ,31 osteo-arthritis (OA) and 76 healthy control .Spearman model analysis was used to analyze the correlation of cytokines with anti-CCP antibody ,rheumatoid factor (RF) ,hypersensitive C-reactive protein (hs-CRP) and erythrocyte sed-imentation rate (ESR) .Results The concentrations of IL-32 ,ICAM-1 and IL-10 in RA and OA were significant-ly higher than that of healthy group (P<0.05) .RA severe active group and stable group in IL-32 ,ICAM-1 con-centration levels were significantly different ;IL-32 and ICAM -1 had significantly positive correlations with anti-CCP antibody ,RF ,hs-CRP ,ESR ,DAS28 ,joint swelling number and joint tenderness number (P<0.01) ,while IL-10 levels were seemly to be positive correlation with hs-CRP ,ESR (P<0.05 or P<0.01) .Conclusion IL-32 , ICAM-1 and IL-10 were likely to play important roles in RA progression ,and were closely related with RA patho-genesis .Study the biological effects of IL-32 ,ICAM-1 and IL-10 on the pathophysiological process in RA will contribute to understand the pathogenesis of RA and provide a basis for its clinical treatment .%目的:通过对类风湿关节炎(RA)患者血清白细胞介素(IL)-32、细胞间黏附分子-1(ICAM-1)、IL-10的检测,探讨IL-32、ICAM-1、IL-10在RA发病、病程发展中的意义及临床相关性。方法采用酶联免疫吸附试验(ELISA),检测115例RA、31例骨关节炎(OA)、76名对照组IL-32、ICAM-1、IL-10的水平,并与抗环瓜氨酸肽(CCP)抗体、类风湿因子(RF)、超敏C反应蛋白(hs-CRP)、红

  14. 单核细胞趋化蛋白-1和细胞间黏附分子-1与动脉粥样硬化和牙周病的关系%Relation of monocyte chemoattractant protein-1 and intercellular adhesion molecule-1 between atherosclerosis and periodontal disease

    Institute of Scientific and Technical Information of China (English)

    焦丽宁

    2012-01-01

    Coronafy heart disease on the pathologic foundation of atherosclerosis is one of the fatal diseases now, however, there is an association exists between periodontitis and atherosclerosis. Both monocyte chemoattractant protein(MCP)-1 and intercellular adhesion molecule(ICAM) -1 play important roles in the occurrence and development of atherosclerosis and periodontitis. In this article the relationship between atherosclerosis and periodontitis by means of MCP-1 and ICAM-1 is reviewed.%以动脉粥样硬化为病理基础的冠心病是目前主要的致死性疾病之一,而牙周病与动脉粥样硬化之间存在着一定的相关性.单核细胞趋化蛋白(MCP)-1和细胞间黏附分子(ICAM)-1在动脉粥样硬化和牙周病的发生发展中起着重要的作用.本文就MCP-1和ICAM-1以及二者与动脉粥样硬化、牙周病间的关系作一综述.

  15. Effect of non-surgical periodontal therapy on level of serum soluble intercellular adhesion molecule-1 and glycated hemoglobin A1c in patients with type 2 diabetes and chronic periodontitis%牙周非手术治疗对2型糖尿病伴牙周炎患者糖化血红蛋白A1c和血清可溶性细胞间黏附分子-1的影响

    Institute of Scientific and Technical Information of China (English)

    袁堂霞; 张彦表; 周云; 王凡涛; 王峰

    2013-01-01

    Objective To evaluate the effects of non-surgical periodontal treatment on clinical periodontal measurements,glycemic control,and level of serum soluble intercellular adhesion molecule-1 (sICAM-1) in type 2 diabetes mellitus with chronic periodontitis patients.Methods Patients with type 2 diabetes and chronic periodontitis were selected and classified into well-controlled group[glycated hemoglobin A1c(GHbA1c)<7.00%,n=30,DMCP1 group] and poorly-controlled group (GHbA1c≥ 7.00%,n=30,DMCP2 group).Thirty systemically healthy patients with chronic periodontitis were recruited as control group (CP group),All subjects underwent non-surgical periodontal therapy.Plaque index(PLI),sulcus bleeding index (SBI),bleeding on probing(BOP),probing depth (PD),clinical attachment loss (CAL),serum sICAM-1 concentration,and the value of fasting plasma glucose(FPG),GHbA1c were recorded at baseline,1 and 3 months after periodontal treatment.Results The three study groups showed significant improvements for the levels of PD,SBI,PLI,BOP,and serum sICAM-1 concentration at 1 and 3 months after non-surgical periodontal treatment (P<0.05).The level of CP group and DMCP1 group also showed significant improvements for the levels of CAL(P<0.05),but no significant change was found in DMCP2 group(P>0.05).At 3 months after periodontal treatment,GHbA1c levels in DMCP2 group significantly decreased by 1.12%(P<0.05),whereas no significant changes were found in CP and DMCP1 groups (P>0.05).Conclusion Non-surgical periodontal treatment can significantly improve periodontal health status in patients with type 2 diabetes and periodontitis,reduce the level of serum sICAM-1,and can reduce the level of GHbA1c in poorly controlled type 2 diabetic patients.%目的 探讨牙周非手术治疗对2型糖尿病伴慢性牙周炎(DMCP)患者牙周状况、糖代谢及血清可溶性细胞间黏附分子-1 (sICAM-1)的影响.方法 选择诊断为2型糖尿病伴慢性牙周炎的

  16. Comparative Study of Serum Soluble Intercellular Adhesion Molecule-1 in Different Obese Women with Polycystic Ovary Syndrome%不同肥胖标准PCOS患者血清可溶性细胞间黏附分子-1水平比较

    Institute of Scientific and Technical Information of China (English)

    黄卡立; 蒋凤艳; 胡芸

    2011-01-01

    目的:比较不同肥胖标准的多囊卵巢综合征(PCOS)患者血清可溶性细胞间黏附分子-1(sICAM-1)水平差异.方法:将PCOS患者以体质量指数(BMI)≥24 ks/m2为肥胖标准分为肥胖A组和非肥胖A组,以腰臀比(WHR)≥0.8为肥胖标准,分为肥胖B组和非肥胖B组,以BMI≥24 kg/m2且WHR≥0.8为肥胖标准分为肥胖C组和非肥胖C组,比较不同组别间的血清sICAM-1水平,并分析sICAM-1水平与BMI、WHR的相关性.结果:肥胖A、B、C组血清sICAM-1水平较对应的非肥胖A、B、C组显著升高(P0.05);非肥胖A组患者血清sICAM-1水平高于非肥胖B组、C组患者(均P0.05);血清sICAM-1水平与BMI、WHR均呈正相关(r分别为0.204和0.360,均P<0.05).结论:PCOS患者血清aICAM-1水平与肥胖有密切联系,PCOS患者sICAM-1水平随着WHR及BMI增大而升高.%Objective:To study the level of serum soluble intercellular adhesion molectle-1 (sICAM-1) in obese women with polycystic ovary syndrome (PCOS). Methods: The obese patients with PCOS were divided into two goups (obese A group and non-obese A group) according to the standard of body mass index (BMI) ≥ 24 kg/m2. The patients were divided into two goups (obese B group and non-obese B group) according to the standard of waist-hip ratio (WHR) ≥ 0.8. The patients were also divided into two groups(obese C groups and non-obese C group) according to the standard of BMI ≥ 24 kg/m2 and WHR≥ 0.8. The serum levels of sICAM-1 were compared between groups. The correlation was analysed between the level of sICAM-1 and the values of BMI and WHR. Results :The serum levels of sICAM-1 were significantly higher in obese A, obese B and obese C groups than those of non-obese A, non-obese B and non-obese C groups (P< 0.05). There were no signficant differences in serum levels of sICAM-1 between obese A, obese B and obese C groups (P > 0.05).The serum level of sICAM-1 was significant higher in non-obese A group than that of non-obese B group and non

  17. Effects on icam-1 Expression and Releasing of Huvec Induced by ox-ldl of Aurantii Fructus Immaturus Extract and its Active Components%枳实提取物及其药效组分对ox-LDL损伤的人脐静脉内皮细胞ICAM-1表达和NO释放的影响

    Institute of Scientific and Technical Information of China (English)

    罗容; 吴霞; 李静宜; 崔湖荣; 张楠; 张贵君

    2012-01-01

    Objective: To investigate the effect of HUVEC treated by ox-LDL of Aurantii Fructus Immaturus extract, hesperidin and neohesperidint on ICAM-1 expression and NO releasing. Methods: HUVEC was cultured in vitro. HUVEC was induced by 50 μg/mL ox-LDL to establish injury model. Cytotoxicity was studied by MTS colorimetry to determine the highest contents of samples in this test. Effect of ICAM-1 expression was studied by cell-ELISA. NO releasing was studied by nitrate/nitrite colorimetric assay kit. Results: ①HUVEC viability was greater than 80 % when 2 mg/mL Aurantii Fructus Immaturus extract, 0.03125 mg/mL hesperidin and 0.25 mg/mL neohesperidin was incubated with culture medium respectively. ②2.0 mg/mL and 1.0 mg/mL Aurantii Fructus Immaturus extract, 15.625 μg/mL hesperidin and 0.2500 mg/mL neohesperidin had significant inhibitory effect on ICAM-1 expression of HUVEC induced by ox-LDL. (3)2.0 mg/mL Aurantii Fructus Immaturus extract could increase the contents of NO in supernatant of normal HUVEC and HUVEC induced by ox-LDL significantly. 7.813 μg/mL, 15.625 μg/mL and 31.250 μg/mL hesperidin can increase the content of NO in supernatant of HUVEC induced by ox-LDL significantly. 31.250^g/mL hesperidin could increase the content of NO in supernatant of normal HUVEC significantly. 0.2500 mg/mL and 0.1250 mg/mL neohesperidin could increase the content of NO in supernatant of HUVEC induced by ox-LDL significantly. Conclusions: Aurantii Fructus Immaturus extract, hesperidin and neohesperidin can inhibit ICAM-1 expression and promote NO releasing of HUVEC induced by ox-LDL.%目的:研究枳实提取物及其药效组分橙皮苷和新橙皮苷对氧化低密度脂蛋白(oxidized low density lipoprotein,Ox-LDL)损伤的人脐静脉内皮细胞(human umbilical vein endothelial cells line,HUVEC)细胞间黏附分子-1(intercellular adhesion molecule-1,ICAM-1)表达和一氧化氮(nitric oxide,NO)释放的影响.方法:体外培养HUVEC,50μg/mL ox-LDL制造HUVEC损

  18. Relation between K469E gene polymorphism of ICAM-1 and recurrence of ACS and cardiovascular mortality

    Institute of Scientific and Technical Information of China (English)

    Ling-Zhi Liu; En-Ping Wu; Heng-Liang Liu

    2013-01-01

    Objective:To explore the relation betweenK469E gene polymorphism of intercellular adhesion molecular-1(ICAM-1) and the recurrence ofACS and cardiovascular mortality.Methods:A total of185 patients withACS hospitalized inDepartment ofCardiology in our hospital fromSep2007 toSep2008 were selected as objectives.Polymerase chain reaction was used to analyzeK469E gene polymorphism ofICAM-1.According to the genotypes, they were divided into two groups: group withK allele(KK+KE) and group withoutK allele(EE).The two groups were followed up prospectively for five years and blood lipid, blood pressure, blood glucose, recurrence and death ofACS were collected when the patients left hospital.The relation betweenICAM-1 gene polymorphism and the recurrence ofACS and cardiovascular mortality was analyzed byLogistic regression.Results:After long-term follow-up, it was found thatACS recurred on71 cases (38.4%) and10 cases died, among which3 cases died of cardiovascular disease.The recurrence ofACS and cardiovascular mortality in group withK allele were remarkably higher than that in group withoutK allele(P0.05).Conclusions:K469E gene polymorphism ofICAM-1 was related toACS recurrence and cardiovascular mortality,K allele probably an independentrisky factor and hypertension and to which the level ofHDL-C were closely related.

  19. Circulating adhesion molecules in patients with virus-related chronic diseases of the liver

    Institute of Scientific and Technical Information of China (English)

    Cosimo Marcello Bruno; Claudio Sciacca; Danila Cilio; Gaetano Bertino; Anna Elisa Marchese; Gaetana Politi; Lucia Chinnici

    2005-01-01

    AIM: In the inflammatory state, intercellular adhesion molecule-1 (ICAM-1) and vascular cellular adhesion molecule-1 (VCAM-1) play a key role in promoting migration of immunological cells from the circulation to target site.Aim of our study was to investigate soluble forms of these molecules in patients with virus-related chronic liver diseases, to assess their behavior in different pathologies and correlation with severity of liver damage.METHODS: Circulating ICAM-1 and VCAM-1 were assayed by EIA commercial kits (R&D System Co.,Abington, UK) in 23 patients with chronic active hepatitis (CH), 50 subjects affected by liver cirrhosis (LC) and 15 healthy controls comparable for sex and age. In patients, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were also detected by autoanalyzer.RESULTS: LC patients had significantly higher ICAM-1 values than CH patients (38.56±7.4 ng/mL vs 20.89±6.42 ng/mL; P<0.001) and these ones had significantly higher values than controls (12.92±1.08 ng/mL; P<0.001). In CH group, ICAM-1 levels were significantly related to inflammatory activity (P= 0.041) and ALT values (r= 0.77;P<0.05). VCAM-1 values were significantly increased only in LC patients (P<0.001) and related to severity of liver impairment.CONCLUSION: These findings suggest that the determination of serum ICAM-1 can be considered as an additional useful marker of hepatocellular necrosis and inflammatory activity in chronic hepatitis, while serum VCAM-1 is an indicator of liver fibrogenesis and severity of disease in cirrhosis.

  20. Omentin inhibits TNF-α-induced expression of adhesion molecules in endothelial cells via ERK/NF-κB pathway.

    Science.gov (United States)

    Zhong, Xia; Li, Xiaonan; Liu, Fuli; Tan, Hui; Shang, Deya

    2012-08-24

    In the present study, we investigated whether omentin affected the expression of intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in tumor necrosis factor-α (TNF-α) induced human umbilical vein endothelial cells (HUVECs). Our data showed that omentin decreased TNF-α-induced expression of ICAM-1 and VCAM-1 in HUVECs. In addition, omentin inhibited TNF-α-induced adhesion of THP-1 cells to HUVECs. Further, we found that omentin inhibited TNF-α-activated signal pathway of nuclear factor-κB (NF-κB) by preventing NF-κB inhibitory protein (IκBα) degradation and NF-κB/DNA binding activity. Omentin pretreatment significantly inhibited TNF-α-induced ERK activity and ERK phosphorylation in HUVECs. Pretreatment with PD98059 suppressed TNF-α-induced NF-κB activity. Omentin, NF-kB inhibitor (BAY11-7082) and ERK inhibitor (PD98059) reduced the up-regulation of ICAM-1 and VCAM-1 induced by TNF-α. These results suggest that omentin may inhibit TNF-α-induced expression of adhesion molecules in endothelial cells via blocking ERK/NF-κB pathway.

  1. Effects of Triptolide on Expression of AIF and ICAM-1 in Rat's Kidney Tissure with Renal Ischemia Reperfusion Injury%雷公藤内酯醇对肾缺血再灌注大鼠凋亡诱导因子及细胞间黏附分子-1表达的影响

    Institute of Scientific and Technical Information of China (English)

    包自阳; 朱彩凤; 李苞芳; 朱斌; 汤绚丽

    2012-01-01

    目的:探讨雷公藤内酯醇(TP)对肾缺血再灌注(I/R)大鼠的肾保护作用,及对凋亡诱导因子、细胞间黏附分子-1的影响.方法:48只雄性Wistar大鼠随机分为假手术组、I/R模型组(I/R组)、TP高、中、低剂量干预组、泼尼松对照组(Pred组).采用夹闭双侧肾动脉30 min,再灌注18 h的方法制作肾I/R大鼠模型.检测血肌酐(Scr)、尿素氮(BUN),原位末端标记法检测肾小管上皮细胞凋亡,观察肾病理改变,计算肾小管损伤(ATN)评分.Western印迹和RT-PCR分别检测AIF、ICAM-1蛋白和基因表达.结果:(1)I/R组血Scr、BUN、ATN评分及细胞凋亡指数较假手术组显著升高(P<0.01);与I/R组比较,TP各组以上指标均改善(P<0.01),pred组血Scr、BUN、ATN评分改善(P<0.01),但细胞凋亡指数无明显变化(P>0.05).(2)I/R组大鼠肾组织AIF、ICAM-1较假手术组高表达(P<0.01);与I/R组比较,TP各组二者表达均减弱(P<0.01),pred组ICAM-1表达减弱(P<0.01)但AIF表达差异无统计学意义(P>0.05).结论:TP对肾I/R大鼠具有肾保护作用,其部分机制可能与抑制肾小管上皮细胞过度凋亡及AIF、ICAM-1表达有关.%Objective: To explore protective effect of Triptolide ( TP ) on rat' s kidney from renal ischemia reperfusion ( 1/ R ) injury and interference effect on expression level of apoptosis - inducing factor ( AIF ) and intercellular adhesion molecule - 1 and ( ICAM - 1 ). Methods:48 male Wistar rats were randomly divided into six groups: sham operation group, ischemia reperfusion injury group ( I/R group ), low TP group, medium TP group, high TP group, prednisone group ( Pred group ). The renal I/R rat model was duplicated by clamping Bilateral renal artery for 30 minutes and then artery reperfusion for 18 hours. The levels of serum creatinine ( Scr ) and Blood urea nitrogen ( Bun ) were detected. Apoptosis of tubular epithelial cell was determined by terminal deoxynucleotidy transferase dUTP nick end labeling

  2. Manassantin A and B isolated from Saururus chinensis inhibit TNF-alpha-induced cell adhesion molecule expression of human umbilical vein endothelial cells.

    Science.gov (United States)

    Kwon, Oh Eok; Lee, Hyun Sun; Lee, Seung Woong; Chung, Mi Yeon; Bae, Ki Hwan; Rho, Mun-Chual; Kim, Young-Kook

    2005-01-01

    Leukocyte adhesion to the vascular endothelium is a critical initiating step in inflammation and atherosclerosis. We have herein studied the effect of manassantin A (1) and B (2), dineolignans, on interaction of THP-1 monocytic cells and human umbilical vein endothelial cells (HUVEC) and expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin in HUVEC. When HUVEC were pretreated with 1 and 2 followed by stimulation with TNF-alpha, adhesion of THP-1 cells to HUVEC decreased in dose-dependent manner with IC50 values of 5 ng/mL and 7 ng/mL, respectively, without cytotoxicity. Also, 1 and 2 inhibited TNF-alpha-induced up-regulation of ICAM-1, VCAM-1 and E-selectin. The present findings suggest that 1 and 2 prevent monocyte adhesion to HUVEC through the inhibition of ICAM-1, VCAM-1 and E-selectin expression stimulated by TNF-alpha, and may imply their usefulness for the prevention of atherosclerosis relevant to endothelial activation.

  3. Ac-SDKP suppresses TNF-α-induced ICAM-1 expression in endothelial cells via inhibition of IκB kinase and NF-κB activation.

    Science.gov (United States)

    Zhu, Liping; Yang, Xiao-Ping; Janic, Branislava; Rhaleb, Nour-Eddine; Harding, Pamela; Nakagawa, Pablo; Peterson, Edward L; Carretero, Oscar A

    2016-05-01

    N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a naturally occurring tetrapeptide that prevents inflammation and fibrosis in hypertension and other cardiovascular diseases. We previously showed that, in angiotensin II-induced hypertension, Ac-SDKP decreased the activation of nuclear transcription factor NF-κB, whereas, in experimental autoimmune myocarditis and hypertension animal models, it also reduced the expression of endothelial leukocyte adhesion molecule ICAM-1. However, the mechanisms by which Ac-SDKP downregulated ICAM-1 expression are still unclear. TNF-α is a proinflammatory cytokine that induces ICAM-1 expression in various cell types via TNF receptor 1 and activation of the classical NF-κB pathway. We hypothesized that in endothelial cells Ac-SDKP suppresses TNF-α-induced ICAM-1 expression by decreasing IKK phosphorylation that as a consequence leads to a decrease of IκB phosphorylation and NF-κB activation. To test this hypothesis, human coronary artery endothelial cells were treated with Ac-SDKP and then stimulated with TNF-α. We found that TNF-α-induced ICAM-1 expression was significantly decreased by Ac-SDKP in a dose-dependent manner. Ac-SDKP also decreased TNF-α-induced NF-κB translocation from cytosol to nucleus, as assessed by electrophoretic mobility shift assay, which correlated with a decrease in IκB phosphorylation. In addition, we found that Ac-SDKP decreased TNF-α-induced IKK phosphorylation and IKK-β expression. However, Ac-SDKP had no effect on TNF-α-induced phosphorylation of p38 MAP kinase or ERK. Thus we conclude that Ac-SDKP inhibition of TNF-α activation of canonical, i.e., IKK-β-dependent, NF-κB pathway and subsequent decrease in ICAM-1 expression is achieved via inhibition of IKK-β.

  4. Three to Tango: MUC1 as a ligand for both E-selectin and ICAM-1 in the breast cancer metastatic cascade

    Directory of Open Access Journals (Sweden)

    Yue eGeng

    2012-07-01

    Full Text Available Cancer cell tethering and rolling on the vascular wall is facilitated by various selectin:glycoprotein interactions which lead to eventual extravasation and metastases. The aberrantly underglycosylated mucin MUC1 has been shown to both abundantly express selectin binding moieties (sialyl Lewis x and a and to consistently expose its core epitope. Flow cytometry was used to determine MUC1 expression on ZR-75-1 and MCF7 cells, while immunofluorescence microscopy was used to confirm the aberrant form of MUC1 and MUC1:ICAM-1 interactions. Each cell line was then perfused through combined E-selectin and ICAM-1 coated microtubes, as a model of the microvascular endothelium. ZR-75-1 and MCF7 were found to express abundant and low levels of underglycosylated MUC1, respectively. The rolling/adhesion profiles showed that ZR-75-1 cells, when compared to MCF7 cells, interact with E-selectin more efficiently resulting in sufficiently slow rolling velocities to form MUC1:ICAM-1 interactions thereby facilitating firm adhesion. The purpose and novelty of this work is the demonstration of the synergistic adhesion capabilities of MUC1 in the metastatic adhesion cascade, where the observed differential adhesion is consistent with the relative metastatic potential of the ZR-75-1 (highly metastatic and MCF7 (weakly metastatic cell lines.

  5. Association of G+1688A Polymorphism of Platelet Endothelial Cell Adhesion Molecule-1 Gene with Myocardial Infarction in the Chinese Han Population

    Institute of Scientific and Technical Information of China (English)

    YANG Ying; CHENG Longxian; Ripen Nsenga; HE Meian; CHANG Zhitang; WU Tangchun

    2007-01-01

    In order to investigate the association of G+1688A (Ser563Asn) polymorphism of platelet endothelial cell adhesion molecule-1 (PECAM-1) gene with myocardial infarction (MI) in the Chi- nese Han population, the G+1688A polymorphism in PECAM-1 gene was detected by polymerase chain reaction-restriction fragment-length polymorphism (PCR-RFLP) method among 502 subjects, including 218 patients with MI and 284 controls. The results showed that there was significant dif-ference in AA frequencies of genotype G+1688A polymorphism between case and control groups (39% vs 24%, P<0.001). A similar trend was observed on the allele frequencies (A/G: 62% vs 49%, P<0.001). Among the subjects with high serum total cholesterol level or high systolic blood pressure level, the variant AA genotype was associated with high risk of MI (adjusted OR, 2.13; 95% CI, 1.08-4.41 and adjusted OR, 2.53; 95%CI, 1.63-3.63). The single nucleotide polymorphism (SNP) at position +1688 in the exon 8 of PECAM-1 gene was associated with MI and the allele A might be a risk factor for MI in the Chinese Han population.

  6. Study on the serum levels of soluble intercellular adhesion molecule—1(slCAM—1) in patients with Helicobacter pylori Infection

    Institute of Scientific and Technical Information of China (English)

    吴勤动; 石益海; 等

    2002-01-01

    Objective:To evaluate the interaction between serum levels of soluble intercellular adhesion molecule-1(sICAM-1) and Helicobacter pylori(H.pylori) infection in patients with chronic gastritis and peptic ulcer.Methods:The serum levels of sICAM-1 in 205 patients with chronic gastric diseases were detected by ELISA method and the status of H.pylori was determined by histologic examination.RUT,14C=UBT,and serology,Ther sera obtained from 18 healthy volunteers served as controls,Results:The serum lervels of sICAM-1 were significantly higher in patients with H.pylori positive than those of H.pylori negative(889.43±32.52ng/mlvs,747.07±30.45ng/ml,P<0.05),The serum levels of sICAM-1 in patients with mild,moderate and severe infection of H.pylori were 841.68±72.36ng/ml,905.43±37.59ng/ml and 1012.54±49.34ng/ml,respectively(P<0.05),The serum levels of sICAM-1 proved to be significantly correlated with the density of H.pylori colonization in gastric mucosa(rs=0.316,P<0.001),The serum levels of sICAM-1 in patients with chronic gastritis and peptic ulcer were significantly higher than those in healthy controls(P<0.05).Conclusions:These results indicated that H.pylori infection up-regulates the expression of sICAM-1.

  7. 抗细胞间黏附分子1靶向液态氟碳微球对大鼠缺血再灌注损伤心肌的靶向结合和抗炎作用的研究%TARGETED COMBINATION AND ANTI-INFLAMMATORY EFFECTS OF ANTI-INTERCELLULAR ADHESION MOLECULE 1 TARGETED PERFLUOROOCTYLBROMIDE PARTICLES ON MYOCARDIAL ISCHEMIA-REPERFUSION INJURY IN RAT MODEL

    Institute of Scientific and Technical Information of China (English)

    尚艳文; 唐红; 韦馨; 侯江龙; 王炼; 李国华; 宋海波; 方华

    2013-01-01

    目的 探讨抗细胞间黏附分子 1 (intercellular adhesion molecule 1,ICAM-1)靶向液态氟碳(perfluorooctylbromide,PFOB)微球对大鼠缺血再灌注损伤心肌的靶向结合和抗炎作用.方法 取成年SD大鼠76只,雌雄不限,体重250~300 g.取30只采用结扎冠状动脉左前降支30 min方法制备心肌缺血再灌注损伤模型,免疫组织化学染色观察缺血再灌注6h心肌细胞表面 ICAM-1蛋白表达情况,以10只正常大鼠作为对照;液相芯片技术检测缺血再灌注6、12、18、24、30、36、42、48 h血清中IL-8含量.另取36只大鼠随机分为6组(n=6):心肌缺血再灌注/靶向PFOB微球组(A组)、心肌缺血再灌注/普通PFOB微球组(B组)、正常大鼠/靶向PFOB微球组(C组)、正常大鼠/普通PFOB微球组(D组)、心肌缺血再灌注/生理盐水组(E组)、假手术组(F组).A、B、E组大鼠同法建立心肌缺血再灌注损伤模型;F组开胸后在冠状动脉下穿线但不结扎.缺血再灌注6h后,A、B、C、D组经颈静脉注入1 mL对应的PFOB微球,E组注入1 mL生理盐水.超声观察A、B、C、D组注入PFOB微球前后心肌显像情况;荧光显微镜观察A、B、C、D组心脏冰冻切片微球结合情况;液相芯片技术检测A、B、E、F组缺血再灌注6h及24 h血清中IL-8含量.结果 缺血再灌注6 h后大鼠心肌细胞表面ICAM-1蛋白表达以前间隔和左室前壁较明显;IL-8含量自缺血再灌注6h起开始增高,24 h达峰值.注入PFOB微球后至缺血再灌注24 hA、B、C、D组超声观察均未见明确受损心肌靶向显影;荧光显微镜下A组前间隔和左室前壁心肌细胞核周围可见绿染的靶向PFOB微球,B、C、D组均未见绿色荧光.缺血再灌注6h,A、B、E组间IL-8含量相似(P>0.05),但均高于F组(P< 0.05); 24h时A、B组间IL-8含量相似(P>0.05),均低于E组(P<0.05).结论 抗ICAM-1靶向PFOB微球可靶向结合大鼠缺血再灌注损伤心肌,通过其抗

  8. 苦参对急性白血病患者 sICA M-1 和 sVCA M-1 水平的影响%Effects of radix sophorae flavescentis on serum levels of sICAM-1 and sVCAM-1 in patients with acute leukemia

    Institute of Scientific and Technical Information of China (English)

    马玲娣; 唐跃华; 董艳芬; 朱志超; 蒋丽佳; 何晓清; 刘娟

    2016-01-01

    目的 探讨苦参对急性白血病患者可溶性细胞间黏附分子-1(sICAM-1)和可溶性血管细胞黏附分子-1(sVCAM-1)水平的影响.方法 选取2013年3月至2015年3月该院收治的急性白血病患者60例 ,按照治疗方式的不同将患者分为常规化疗组和苦参治疗组 ,每组各30例.常规化疗组患者给予常规化疗方案实施治疗 ,苦参治疗组患者在常规化疗基础上加用苦参治疗.另选取同期该院健康体检者60例作为健康对照组.采用酶联免疫吸附试验(ELISA)分析急性白血病患者治疗前后和健康体检者血清sICAM-1、sVCAM-1水平.结果 急性白血病患者血清sICAM-1、sVCAM-1水平在治疗前及治疗后均明显高于健康对照组 ,两者比较差异有统计学意义(P<0 .05).常规化疗组及苦参治疗组 ,治疗后患者血清sICAM-1、sVCAM-1水平均有下降 ,苦参治疗组sICAM-1、sV-CAM-1的水平下降程度较常规化疗组更明显 ,差异有统计学意义(P<0 .05).苦参治疗组治疗有效率为90 .00% ,高于常规化疗组的67 .67% ,差异有统计学意义(P<0 .05).结论 苦参可明显降低急性白血病患者血清sICAM-1、sVCAM-1水平 ,改善常规化疗药物疗效 ,促进患者康复.%Objective To investigate the effect of radix sophorae flavescentis on the levels of soluble intercellu-lar adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1(sVCAM-1) in the patients with a-cute leukemia .Methods 60 cases of acute leukemia in our hospital from March 2013 to March 2015 were selected and divided into the conventional chemotherapy group and the radix sophorae flavescentis therapy group according to dif-ferent therapeutic methods ,30 cases in each group .The conventional chemotherapy group was given the routine chemotherapy regimen for implementing the therapy ,while on this basis the radix sophorae flavescentis therapy group was added with radix sophorae flavescentis .Contemporaneous 60 individuals undergoing

  9. 连接粘附分子-1在人角膜上皮中的表达%Expression of junctional adhesion molecule-1 in human Corneal epithelium

    Institute of Scientific and Technical Information of China (English)

    陈立忠; 洪晶; 海老原 伸行; 村上晶

    2007-01-01

    AIM:To investigate the expression and distribution of junction adhesion molecule-1(JAM-1)in human corneal epithelium and compare with that of occludin.METHODS:The expression in RNAs of JAM-1 and occludin was revealed by RT-PCR and the presence of protein was analyzed by the FACS method.Double immunofluorescent staining was used to determine the tissue distribution of JSM-1 and occludin in human corneal epithelium.RESULTS:The expression of JAM-1 and occludin was found in cultured human corneal epithelial cells.The double immunofluorescent study showed positive staining for JAM-1 at cell borders in the entire epithelial layer,while relatively extensive staining was seen in the superficial layer,where it COexisted with the expression of ocdudin.CONCLUSION:JAM-1 was expressed in entire layer of human corneal epithelium encircling the cells.%目的:检测连接粘附分子-1(junction adhesion molecule,JAM-1)在正常人角膜上皮各层中的表达及分布特点并与咬合蛋白(occludin)进行比较.方法:培养人角膜上皮细胞提取细胞总RNA.以逆转录后获得的cDNA为模板PCR扩增目的基因JAM-1及occludin.流式细胞仪检测JAM-1蛋白表达.双重免疫荧光观察JAM-1与occludin在正常人角膜上皮组织的原位表达.结果:通过RT-PCR在培养人角膜上皮细胞中检测到JAM-1与occludin扩增片段;流式细胞仪检测到JAM-1蛋白表达;双重免疫荧光结果显示occludin染色主要位于表层上皮层细胞之间;而JAM-1荧光染色不仅见于上皮表层,在整个上皮层细胞之间均可见其荧光反应.结论:Occludin主要位于正常人角膜上皮表层细胞之间,JAM-1在正常人角膜上皮的全层中均有表达.

  10. Expression of platelet-endothelial cell adhesion molecule-1 in human umbilical vein endothelial cells by exposure to advanced glycosylation end products and inflammatory mediators

    Institute of Scientific and Technical Information of China (English)

    孟丹; 刘乃丰

    2003-01-01

    Objective To determine whether advanced glycosylation end products modified bovine serum albumin (AGEs-BSA) affects endothelial cell lateral junction protein, platelet-endothelial cell adhesion molecule-1 (PECAM-1) in the presence or absence of inflammatory mediators.Methods Cultured human umbilical vein endothelial cells (HUVECs) were exposed to AGEs-BSA for 6, 12, 24, and 36 hours, and exposed to AGEs-BSA glycosylated with different concentrations of glucose, tumor necrosis factord-α (TNF-α), interferon (IFN-γ), TNF-α+IFN-γ and AGEs-BSA+TNF-α for 24 hours, respectively. Expression of PECAM-1 mRNA was measured by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) with β-actin as an internal standard, and sequencing of RT-PCR products was performed to confirm the specificity of amplification for PECAM-1 gene. The endothelial cell surface expression of PECAM-1 was determined by flow cytometry (FCM).Results There were no significant changes in the expression of PECAM-1 mRNA and protein when the cells were exposed to AGEs-BSA with different concentrations or periods (P> 0.05). However, PECAM-1 expression was reduced in the cells treated with TNF-α, IFN-γ, TNF-α+IFN-γ and AGEs-BSA+TNF-α. The level of PECAM-1 treated with AGEs-BSA+TNF-α was lower than that of TNF-α treated alone (P<0.01).Conclusions AGEs-BSA had no effect on the expression of PECAM-1 mRNA and protein in cultured HUVEC. With the presence of inflammatory mediator TNF-α, AGEs-BSA decreased the level of PECAM-1, which might reduce the adhesion interaction between adjacent endothelial cells, enhance the permeability of endothelial cells, and might be implicated in the endothelial dysfunction and pathogenesis of atherosclerosis in patients with diabetes mellitus. The significance of this phenomenon in intracellular signal transduction remains to be determined.

  11. Circulating Adhesion Molecules in Patients with Keshan Disease and Their Relationship with Coxsackie B Virus Infection

    Institute of Scientific and Technical Information of China (English)

    Congsheng LI; Xiaolin NIU; Cong LEI

    2009-01-01

    This study determined the levels of serum soluble intercellular adhesion molecule-1 (sI-CAM-1) and soluble vascular cell adhesion molecular-1 (sVCAM-1) in patients with different types of Keshan disease (KD),examined the relationship between Coxsackie B virus-specific lgM antibody (CBV-IgM) and sICAM-1 or sVCAM-1 in KD patients,and investigated the role of these adhesion molecules in the pathogenesis of KD and their clinical implications.The levels of serum slCAM-1,sVCAM-1 and CBV-IgM were measured by using enzyme-linked immunosorbent assay in 22 patients with chronic Keshan disease (CKD),27 with latent Keshan disease (LKD) and 28 healthy controis.The subjects in different groups were adjusted for sex and age.Echocardiography was adopted to determine left ventrieular ejection fraction (LVEF) in 22 patients with CKD.The results showed that CKD patients had significantly higher levels of sICAM-1 and sVCAM-1 than LKD patients and healthy controls (P<0.01 for all).And there was significant difference in the levels of the 2 adhesion molecules between LKD patients and healthy controls (P<0.05).A negative correlation was found between LVEF and sICAM-1 or sVCAM-1 in CKD patients.The percentage of CBV-specific IgM positive individuals in KD patients was significantly higher than that of healthy controls.In CVB-specific IgM positive patients,the levels of serum sICAM-1 and sVCAM-1 were significantly greater than those in CBV-specific IgM negative counterpart.It was concluded that the increase in the levels of sICAM-1 and sVCAM-1 suggests the progression of inflammation in KD.sICAM-1 and sVCAM-1 can promote the development of myocardial pathology and lead to poor myocardial function.The increased serum sICAM-1 and sVCAM-1 in KD patients may be related to CBV infection.

  12. High throughput functional assays of the variant antigen PfEMP1 reveal a single domain in the 3D7 Plasmodium falciparum genome that binds ICAM1 with high affinity and is targeted by naturally acquired neutralizing antibodies.

    Directory of Open Access Journals (Sweden)

    Andrew V Oleinikov

    2009-04-01

    Full Text Available Plasmodium falciparum-infected erythrocytes bind endothelial receptors to sequester in vascular beds, and binding to ICAM1 has been implicated in cerebral malaria. Binding to ICAM1 may be mediated by the variant surface antigen family PfEMP1: for example, 6 of 21 DBLbetaC2 domains from the IT4 strain PfEMP1 repertoire were shown to bind ICAM1, and the PfEMP1 containing these 6 domains are all classified as Group B or C type. In this study, we surveyed binding of ICAM1 to 16 DBLbetaC2 domains of the 3D7 strain PfEMP1 repertoire, using a high throughput Bioplex assay format. Only one DBL2betaC2 domain from the Group A PfEMP1 PF11_0521 showed strong specific binding. Among these 16 domains, DBL2betaC2(PF11_0521 best preserved the residues previously identified as conserved in ICAM1-binding versus non-binding domains. Our analyses further highlighted the potential role of conserved residues within predominantly non-conserved flexible loops in adhesion, and, therefore, as targets for intervention. Our studies also suggest that the structural/functional DBLbetaC2 domain involved in ICAM1 binding includes about 80 amino acid residues upstream of the previously suggested DBLbetaC2 domain. DBL2betaC2(PF11_0521 binding to ICAM1 was inhibited by immune sera from east Africa but not by control US sera. Neutralizing antibodies were uncommon in children but common in immune adults from east Africa. Inhibition of binding was much more efficient than reversal of binding, indicating a strong interaction between DBL2betaC2(PF11_0521 and ICAM1. Our high throughput approach will significantly accelerate studies of PfEMP1 binding domains and protective antibody responses.

  13. Differential effects of fenofibrate versus atorvastatin on the concentrations of E-selectin and vascular cellular adhesion molecule-1 in patients with type 2 diabetes mellitus and mixed hyperlipoproteinemia: a randomized cross-over trial

    Directory of Open Access Journals (Sweden)

    Otto Carsten

    2003-12-01

    Full Text Available Abstract Background Diabetic dyslipoproteinemia is characterized by hypertriglyceridemia, low HDL-cholesterol and often elevated LDL-cholesterol and is a strong risk factor for atherosclerosis. Adhesion molecule levels are elevated both in hyperlipoproteinemia and diabetes mellitus. It is unclear whether fibrate or statin therapy has more beneficial effects on adhesion molecule concentrations. Methods Atorvastatin (10 mg/d was compared to fenofibrate (200 mg/d each for 6 weeks separated by a 6 week washout period in 11 patients (6 male, 5 female; 61.8 ± 8.2 years; body mass index 29.8 ± 3.1 kg/m2 with type 2 diabetes mellitus (HbA1c 7.3 ± 1.1 % and mixed hyperlipoproteinemia using a randomized, cross-over design. Fasting blood glucose, HbA1c, lipid parameters, E-selectin, ICAM-1, VCAM-1, and fibrinogen concentrations were determined before and after each drug. Results Glucose and HbA1c concentrations remained unchanged during the whole study period. LDL cholesterol was reduced during atorvastatin therapy, triglycerides were lowered more effectively with fenofibrate. Comparison of pre- and postreatment concentrations of E-selectin showed a reduction during atorvastatin (-7 %, p = 0.11 and fenofibrate (-10 %, p Conclusions In addition to the different beneficial effects on lipid metabolism, both drugs appear to lower adhesion molecule plasma concentrations in a different manner in patients with type 2 diabetes and mixed hyperlipoproteinemia. Our observations should be confirmed in a larger cohort of such patients.

  14. Regulation of ICAM-1 in cells of the monocyte/macrophage system in microgravity.

    Science.gov (United States)

    Paulsen, Katrin; Tauber, Svantje; Dumrese, Claudia; Bradacs, Gesine; Simmet, Dana M; Gölz, Nadine; Hauschild, Swantje; Raig, Christiane; Engeli, Stephanie; Gutewort, Annett; Hürlimann, Eva; Biskup, Josefine; Unverdorben, Felix; Rieder, Gabriela; Hofmänner, Daniel; Mutschler, Lisa; Krammer, Sonja; Buttron, Isabell; Philpot, Claudia; Huge, Andreas; Lier, Hartwin; Barz, Ines; Engelmann, Frank; Layer, Liliana E; Thiel, Cora S; Ullrich, Oliver

    2015-01-01

    Cells of the immune system are highly sensitive to altered gravity, and the monocyte as well as the macrophage function is proven to be impaired under microgravity conditions. In our study, we investigated the surface expression of ICAM-1 protein and expression of ICAM-1 mRNA in cells of the monocyte/macrophage system in microgravity during clinostat, parabolic flight, sounding rocket, and orbital experiments. In murine BV-2 microglial cells, we detected a downregulation of ICAM-1 expression in clinorotation experiments and a rapid and reversible downregulation in the microgravity phase of parabolic flight experiments. In contrast, ICAM-1 expression increased in macrophage-like differentiated human U937 cells during the microgravity phase of parabolic flights and in long-term microgravity provided by a 2D clinostat or during the orbital SIMBOX/Shenzhou-8 mission. In nondifferentiated U937 cells, no effect of microgravity on ICAM-1 expression could be observed during parabolic flight experiments. We conclude that disturbed immune function in microgravity could be a consequence of ICAM-1 modulation in the monocyte/macrophage system, which in turn could have a strong impact on the interaction with T lymphocytes and cell migration. Thus, ICAM-1 can be considered as a rapid-reacting and sustained gravity-regulated molecule in mammalian cells.

  15. Regulation of ICAM-1 in Cells of the Monocyte/Macrophage System in Microgravity

    Directory of Open Access Journals (Sweden)

    Katrin Paulsen

    2015-01-01

    Full Text Available Cells of the immune system are highly sensitive to altered gravity, and the monocyte as well as the macrophage function is proven to be impaired under microgravity conditions. In our study, we investigated the surface expression of ICAM-1 protein and expression of ICAM-1 mRNA in cells of the monocyte/macrophage system in microgravity during clinostat, parabolic flight, sounding rocket, and orbital experiments. In murine BV-2 microglial cells, we detected a downregulation of ICAM-1 expression in clinorotation experiments and a rapid and reversible downregulation in the microgravity phase of parabolic flight experiments. In contrast, ICAM-1 expression increased in macrophage-like differentiated human U937 cells during the microgravity phase of parabolic flights and in long-term microgravity provided by a 2D clinostat or during the orbital SIMBOX/Shenzhou-8 mission. In nondifferentiated U937 cells, no effect of microgravity on ICAM-1 expression could be observed during parabolic flight experiments. We conclude that disturbed immune function in microgravity could be a consequence of ICAM-1 modulation in the monocyte/macrophage system, which in turn could have a strong impact on the interaction with T lymphocytes and cell migration. Thus, ICAM-1 can be considered as a rapid-reacting and sustained gravity-regulated molecule in mammalian cells.

  16. Lung ICAM-1 and ICAM-2 support spontaneous intravascular effector lymphocyte entrapment but are not required for neutrophil entrapment or emigration inside endotoxin-inflamed lungs.

    Science.gov (United States)

    Petrovich, Ekaterina; Feigelson, Sara W; Stoler-Barak, Liat; Hatzav, Miki; Solomon, Adam; Bar-Shai, Amir; Ilan, Neta; Li, Jin-Ping; Engelhardt, Britta; Vlodavsky, Israel; Alon, Ronen

    2016-05-01

    The pulmonary vasculature constitutively expresses the integrin lymphocyte function-associated antigen-1 ligands intercellular adhesion molecule (ICAM)-1 and -2. In this study, effector T cells were temporarily entrapped by the lung vasculature on their way to inflamed lymph nodes, and this entrapment was strongly reduced in ICAM-1 and -2 double-deficient mice (79 and 86% reduction for CD8(+) and CD4(+) effectors, respectively, compared with wild-type mice). Although the pulmonary vasculature has been suggested to be masked by the heparan sulfate-containing glycocalyx, which is susceptible to heparanase-mediated shedding, lung and lymphocyte heparanase have been found to be unnecessary for this entrapment. Systemic LPS induced rapid neutrophil entrapment in the lung vasculature, but in contrast to T-cell entrapment, this sequestration was ICAM-1, ICAM-2, and heparanase independent. Furthermore, neutrophil migration into the bronchoalveolar space induced by LPS inhalation and LPS-induced leakage of red blood cells into this space were not dependent on lung ICAMs or heparanase activity. Nevertheless, heparanase was critical for neutrophil accumulation in smoke-exposed lungs. Our results indicate that, whereas T cells use ICAM-1 and -2 for temporary pulmonary entrapment, neutrophils get sequestered and extravasate into inflamed lungs independent of ICAMs. This is the first demonstration that the pulmonary vasculature is differentially recognized by T cells and neutrophils.-Petrovich, E., Feigelson, S. W., Stoler-Barak, L., Hatzav, M., Solomon, A., Bar-Shai, A., Ilan, N., Li, J.-P., Engelhardt, B., Vlodavsky, I., Alon, R. Lung ICAM-1 and ICAM-2 support spontaneous intravascular effector lymphocyte entrapment but are not required for neutrophil entrapment or emigration inside endotoxin-inflamed lungs.

  17. Plasmodium Falciparum: Adhesion Phenotype of Infected Erythrocytes Using Classical and Mini-Column Cytoadherence Techniques

    Directory of Open Access Journals (Sweden)

    N Kalantari

    2013-03-01

    Full Text Available Background: Cytoadherence of Plasmodium falciparum- infected erythrocytes to host cells is an impor­tant trait for parasite survival and has a major role in pathology of malaria disease. Infections with P. falciparum usually consist of several subpopulations of parasites with different adhesive proper­ties. This study aimed to compare relative sizes of various binding subpopulations of different P. falciparum isolates. It also investigated the adhesive phenotype of a laboratory P. falciparum line, A4, using different binding techniques.Methods: Seven different P. falciparum isolates (ITG, A4, 3D7 and four field isolates were cultivated to late trophozoite and schizont and then cytoadherence to cell differentiation 36 (CD36, intercellu­lar cell adhesion molecule-1 (ICAM-1, and vascular cell adhesion molecule (V-CAM and E-selectin were examined. The relative binding sizes of parasite subpopulations to human receptors were meas­ured by mini-column cytoadherence method. The adhesion phenotype of P. falciparum-A4 line was evaluated by in vitro static, flow-based and mini-column binding assays.Results: The relative binding size of ITG, A4 and 3D7 clones to a column made with CHO/ICAM-1 was 68%, 54% and 0%, respectively. The relative binding sizes of these lines to CHO/CD36 were 59.7%, 28.7% and 0%, respectively. Different field isolates had variable sizes of respective CD36 and ICAM1-binding subpopulations. A4 line had five different subpopulations each with different binding sizes.Conclusion: This study provided further evidence that P. falciparum isolates have different binding subpopulations sizes in an infection. Furthermore, measurement of ICAM-1 or CD36 binding subpopula­tions may practical to study the cytoadherence phenotypes of P. falciparum field isolates at the molecular level.

  18. Polymorphisms of the ICAM-1 exon 6 (E469K) are associated with differentiation of colorectal cancer

    OpenAIRE

    Wen Jin-Kun; Han Yi; Liu Yue-Ping; Miao Sui-Bing; Liu Ya-bin; Liu Bin; Li Bing-hui; Wang Qing-lei; Han Mei

    2009-01-01

    Abstract Background Genetic factors are thought to play a role in development for colorectal carcinogenesis. ICAM-1 is a polymorphic gene, thus, the present study investigated the relationship between the polymorphisms of ICAM-1 and the susceptibility and phenotypical characteristics of colorectal cancer (CRC). Methods The polymorphisms at ICAM-1 exon 4 (G241R) and exon 6 (E469K) were detected by PCR with sequence-specific primers. The relationship between specific genotypes of ICAM-1 and dif...

  19. Effects of ulinastatin on the mRNA expression of intercellular adhesion molecule-1 and P-selection in pulmonary tissue after ischemia reperfusion%乌司他丁对缺血再灌注肺组织细胞间黏附分子-1和P-选择素基因mRNA表达的影响

    Institute of Scientific and Technical Information of China (English)

    常忠路; 康炳玲; 陈庆伟

    2011-01-01

    OBJECTIVE To explore the effects of ulinastatin ( UTI ) on the mRNA expression of intercellular adhesion molecule ( ICAM ) - 1 and P - selection in pulmonary tissue after ischemia reperfusion. METHODS Eighteen New Zealand rabbits were randomly divided into 3 groups of 6 each: low potassium dextran ( LPD ) group, UTI group and control group. In vivo lung ischemia reperfusion model was established in rabbit, after hilum of left lung was clamped, the left lower lung lobe was stored at 10℃ in a special made lung preservation container for 2 hours and reperfused for another 2 hours. In LPD group and UTI group the left lower lobe was perfused with LPD solution or LPD solution contained ulinastatin respectively, without anything perfused in control group. The pulmonary tissue was obtained at three time intervals and the mRNA expression of ICAM - 1 and P - selection in pulmonary tissue was measured using RT - PCR technique. RESULTS The mRNA expression of ICAM - 1 at 2 hours after ischemia and 2 hours after perfusion in UTI group was significantly lower than that in LPD group and control group. The P - selection mRNA expression at 2 hours after perfusion in LPD group and control group was significantly higher than pre - ischemia and 2 hours after clamping hilum of left lung.There was no such significant difference in UTI group. CONCLUSION UTI can inhibit the upregulation of the mRNA expression of ICAM -1 and P -selection after ischemia reperfusion in pulmonary tissue, so it is profitable for pulmonary protection.%目的 探讨乌司他丁(UTI)对在体缺血再灌注后肺组织细胞间黏附分子(ICAM)-1和P-选择素基因mRNA表达的影响.方法 新西兰兔18只随机分为3组:低钾右旋糖酐液(LPD)组、UTI组和对照组.建立兔在体肺缺血冷存再灌注模型,阻断左肺门后将左肺下叶在体冷存于10℃肺保存器内2 h,再灌注2 h.LPD组灌注LPD液,UTI组灌注含UTI的LPD液,对照组不灌注肺保护液.分别

  20. Effects of Interleukin-1β,-1Rα on the Expression of Matrix Metalloproteinases-9 and Intercellular Adhesion Molecule-1 in the Embryo and Endometrium Co-Culture System%白细胞介素-1β,-1Rα对胚胎-内膜共培养体系分泌基质金属蛋白酶-9/细胞间黏附分子-1的影响

    Institute of Scientific and Technical Information of China (English)

    张宁; 刘萍; 郝翠芳; 王昕荣

    2012-01-01

    epithelial cells were collected and the endometrial cells were primarily cultured.There were 7 copies primary endometrial cells were successful cultured and were inoculated into 35 holes respectively.Control group were 5 hole cells without any treatment (n=5 × 7).30 holes was divided into 6 groups according to different concentrations of IL-1β and different raio of IL-1β3+IL-1Ra.3 groups were GⅡ with 1 ng/mL IL-1β,10 ng/mL IL1β and 100 ng/mL IL-1β,3 groups were G Ⅱ with 1 ng/mL IL-1β+ 10 μg/mL IL 1Rα,10 ng/mL IL-1β+ 10μg/mL IL-1Rα and 100 ng/mL IL 1β+ 10 μg/mL IL-1Rα (n=5 × 7).8 cell embryos were co-cultured with endometrial glandular epithelial cells in different media (6 embryos each hole).Supernatant were collected after 48 h co-culture,and the levels of matrix metalloproteinase-9 (MMP-9) / intercellular adhesion molecule-1 (ICAM-1) were measured by ELISA.Results Expressions of MMP-9 / ICAM 1 were significantly increased in 1 ng/mL IL-1β group and 10 ng/mL IL-1β group compared with those in control group respectively (P<0.05).While expression of MMP 9/ICAM1 levels had no significant differences in 1 ng/mL IL-1β group and in 10 ng/mL IL-1β group,and also in 100 ng/mL IL-1β group and in control group (P>0.05).MMP-9/ICAM-1 levels were significant decreased in 10 ng/mL IL-1β+ 10 μg/mL IL-1Ra group compared with those control group (P<0.05); While expression of MMP-9/ICAM-1 levels had no significant differences in 1 ng/mL IL-1β+ 10 μg/mL IL-1Ra group and in control group,and also had no significant in 100 ng/mL IL-1β+10 μg/mL IL-1Ra group and in control group (P>0.05).They also had no significant difference in 1 ng/mL IL-1β+10 μg/mL IL-1Ra group compared with those in 100 ng/mL IL-1β +10 μg/mL IL-1Ra group (P>0.05).Conclusions Appropriate proportion of IL-1β and IL-1Rα can regulate embryo implantation.

  1. Effects of trans-3,5,4′-trimethoxystilbene on the expressions of NO,ICAM-1 and NF-κB in human umbilical vein endothelial cells induced by lipopolysaccharide in vitro%白藜芦醇衍生物 TMS 对脂多糖诱导血管内皮细胞表达 NO、ICAM-1和 NF-κB 的影响

    Institute of Scientific and Technical Information of China (English)

    付海燕; 胡占升; 杜红阳

    2015-01-01

    Objective To explore the effects of trans-3,5,4′-trimethoxystilbene (TMS)on the expressions of NO, intercellular adhesion molecule-1 (ICAM-1)and nuclear factor-κB (NF-κB)in human umbilical vein endothelial cells (HUVEs)induced by lipopolysaccharide (LPS)in vitro.Methods The cell viabilities influenced by the different concentrations of TMS were assessed by CCK-8 assay.The cells were divided into the control group (CON group), LPS group,low-concentration TMS plus LPS group,medium-concentration TMS plus LPS group,high-concentration TMS plus LPS group and ammonium pyrrolidine dithiocarbamate (PDTC)plus LPS group.HUVEs were pretreated with the different concentrations of TMS and 10 μmol/L PDTC,and then were stimulated with 0.1 μg /mL LPS.After incubation,the level of NO was determined by Griess assay.The mRNA expressions of ICAM-1 and NF-κB p65 were detected by Real-time PCR,the protein expressions of ICAM-1,NF-κB p65 and IκBαby Western blotting assay,and the protein expressions of ICAM-1 and NF-κB p65 by immunocytochemetry assay.Results There was little effect of low-concentration TMS (5 or 10 μmol/L)on the cell viability,but the cell viability decreased significantly when trea-ted with high-concentration TMS (50 or 100 μmol/L)in time-or concentration-dependent manners.Griess results showed that the level of NO in the low-,medium-and high-concentration TMS plus LPS groups and PDTC plus LPS group decreased compared with that in LPS group (P <0.05 ).The results of Real-time PCR and Western blotting showed that compared with LPS group and CON group,there were significant difference of mRNA and protein expressions of ICAM-1 and NF-κB p65 in medium-concentration TMS plus LPS group and PDTC plus LPS group (P <0.05;P <0.01).Furthermore,there were nuclear expressions of NF-κB p65 protein in medium-concentration TMS plus LPS group,PDTC plus LPS group and LPS group except for CON group.The protein expression of IκBαdecreased significantly in LPS group compared

  2. Colonic epithelial cell expression of ICAM-1 relates to loss of surface continuity

    DEFF Research Database (Denmark)

    Vainer, Ben; Horn, Thomas; Nielsen, Ole Haagen

    2006-01-01

    . The aim of this study was to assess the ICAM-1 expression in human colonic tissue representing UC, Crohn's disease (CD), adenomas, and adenocarcinomas, with special attention to the epithelium. MATERIAL AND METHODS: Formalin-fixed and paraffin-embedded tissue from the archives of the Department...... of Pathology of Rigshospitalet University of Copenhagen was examined. Colonic tissue from 10 patients with UC, 10 with CD, 32 adenomas, 27 adenocarcinomas, and 10 lymph node metastases were included. The expression of ICAM-1 was assessed by using the EnVision(+)technique (DakoCytomation). RESULTS: Endothelial...... ICAM-1 was up-regulated in areas with dense lymphocyte infiltration and near crypt abscesses and ulcerations. Ulcerations were covered by a continuous layer of macrophages and epithelial cells expressing ICAM-1. Similar observations were made in the case of adenomas and adenocarcinomas...

  3. Levels of soluble adhesion molecules in patients with various clinical presentations of coronary atherosclerosis

    Institute of Scientific and Technical Information of China (English)

    LU Hui-he; SHENG Zheng-qiang; WANG Yi; ZHANG Li

    2010-01-01

    Background Adhesion molecules play an important role in the development and progression of coronary atherosclerosis. The aim of this study was to compare concentrations of soluble forms of adhesion molecules in patients with different clinical presentations of coronary artery disease (CAD).Methods One hundred and twenty-eight patients with CAD were divided into three groups; the first group was acute myocardial infarction group (AMI group, n=45), the second group was unstable angina pectoris group (UAP group, n=48),the third group was stable angina pectoris group (SAP group, n=35). We compared them with patients with normal coronary arteries (control group, n=31). The serum levels of vascular cell adhesion molecule (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), E-selectin and P-selectin were measured in all subjects.Results The serum level of VCAM-1 in the AMI group was significantly higher than in the UAP, SAP and control groups (P <0.01). The level in the UAP group was significantly higher than the SAP group and control group (P <0.01) and the level in the SAP group was significantly higher than in the control group (P <0.01). The serum ICAM-1 level was significantly elevated in the AMI, UAP and SAP groups as compared to the control group (P <0.01). The levels of serum E-selectin and P-selectin in the AMI and UAP groups were significantly higher than in the SAP and control groups (P<0.01).Conclusions Increased levels of VCAM-1 and ICAM-1, E-selectin and P-selectin, as markers of inflammation, showed the importance of inflammatory processes in the development of atherosclerosis and clinical expression of CAD. Soluble ICAM-1, VCAM-1, E-selectin and P-selectin concentrations are useful indicators of the presence of atherosclerosis and the severity of CAD clinical presentation.

  4. Differential modulation of IL-1-induced endothelial adhesion molecules and transendothelial migration of granulocytes by G-CSF.

    Science.gov (United States)

    Eissner, G; Lindner, H; Reisbach, G; Klauke, I; Holler, E

    1997-06-01

    Granulocyte colony stimulating factor (G-CSF) is widely used for mobilization of haemopoietic stem cells into the peripheral blood. However, little is known about the mechanisms involved in mobilization and the immune modulatory effects of this growth factor. In this report we show that G-CSF down-regulated intercellular adhesion molecule 1 (ICAM-1) induced by Interleukin-1 (IL-1) on human endothelial cells. Interestingly, the G-CSF-mediated down-modulation of IL-1-induced ICAM-1 appeared to be biphasic. In pharmacological concentrations (> 300 ng/ml), and in dose ranges of plasma G-CSF levels above that of nonfebrile healthy individuals (30 pg/ml), a significant decrease in surface ICAM-1 could be observed. This could be explained, at least in part, by an increased autocrine G-CSF production by endothelial cells in response to IL-1 and exogenous G-CSF. In contrast to ICAM-1, IL-1-triggered VCAM-1 expression was superinduced by G-CSF with the optimal concentration of 30 pg/ml. To evaluate the functional significance of these findings, 51Cr adhesion assays with peripheral blood mononuclear cells (PBMC) or granulocytes known to lack the VCAM-1 counter-receptor very late antigen 4 (VLA-4) and IL-1-stimulated endothelial cells, in the presence or absence of G-CSF, were performed. G-CSF could not inhibit the IL-1-induced adhesion of PBMC to endothelial cells, which may be due to the differential adhesion molecule modulation. In contrast, granulocyte adhesion induced by IL-1 could effectively be blocked by co-incubation with G-CSF. Finally, G-CSF also inhibited transendothelial migration of granulocytes through IL-1-activated endothelial cells in a concentration-dependent manner.

  5. Highly sensitivity adhesion molecules detection in hereditary haemochromatosis patients reveals altered expression.

    LENUS (Irish Health Repository)

    Norris, S

    2012-02-01

    Several abnormalities in the immune status of patients with hereditary haemochromatosis (HH) have been reported, suggesting an imbalance in their immune function. This may include persistent production of, or exposure to, altered immune signalling contributing to the pathogenesis of this disorder. Adhesion molecules L-, E- and P-Selectin, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) are some of the major regulators of the immune processes and altered levels of these proteins have been found in pathological states including cardiovascular diseases, arthritis and liver cancer. The aim of this study was to assess L-, E- and P-Selectin, ICAM-1 and VCAM-1 expression in patients with HH and correlate these results with HFE mutation status and iron indexes. A total of 139 subjects were diagnosed with HH (C282Y homozygotes = 87, C282Y\\/H63D = 26 heterozygotes, H63D homozygotes = 26), 27 healthy control subjects with no HFE mutation (N\\/N), 18 normal subjects heterozygous for the H63D mutation served as age-sex-matched controls. We observed a significant decrease in L-selectin (P = 0.0002) and increased E-selectin and ICAM-1 (P = 0.0006 and P = 0.0059) expression in HH patients compared with healthy controls. This study observes for the first time that an altered adhesion molecules profile occurs in patients with HH that is associated with specific HFE genetic component for iron overload, suggesting that differential expression of adhesion molecules may play a role in the pathogenesis of HH.

  6. Olive oil phenolic compounds inhibit homocysteine-induced endothelial cell adhesion regardless of their different antioxidant activity.

    Science.gov (United States)

    Manna, Caterina; Napoli, Daniela; Cacciapuoti, Giovanna; Porcelli, Marina; Zappia, Vincenzo

    2009-05-13

    In this study, we examine the effect of extra virgin olive oil phenolic compounds on homocysteine-induced endothelial dysfunction and whether the protective effects are related to their different scavenging activities. Structurally related compounds have been assayed for their ability to reduce homocysteine-induced monocyte adhesion as well as the cell surface expression of intercellular adhesion molecule-1 (ICAM-1) in EA.hy.926 cells. As well-known, among the selected phenolic compounds, hydroxytyrosol, homovanillyl alcohol, and the hydroxycinnamic acid derivatives caffeic and ferulic acid display high scavenging activities, while tyrosol and p-coumaric acid are poorly active. All of the tested compounds, approaching potential in vivo concentrations, significantly reduce homocysteine-induced cell adhesion and ICAM-1 expression. Interestingly, we report the first evidence that monophenols tyrosol and p-coumaric acid are selectively protective only in homocysteine-activated cells, while they are ineffective in reducing ICAM-1 expression induced by TNFalpha. Finally, we report the synergistic effect of o-diphenolic and monophenolic compounds.

  7. Degraded carrageenan causing colitis in rats induces TNF secretion and ICAM-1 upregulation in monocytes through NF-kappaB activation.

    Directory of Open Access Journals (Sweden)

    Claudine Benard

    Full Text Available Carrageenan (CGN is a high molecular weight sulphated polysaccharide derived from red seaweeds. In rodents, its degraded forms (dCGN can induce intestinal inflammation associated with macrophage recruitment and activation. The aim of this study was: 1 to analyze the size-dependent effects of dCGN on colon inflammation in vivo, and 2 to correlate these effects with monocyte/macrophage proliferation, cytokine production and expression of various cell surface antigens including ICAM-1 adhesion molecule. Peripheral blood monocytes (PBM and THP-1 monocytic cells were cultured in the presence of either 10 or 40 kDa, dCGN. The 40 kDa, but not the 10 kDa dCGN, induced colitis in in vivo. Degraded CGN inhibited THP-1 cell proliferation in vitro, arresting the cells in G1 phase. In addition, dCGN increased ICAM-1 expression in both PBM and THP-1 cells with a major effect seen after 40 kDa dCGN exposure. Also, dCGN stimulated monocyte aggregation in vitro that was prevented by incubation with anti-ICAM-1 antibody. Finally, dCGN stimulated TNF-alpha expression and secretion by both PBM and THP-1 cells. All these effects were linked to NF-kappaB activation. These data strongly suggest that the degraded forms of CGN have a pronounced effect on monocytes, characteristic of an inflammatory phenotype.

  8. FOXO1 regulates dendritic cell activity through ICAM-1 and CCR7.

    Science.gov (United States)

    Dong, Guangyu; Wang, Yu; Xiao, Wenmei; Pacios Pujado, Sandra; Xu, Fanxing; Tian, Chen; Xiao, E; Choi, Yongwon; Graves, Dana T

    2015-04-15

    The transcription factor FOXO1 regulates cell function and is expressed in dendritic cells (DCs). We investigated the role of FOXO1 in activating DCs to stimulate a lymphocyte response to bacteria. We show that bacteria induce FOXO1 nuclear localization through the MAPK pathway and demonstrate that FOXO1 is needed for DC activation of lymphocytes in vivo. This occurs through FOXO1 regulation of DC phagocytosis, chemotaxis, and DC-lymphocyte binding. FOXO1 induces DC activity by regulating ICAM-1 and CCR7. FOXO1 binds to the CCR7 and ICAM-1 promoters, stimulates CCR7 and ICAM-1 transcriptional activity, and regulates their expression. This is functionally important because transfection of DCs from FOXO1-deleted CD11c.Cre(+)FOXO1(L/L) mice with an ICAM-1-expressing plasmid rescues the negative effect of FOXO1 deletion on DC bacterial phagocytosis and chemotaxis. Rescue with both CCR7 and ICAM-1 reverses impaired DC homing to lymph nodes in vivo when FOXO1 is deleted. Moreover, Ab production following injection of bacteria is significantly reduced with lineage-specific FOXO1 ablation. Thus, FOXO1 coordinates upregulation of DC activity through key downstream target genes that are needed for DCs to stimulate T and B lymphocytes and generate an Ab defense to bacteria.

  9. Association of TLR2 S450S and ICAM1 K469E polymorphisms with polycystic ovary syndrome (PCOS) and obesity.

    Science.gov (United States)

    Ojeda-Ojeda, Miriam; Martínez-García, M Ángeles; Alpañés, Macarena; Luque-Ramírez, Manuel; Escobar-Morreale, Héctor F

    2016-02-01

    Toll-like receptors (TLRs) are activated by inflammatory stimuli and influence endothelial functions, contributing to the pathogenesis of atherosclerosis. We investigate the influence of polymorphisms in the genes encoding toll-like receptor 2 (TLR2) and 4 (TLR4) and endothelial adhesion molecules on polycystic ovary syndrome (PCOS) and its interaction with obesity. Ten single nucleotide polymorphisms were genotyped in 305 women with PCOS and 166 non-hyperandrogenic control women. In obese women, TLR2 S450S and ICAM1 K469E polymorphisms differently influenced metabolic variables and PCOS, respectively. Irrespective of PCOS, variant alleles of TLR2 S450S increased triglycerides, fasting insulin levels, and insulin resistance in obese women. TLR2 S450S interacted with obesity and PCOS on androstenedione levels, mutant alleles were associated with increased androstenedione concentrations in all women, with the exception of obese patients with PCOS (P=0.034). Regarding ICAM1 K469E, homozygosis for K469 alleles was more frequent in PCOS, but only in obese women (P=0.014). K469 alleles were also related to increased body mass index (P=0.017) and diastolic blood pressure (P=0.034). Moreover, ICAM1 K469E interacted with obesity and PCOS on serum triglyceride levels (P=0.019) and with PCOS on serum sex hormone-binding globulin concentrations (P=0.006). In conclusion, TLR2 S450S and ICAM1 K469E polymorphisms may be associated with PCOS and metabolic comorbidities in obese women.

  10. The carbon monoxide releasing molecule (CORM-3) inhibits expression of vascular cell adhesion molecule-1 and E-selectin independently of haem oxygenase-1 expression

    NARCIS (Netherlands)

    Song, H.; Bergstrasser, C.; Rafat, N.; Hoeger, S.; Schmidt, M.; Endres, N.; Goebeler, M.; Hillebrands, J. L.; Brigelius-Flohe, R.; Banning, A.; Beck, G.; Loesel, R.; Yard, B. A.

    2009-01-01

    Background and purpose: Although carbon monoxide (CO) can modulate inflammatory processes, the influence of CO on adhesion molecules is less clear. This might be due to the limited amount of CO generated by haem degradation. We therefore tested the ability of a CO releasing molecule (CORM-3), used i

  11. Effect of irradiation on gene expression of rat liver adhesion molecules. In vivo and in vitro studies

    Energy Technology Data Exchange (ETDEWEB)

    Moriconi, Federico; Malik, Ihtzaz; Ahmad, Ghayyor; Dudas, Joszef; Ramadori, Giuliano [Dept. of Gastroenterology and Endocrinology, Goettingen Univ. (Germany); Rave-Fraenk, Margret; Vorwerk, Hilke; Hille, Andrea; Hess, Clemens Friedrich; Christiansen, Hans [Dept. of Radiotherapy, Goettingen Univ. (Germany)

    2009-07-15

    Background and purpose: Migration of leukocytes into tissue is a key element of innate and adaptive immunity. An animal study showed that liver irradiation, in spite of induction of chemokine gene expression, does not lead to recruitment of leukocytes into the parenchyma. The aim of this study was to analyze gene expression of adhesion molecules, which mediate leukocyte recruitment into organs, in irradiated rat liver in vivo and rat hepatocytes in vitro. Material and methods: Rat livers in vivo were irradiated selectively at 25 Gy. Isolated hepatocytes in vitro were irradiated at 8 Gy. RNA extracted within 48 h after irradiation in vivo and in vitro was analyzed by real-time PCR (polymerase chain reaction) and Northern blot. Adhesion molecule concentration in serum was measured by ELISA (enzyme-linked immunosorbent assay). Cryostat sections of livers were used for immunohistology. Results: Significant radiation-induced increase of ICAM-1 (intercellular adhesion molecule-1), VCAM-1 (vascular cell adhesion molecule-1), JAM-1 (junctional adhesion molecule-1), {beta}{sub 1}-integrin, {beta}{sub 2}-integrin, E-cadherin, and P-selectin gene expression could be detected in vivo, while PECAM-1 (platelet-endothelial cell adhesion molecule-1) gene expression remained unchanged. In vitro, {beta}{sub 1}-integrin, JAM-1, and ICAM-2 showed a radiation-induced increased expression, whereas the levels of P-selectin, ICAM-1, PECAM-1, VCAM-1, Madcam-1 (mucosal addressin cell adhesion molecule-1), {beta}{sub 2}-integrin, and E-cadherin were downregulated. However, incubation of irradiated hepatocytes with either tumor necrosis factor-(TNF-){alpha}, interleukin-(IL-)1{beta}, or IL-6 plus TNF-{alpha} led to an upregulation of P-selectin, ICAM-1 and VCAM-1. Conclusion: The findings suggest that liver irradiation modulates gene expression of the main adhesion molecules in vivo and in cytokine-activated hepatocytes, with the exception of PECAM-1. This may be one reason for the lack of

  12. 粘附分子在复发性口腔溃疡的发病机制中作用的探讨%Expression of vascular cell adhesion molecule-1 in recurrent oral ulceration

    Institute of Scientific and Technical Information of China (English)

    孙睿; 董玙; 晁海英; 孙晓震

    2003-01-01

    目的:探讨可溶性血管内皮细胞粘附分子(sVCAM-1)、可溶性细胞间粘附分子(sICAM-1)在复发性口腔溃疡(recurrent oral ulceration,ROU)发病机制中的作用.方法:采用双抗体夹心酶联免疫吸附实验法检测血清中的sVCAM-1、sICAM-1浓度.结果:ROU患者的sVCAM-1浓度高于健康对照组,差异有显著性.ROU患者的sICAM-1浓度与健康对照组相比无显著性差异.sVCAM-1、sICAM-1两者浓度在活动期与静止期差异无显著性.结论:sVCAM 1在复发性口腔溃疡发病机制中可能有重要意义.

  13. CXC-chemokine regulation and neutrophil trafficking in hepatic ischemia-reperfusion injury in P-selectin/ICAM-1 deficient mice

    Directory of Open Access Journals (Sweden)

    Crockett Elahé T

    2007-05-01

    Full Text Available Abstract Background Neutrophil adhesion and migration are critical in hepatic ischemia and reperfusion injury (I/R. P-selectin and the intercellular adhesion molecule (ICAM-1 can mediate neutrophil-endothelial cell interactions, neutrophil migration, and the interactions of neutrophils with hepatocytes in the liver. Despite very strong preclinical data, recent clinical trials failed to show a protective effect of anti-adhesion therapy in reperfusion injury, indicating that the length of injury might be a critical factor in neutrophil infiltration. Therefore, the aim of this study was to assess the role of P-selectin and ICAM-1 in neutrophil infiltration and liver injury during early and late phases of liver I/R. Methods Adult male wild-type and P-selectin/ICAM-1-deficient (P/I null mice underwent 90 minutes of partial liver ischemia followed by various periods of reperfusion (6, 15 h, and a survival study. Liver injury was assessed by plasma level of alanine aminotransferase (ALT and histopathology. The plasma cytokines, TNF-α, IL-6, MIP-2 and KC, were measured by ELISA. Results Reperfusion caused significant hepatocellular injury in both wild-type and P/I null mice as was determined by plasma ALT levels and liver histopathology. The injury was associated with a marked neutrophil infiltration into the ischemic livers of both wild-type and P/I null mice. Although the levels of ALT and neutrophil infiltration were slightly lower in the P/I null mice compared with the wild-type mice the differences were not statistically significant. The plasma cytokine data of TNF-α and IL-6 followed a similar pattern to ALT data, and no significant difference was found between the wild-type and P/I null groups. In contrast, a significant difference in KC and MIP-2 chemokine levels was observed between the wild-type and P/I null mice. Additionally, the survival study showed a trend towards increased survival in the P/I null group. Conclusion While ICAM-1 and P

  14. Gene deletion of P-Selectin and ICAM-1 does not inhibit neutrophil infiltration into peritoneal cavity following cecal ligation-puncture

    Directory of Open Access Journals (Sweden)

    Hess Karen

    2004-07-01

    Full Text Available Abstract Background Neutrophil infiltration is one of the critical cellular components of an inflammatory response during peritonitis. The adhesion molecules, P-selectin and intercellular adhesion molecule (ICAM-1, mediate neutrophil-endothelial cell interactions and the subsequent neutrophil transendothelial migration during the inflammatory response. Despite very strong preclinical data, recent clinical trials failed to show a protective effect of anti-adhesion therapy, suggesting that the length of injury might be a critical factor in neutrophil infiltration. Therefore, the objective of this study was to determine the role of P-selectin and ICAM-1 in neutrophil infiltration into the peritoneal cavity during early and late phases of peritonitis. Methods Peritonitis was induced in both male wild-type and P-selectin/ICAM-1 double deficient (P/I null mice by cecal ligation-puncture (CLP. Peripheral blood and peritoneal lavage were collected at 6 and 24 hours after CLP. The total leukocyte and neutrophil contents were determined, and neutrophils were identified with the aid of in situ immunohistochemical staining. Comparisons between groups were made by applying ANOVA and student t-test analysis. Results CLP induced a severe inflammatory response associated with a significant leukopenia in both wild-type and P/I null mice. Additionally, CLP caused a significant neutrophil infiltration into the peritoneal cavity that was detected in both groups of mice. However, neutrophil infiltration in the P/I null mice at 6 hours of CLP was significantly lower than the corresponding wild-type mice, which reached a similar magnitude at 24 hours of CLP. In contrast, in peritonitis induced by intraperitoneal inoculation of 2% glycogen, no significant difference in neutrophil infiltration was observed between the P/I null and wild-type mice at 6 hours of peritonitis. Conclusions The data suggest that alternative adhesion pathway(s independent of P-selectin and ICAM

  15. Opiates Upregulate Adhesion Molecule Expression in Brain MicroVascular Endothelial Cells (BMVEC: Implications for Altered Blood Brain Barrier (BBB Permeability

    Directory of Open Access Journals (Sweden)

    Madhavan P.N. Nair

    2006-01-01

    Full Text Available The blood-brain barrier (BBB is an intricate cellular system composed of vascular endothelial cells and perivascular astrocytes that restrict the passage of immunocompetent cells into the central nervous system (CNS. Expression of the adhesion molecules, intercellular adhesion molecule 1 (ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1 on brain microvascular endothelial cells (BMVEC and their interaction with human immunodeficiency virus (HIV-1 viral proteins may help enhance viral adhesion and virus-cell fusion resulting in increased infectivity. Additionally, transmigration through the BBB is facilitated by both endothelial and monocyte/macrophage-derived nitric oxide (NO. Dysregulated production of NO by BMVEC due to opiates and HIV-1 viral protein interactions play a pivotal role in brain endothelial injury, resulting in the irreversible loss of BBB integrity, which may lead to enhanced infiltration of virus-carrying cells across the BBB. Opioids act as co-factors in the neuropathogenesis of HIV-1 by facilitating BBB dysfunction however, no studies have been done to investigate the role of opiates alone or in combination with HIV-1 viral proteins on adhesion molecule expression in BMVEC. We hypothesize that opiates such as heroin and morphine in conjunction with the HIV-1 viral protein gp120 increase the expression of adhesion molecules ICAM-1 and VCAM-1 and these effects are mediated via the modulation of NO. Results show that opiates alone and in synergy with gp120 increase both the genotypic and phenotypic expression of ICAM-1 and VCAM-1 by BMVEC, additionally, these opiate induced effects may be the result of increased NO production. These studies will provide a better understanding of how opiate abuse in conjunction with HIV-1 infection facilitates the breakdown of the BBB and exacerbates the neuropathogenesis of HIV-1. Elucidation of the mechanisms of BBB modulation will provide new therapeutic approaches to maintain BBB integrity

  16. C1q/TNF-related protein-9 inhibits cytokine-induced vascular inflammation and leukocyte adhesiveness via AMP-activated protein kinase activation in endothelial cells.

    Science.gov (United States)

    Jung, Chang Hee; Lee, Min Jung; Kang, Yu Mi; Lee, Yoo La; Seol, So Mi; Yoon, Hae Kyeong; Kang, Sang-Wook; Lee, Woo Je; Park, Joong-Yeol

    2016-01-05

    Although recent studies have reported cardioprotective effects of C1q/TNF-related protein 9 (CTRP9), the closet adiponectin paralog, its role on cytokine-induced endothelial inflammation is unknown. We investigated whether CTRP9 prevented inflammatory cytokine-induced nuclear factor-kappa B (NF-κB) activation and inhibited the expression of adhesion molecules and a chemokine in the vascular endothelial cell. We used human aortic endothelial cells (HAECs) to examine the effects of CTRP9 on NF-κB activation and the expression of NF-κB-mediated genes, including intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and monocyte chemoattractant protein-1 (MCP-1). Tumor necrosis factor alpha (TNFα) was used as a representative proinflammatory cytokine. In an adhesion assay using THP-1 cells, CTRP9 reduced TNFα-induced adhesion of monocytes to HAECs. Treatment with CTRP9 significantly decreased TNFα-induced activation of NF-κB, as well as the expression of ICAM-1, VCAM-1, and MCP-1. In addition, treatment with CTRP9 significantly increased the phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC), the downstream target of AMPK. The inhibitory effect of CTRP9 on the expression of ICAM-1, VCAM-1, and MCP-1 and monocyte adhesion to HAECs was abolished after transfection with an AMPKα1-specific siRNA. Our study is the first to demonstrate that CTRP9 attenuates cytokine-induced vascular inflammation in endothelial cells mediated by AMPK activation.

  17. NADPH OXIDASE AND LIPID RAFT-ASSOCIATED REDOX SIGNALING ARE REQUIRED FOR PCB153-INDUCED UPREGULATION OF CELL ADHESION MOLECULES IN HUMAN BRAIN ENDOTHELIAL CELLS

    Science.gov (United States)

    Eum, Sung Yong; Andras, Ibolya; Hennig, Bernhard; Toborek, Michal

    2009-01-01

    Exposure to persistent organic pollutants, such as polychlorinated biphenyls (PCBs), can lead to chronic inflammation and the development of vascular diseases. Because cell adhesion molecules (CAMs) of the cerebrovascular endothelium regulate infiltration of inflammatory cells into the brain, we have explored the molecular mechanisms by which ortho-substituted polychlorinated biphenyls (PCBs), such as PCB153, can upregulate CAMs in brain endothelial cells. Exposure to PCB153 increased expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), as well as elevated adhesion of leukocytes to brain endothelial cells. These effects were impeded by inhibitors of EGFR, JAKs, or Src activity. In addition, pharmacological inhibition of NADPH oxidase or disruption of lipid rafts by cholesterol depleting agents blocked PCB153-induced phosphorylation of JAK and Src kinases and upregulation of CAMs. In contrast, silencing of caveolin-1 by siRNA interference did not affect upregulation of ICAM-1 and VCAM-1 in brain endothelial cells stimulated by PCB153. Results of the present study indicate that lipid raft-dependent NADPH oxidase/JAK/EGFR signaling mechanisms regulate the expression of CAMs in brain endothelial cells and adhesion of leukocytes to endothelial monolayers. Due to its role in leukocyte infiltration, induction of CAMs may contribute to PCB-induced cerebrovascular disorders and neurotoxic effects in the CNS. PMID:19632255

  18. Rolling adhesion of alphaL I domain mutants decorrelated from binding affinity.

    Science.gov (United States)

    Pepper, Lauren R; Hammer, Daniel A; Boder, Eric T

    2006-06-30

    Activated lymphocyte function-associated antigen-1 (LFA-1, alphaLbeta2 integrin) found on leukocytes facilitates firm adhesion to endothelial cell layers by binding to intercellular adhesion molecule-1 (ICAM-1), which is up-regulated on endothelial cells at sites of inflammation. Recent work has shown that LFA-1 in a pre-activation, low-affinity state may also be involved in the initial tethering and rolling phase of the adhesion cascade. The inserted (I) domain of LFA-1 contains the ligand-binding epitope of the molecule, and a conformational change in this region during activation increases ligand affinity. We have displayed wild-type I domain on the surface of yeast and validated expression using I domain specific antibodies and flow cytometry. Surface display of I domain supports yeast rolling on ICAM-1-coated surfaces under shear flow. Expression of a locked open, high-affinity I domain mutant supports firm adhesion of yeast, while yeast displaying intermediate-affinity I domain mutants exhibit a range of rolling phenotypes. We find that rolling behavior for these mutants fails to correlate with ligand binding affinity. These results indicate that unstressed binding affinity is not the only molecular property that determines adhesive behavior under shear flow.

  19. Modulation of Sickle Red Blood Cell Adhesion and its Associated Changes in Biomarkers by Sulfated Nonanticoagulant Heparin Derivative.

    Science.gov (United States)

    Alshaiban, Abdulelah; Muralidharan-Chari, Vandhana; Nepo, Anne; Mousa, Shaker A

    2016-04-01

    Abnormal cellular adhesion is one of the primary causes of vaso-occlusive crisis in sickle cell disease (SCD). Levels of intercellular adhesion molecule 1 (ICAM-1) and P-selectin are upregulated, resulting in increased adhesion of leukocytes and sickle red blood cells (RBCs) to endothelium. This study compares the inhibitory effect of a sulfated nonanticoagulant heparin (S-NACH) derivative with a low-molecular-weight heparin, tinzaparin, on the adhesion of sickle RBCs to endothelium. The S-NACH exhibits minimum effects on hemostasis and bleeding and interferes with the binding of pancreatic cancer cells to endothelial cells via P-selectin. We show by static binding assay that pretreatment of both erythrocytes and endothelial cells with S-NACH significantly inhibits the increased adhesion of sickle RBCs to endothelial cells. The S-NACH treatment also decreases the higher plasma levels of (adhesion biomarkers) ICAM-1 and P-selectin in SCD mice. This investigation signals further research into the potential use of S-NACH in treating vaso-occlusions with minimal bleeding events in patients with SCD.

  20. Plasma concentrations of VCAM-1 and ICAM-1 are elevated in patients with Type 1 diabetes mellitus with microalbuminuria and overt nephropathy

    DEFF Research Database (Denmark)

    Clausen, P; Jacobsen, P; Rossing, K

    2000-01-01

    diabetic patients, but the concentrations were increased by the presence of microalbuminuria and overt nephropathy (P differ between diabetic patients and controls. CONCLUSIONS: Plasma concentration of sICAM-1 is elevated in Type 1......AIMS: Elevated urinary albumin excretion is associated with macrovascular atherosclerotic complications in Type 1 diabetes mellitus. Adhesion molecules mediate leucocyte adhesion to the endothelium early in the atherosclerotic process. The present study tests the hypothesis that microalbuminuria...... disease in diabetic patients with renal complications. METHODS: Soluble adhesion molecule concentrations were measured by enzyme-linked immunosorbent assays (ELISA) in healthy controls (n = 16) and in 59 Type 1 diabetic patients: group 1-patients with normoalbuminuria (n = 16); group 2-patients...

  1. Pentosan polysulfate treatment ameliorates motor function with increased serum soluble vascular cell adhesion molecule-1 in HTLV-1-associated neurologic disease.

    Science.gov (United States)

    Nakamura, Tatsufumi; Satoh, Katsuya; Fukuda, Taku; Kinoshita, Ikuo; Nishiura, Yoshihiro; Nagasato, Kunihiko; Yamauchi, Atsushi; Kataoka, Yasufumi; Nakamura, Tadahiro; Sasaki, Hitoshi; Kumagai, Kenji; Niwa, Masami; Noguchi, Mitsuru; Nakamura, Hideki; Nishida, Noriyuki; Kawakami, Atsushi

    2014-06-01

    The main therapeutic strategy against human T lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) characterized by lower extremity motor dysfunction is immunomodulatory treatment, with drugs such as corticosteroid hormone and interferon-α, at present. However, there are many issues in long-term treatment with these drugs, such as insufficient effects and various side effects. We now urgently need to develop other therapeutic strategies. The heparinoid, pentosan polysulfate sodium (PPS), has been safely used in Europe for the past 50 years as a thrombosis prophylaxis and for the treatment of phlebitis. We conducted a clinical trial to test the effect of subcutaneous administration of PPS in 12 patients with HAM/TSP in an open-labeled design. There was a marked improvement in lower extremity motor function, based on reduced spasticity, such as a reduced time required for walking 10 m and descending a flight of stairs. There were no significant changes in HTLV-I proviral copy numbers in peripheral blood contrary to the inhibitory effect of PPS in vitro for intercellular spread of HTLV-I. However, serum soluble vascular cell adhesion molecule (sVCAM)-1 was significantly increased without significant changes of serum level of chemokines (CXCL10 and CCL2). There was a positive correlation between increased sVCAM-1and reduced time required for walking 10 m. PPS might induce neurological improvement by inhibition of chronic inflammation in the spinal cord, through blocking the adhesion cascade by increasing serum sVCAM-1, in addition to rheological improvement of the microcirculation. PPS has the potential to be a new therapeutic tool for HAM/TSP.

  2. Expression of adhesion molecules, chemokines and matrix metallo- proteinases (MMPs) in viable and degenerating stage of Taenia solium metacestode in swine neurocysticercosis.

    Science.gov (United States)

    Singh, Satyendra K; Singh, Aloukick K; Prasad, Kashi N; Singh, Amrita; Singh, Avinash; Rai, Ravi P; Tripathi, Mukesh; Gupta, Rakesh K; Husain, Nuzhat

    2015-11-30

    Neurocysticercosis (NCC) is a parasitic infection of central nervous system (CNS). Expression of adhesion molecules, chemokines and matrix metalloproteinases (MMPs) were investigated on brain tissues surrounding viable (n=15) and degenerating cysticerci (n=15) of Taenia solium in swine by real-time RT-PCR and ELISA. Gelatin gel zymography was performed for MMPs activity. ICAM-1 (intercellular adhesion molecule-1), E-selectin, MIP-1α (macrophage inflammatory protein-1α), Eotaxin-1 and RANTES (regulated on activation, normal T cell expressed and secreted) were associated with degenerating cysticerci (cysts). However, VCAM-1 (vascular cell adhesion molecule-1), MCP-1 (monocyte chemotactic protein-1), MMP-2 and MMP-9 were associated with both viable and degenerating cysts. In conclusion, viable and degenerating cysticerci have different immune molecule profiles and role of these molecules in disease pathogenesis needs to be investigated.

  3. Impaired sensitivity to beta 2 integrin-blocking in ICAM-1-mediated neutrophil migration in ulcerative colitis

    DEFF Research Database (Denmark)

    Vainer, B; Brimnes, J; Claesson, M H

    2001-01-01

    -mediated migration. METHODS: The chemotactic effect of ICAM-1 on neutrophils isolated from 13 UC patients and 17 healthy volunteers was studied in microchemotaxis chambers. Physiological concentrations of ICAM-1 (0.05-500 pM) were separated from neutrophils by nitrocellulose filters, and cell migration...... response curve with peak migration at 5 pM ICAM-1 (30.0 microns; interquartile range 22.9-35.7; P effect of ICAM-1 by 43.6%-58.0%, whereas the migration was decreased by only 20% in UC under similar blocking conditions...... (P effect. Inhibition of protein kinases with staurosporin only slightly decreased the ICAM-1-mediated migration, whereas incubation with staurosporin and CD11 antibodies showed additive effects on UC neutrophils and synergistic effects on control cells. No quantitative...

  4. The Expression of TNF-α and ICAM-1 in Lesions of Lichen Planus and Its Implication

    Institute of Scientific and Technical Information of China (English)

    CHEN Xue; LIU Zhixiang; YUE Qing; LIU Houjun; WU Yan; LI Jiawen

    2007-01-01

    In order to investigate the role of TNF-α and ICAM-1 in the pathogenesis of lichen planus, immunohistechemistty was used to detect the expression of TNF-α and ICAM-1 in skin le- sions of the patients with lichen planus and skin tissues of normal subjects. The results showed that positive rates of TNF-α and ICAM-1 expressions in lichen planus were significantly higher than those in normal skins (both P<0.05). Meanwhile, there was a obvious correlation between the in- crease of TNF-α and that of ICAM-1 in lichen planus. The expression of TNF-α and ICAM-1 might play an important role in the development of lichen planus.

  5. s-ICAM-1 and s-VCAM-1 in healthy men are strongly associated with traits of the metabolic syndrome, becoming evident in the postprandial response to a lipid-rich meal

    Directory of Open Access Journals (Sweden)

    Nothnagel Michael

    2008-09-01

    Full Text Available Abstract Background The importance of the postprandial state for the early stages of atherogenesis is increasingly acknowledged. We conducted assessment of association between postprandial triglycerides, insulin and glucose after ingestion of a standardized lipid-rich test meal, and soluble cellular adhesion molecules (sCAM in young healthy subjects. Methods Metabolic parameters and sICAM-1, sVCAM-1 and E-selectin were measured before and hourly until 6 hours after ingestion of a lipid-rich meal in 30 healthy young men with fasting triglycerides 260 mg/dl. Levels of CAM were compared in HR and NR, and correlation with postprandial triglyceride, insulin and glucose response was assessed. Results Fasting sICAM-1 and sVCAM-1 levels were significantly higher in HR as compared to NR (p = 0.046, p = 0.03. For sE-selectin there was such a trend (p = 0.05. There was a strong positive and independent correlation between sICAM-1 and postprandial insulin maxima (r = 0.70, p Conclusion This independent association of postprandial triglycerides with sICAM-1 may indicate a particular impact of postprandial lipid metabolism on endothelial reaction.

  6. Detection of Adhesion Molecules on Inflamed Macrophages at Early-Stage Using SERS Probe Gold Nanorods

    Institute of Scientific and Technical Information of China (English)

    Dakrong Pissuwan; Yusuke Hattori

    2017-01-01

    In recent years, it has been shown that inflammatory biomarkers can be used as an effective signal for disease diagnoses. The early detection of these signals provides useful information that could prevent the occurrence of severe diseases. Here, we employed surface-enhanced Raman scattering (SERS) probe gold nanorods (GNRs) as a tool for the early detection of inflammatory molecules in inflamed cells. A murine macrophage cell line (Raw264.7) stimulated with lipopolysaccharide (LPS) was used as a model in this study. The prepared SERS probe GNRs containing 4-mercapto-benzoic acid as a Raman reporter to generate SERS signals were used for detection of intracellular adhesion molecule-1 (ICAM-1) in macrophages after treatment with LPS for varying lengths of time. Our results show that SERS probe GNRs could detect significant differences in the expression of ICAM-1 molecules in LPS-treated macrophages compared to those in untreated macrophages after only 1 h of LPS treatment. In contrast, when using fluorescent labeling or enzyme-linked immunosorbent assays (ELISA) to detect ICAM-1, significant differences between inflamed and un-inflamed macrophages were not seen until the cells had been treated with LPS for 5 h. These results indicate that our SERS probe GNRs provide a higher sensitivity for detecting biomarker molecules in inflamed macrophages than the conventional fluorescence and ELISA techniques, and could therefore be useful as a potential diagnostic tool for managing disease risk.

  7. 大鼠小肠移植排斥反应期移植肠基因表达、ICAM-1和IL-2R分子表达及上皮细胞凋亡的变化%Up-regulated intragraft gene expression,ICAM-1 and IL-2R molecules,and apoptotic epithelial cells during rejection of rat small intestine allografts

    Institute of Scientific and Technical Information of China (English)

    李元新; 李宁; 李幼生; 吴波; 黎介寿

    2001-01-01

    adhesion molecule-1 ( ICAM-1 ) during acute rejection episodes, and to analyze the changes in apoptosis in small intestinal allograft rejection. Methods Heterotopic small intestine transplantation was performed with inbred rats F344/N (RT11) and Wistar/A (RT1-Ak, RT1-Ed). All recipients were divided into four groups: group 1 : Wistar, native control; group 2: Wistar→Wistar; group 3: F344→Wistar and group 4: F344→Wistar + cyclosporine A (6 mg·kg-1 ·d-1 I.M. ). The grafts were harvested on postoperative days (PODs) 3, 5 and 7. All samples were examined pathologically. Intragraft mRNA expression of IL-2, IFN-γ, perforin and granzyme B were detected with reverse transcriptase polymerase chain reaction (RT-PCR) and intragraft expression of IL-2R and ICAM-1 were stained using immunohistochemistry. We also analyzed the change in apoptosis rejection with terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL). Results Mild acute rejection occurred on POD 3 in the ailograft group, moderate acute rejection on POD 5, and severe acute rejection on POD 7, while none of the isografts had histological evidence of acute rejection. Cyclosporine A could effectively control rejection. Gene expression was virtually negative in the native control. Only on POD 5 was IL-2 mRNA expression of ailografts significantly higher than that of isografts ( P < 0.05). IFN-γ mRNA expression was significantly higher than that of the control groups ( P < 0.01 ) on PODs 3, 5 and 7, and the level of perforin and granzyme B mRNA expression reached significantly higher levels than in the other two control groups on POD 5 and POD 7. Intragraft IL-2R expression of the allograft was significantly higher than that of the other three control groups. Only on POD 3 was intragraft ICAM-1 expression of allografts significantly higher than isografts. The number of apoptotic cells per crypt of allografts was significantly higher than that of the other three control groups on POD 3 and POD

  8. Neisserial outer membrane vesicles bind the coinhibitory receptor carcinoembryonic antigen-related cellular adhesion molecule 1 and suppress CD4+ T lymphocyte function.

    Science.gov (United States)

    Lee, Hannah S W; Boulton, Ian C; Reddin, Karen; Wong, Henry; Halliwell, Denise; Mandelboim, Ofer; Gorringe, Andrew R; Gray-Owen, Scott D

    2007-09-01

    Pathogenic Neisseria bacteria naturally liberate outer membrane "blebs," which are presumed to contribute to pathology, and the detergent-extracted outer membrane vesicles (OMVs) from Neisseria meningitidis are currently employed as meningococcal vaccines in humans. While the composition of these vesicles reflects the bacteria from which they are derived, the functions of many of their constituent proteins remain unexplored. The neisserial colony opacity-associated Opa proteins function as adhesins, the majority of which mediate bacterial attachment to human carcinoembryonic antigen-related cellular adhesion molecules (CEACAMs). Herein, we demonstrate that the Opa proteins within OMV preparations retain the capacity to bind the immunoreceptor tyrosine-based inhibitory motif-containing coinhibitory receptor CEACAM1. When CD4(+) T lymphocytes were exposed to OMVs from Opa-expressing bacteria, their activation and proliferation in response to a variety of stimuli were effectively halted. This potent immunosuppressive effect suggests that localized infection will generate a "zone of inhibition" resulting from the diffusion of membrane blebs into the surrounding tissues. Moreover, it demonstrates that OMV-based vaccines must be developed from strains that lack CEACAM1-binding Opa variants.

  9. Fu dragon antithrombotic pill on cerebral ischemia reperfusion injury in rat tissue expression of ICAM -1%蝮龙抗栓丸对脑缺血再灌注损伤大鼠脑组织ICAM-1表达的影响

    Institute of Scientific and Technical Information of China (English)

    宋慧峰

    2015-01-01

    目的:观察蝮龙抗栓丸对脑缺血再灌注损伤大鼠脑组织中细胞间黏附因子-1(ICAM-1)含量的影响。方法:利用完全随机法将75只SD大鼠分为:假手术组(15只)、模型组(15只)、治疗I组(15只)、治疗II组(15只)、对照治疗组(15只),予以治疗I组蝮龙抗栓丸0.65mg/g、治疗II组蝮龙抗栓丸1.29mg/g、对照治疗组银杏叶软胶囊0.13mg/g,灌胃1次/天,共计7天。末次灌胃后应用线栓法制备脑缺血再灌注大鼠模型,采用ELISA方法测定各组大鼠脑组织中ICAM-1含量的变化。结果:与模型组比较,各治疗组大鼠脑组织ICAM-1含量比模型组降低(P<0.05)。结论:蝮龙抗栓丸能明显改善大鼠脑缺血再灌注损伤,其机制与降低脑缺血区域中ICAM-1含量有关。%Objective Fu dragon antithrombotic pill on cerebral ischemia reperfusion injury in rat tissues intercellular adhesion factor 1 (ICAM - 1) content.Methods With completely random method, 75 SD rats can be divided into: the control group (15), model group (15), treatment group I (15), treatment group II (15), contrast the treatment group (15), the treatment group I Fu dragon antithrombotic pill 0.65 mg/g, treatment group II Fu dragon antithrombotic pill 1.29 mg/g, contrast treatment group ginkgo biloba soft capsule 0.13 mg/g, lavage 1 time/day, a total of 7 days. After lavage application line plug at the end of the preparation of cerebral ischemia reperfusion model in rats, using ELISA method in the determination of each group rats had changes in concentrations of ICAM - 1.Results Compared with model group, content of ICAM - 1 in each treatment group rats had lower than model group (p < 0.05).Conclusions Fu dragon antithrombotic pill has obvious improvement in ischemia reperfusion injury in rats and its mechanism and reduce ICAM - 1 content in the area of cerebral ischemia.

  10. The RhoA/ROCK Pathway Ameliorates Adhesion and Inflammatory Infiltration Induced by AGEs in Glomerular Endothelial Cells.

    Science.gov (United States)

    Rao, Jialing; Ye, Zengchun; Tang, Hua; Wang, Cheng; Peng, Hui; Lai, Weiyan; Li, Yin; Huang, Wanbing; Lou, Tanqi

    2017-01-05

    A recent study demonstrated that advanced glycation end products (AGEs) play a role in monocyte infiltration in mesangial areas in diabetic nephropathy. The Ras homolog gene family, member A Rho kinase (RhoA/ROCK) pathway plays a role in regulating cell migration. We hypothesized that the RhoA/ROCK pathway affects adhesion and inflammation in endothelial cells induced by AGEs. Rat glomerular endothelial cells (rGECs) were cultured with AGEs (80 μg/ml) in vitro. The ROCK inhibitor Y27632 (10 nmol/l) and ROCK1-siRNA were used to inhibit ROCK. We investigated levels of the intercellular adhesion molecule 1 (ICAM-1) and monocyte chemoattractant protein1 (MCP-1) in rGECs. Db/db mice were used as a diabetes model and received Fasudil (10 mg/kg/d, n = 6) via intraperitoneal injection for 12 weeks. We found that AGEs increased the expression of ICAM-1 and MCP-1 in rGECs, and the RhoA/ROCK pathway inhibitor Y27632 depressed the release of adhesion molecules. Moreover, blocking the RhoA/ROCK pathway ameliorated macrophage transfer to the endothelium. Reduced expression of adhesion molecules and amelioration of inflammatory cell infiltration in the glomerulus were observed in db/db mice treated with Fasudil. The RhoA/ROCK pathway plays a role in adhesion molecule expression and inflammatory cell infiltration in glomerular endothelial cells induced by AGEs.

  11. Ambient pollutants, polymorphisms associated with microRNA processing and adhesion molecules: the Normative Aging Study

    Directory of Open Access Journals (Sweden)

    Vokonas Pantel S

    2011-05-01

    Full Text Available Abstract Background Particulate air pollution has been associated with cardiovascular morbidity and mortality, but it remains unclear which time windows and pollutant sources are most critical. MicroRNA (miRNA is thought to be involved in cardiovascular regulation. However, little is known about whether polymorphisms in genes that process microRNAs influence response to pollutant exposure. We hypothesized that averaging times longer than routinely measured one or two day moving averages are associated with higher soluble intercellular adhesion molecule-1 (sICAM-1 and vascular cell adhesion molecule-1 (sVCAM-1 levels, and that stationary and mobile sources contribute differently to these effects. We also investigated whether single nucleotide polymorphisms (SNPs in miRNA-processing genes modify these associations. Methods sICAM-1 and sVCAM-1 were measured from 1999-2008 and matched to air pollution monitoring for fine particulate matter (PM2.5 black carbon, and sulfates (SO42-. We selected 17 SNPs in five miRNA-processing genes. Mixed-effects models were used to assess effects of pollutants, SNPs, and interactions under recessive inheritance models using repeated measures. Results 723 participants with 1652 observations and 1-5 visits were included in our analyses for black carbon and PM2.5. Sulfate data was available for 672 participants with 1390 observations. An interquartile range change in seven day moving average of PM2.5 (4.27 μg/m3 was associated with 3.1% (95%CI: 1.6, 4.6 and 2.5% (95%CI: 0.6, 4.5 higher sICAM-1 and sVCAM-1. Interquartile range changes in sulfates (1.39 μg/m3 were associated with 1.4% higher (95%CI: 0.04, 2.7 and 1.6% (95%CI: -0.4, 3.7 higher sICAM-1 and sVCAM-1 respectively. No significant associations were observed for black carbon. In interaction models with PM2.5, both sICAM-1 and sVCAM-1 levels were lower in rs1062923 homozygous carriers. These interactions remained significant after multiple comparisons

  12. ICAM-1 targeted catalase encapsulated PLGA-b-PEG nanoparticles against vascular oxidative stress.

    Science.gov (United States)

    Sari, Ece; Tunc-Sarisozen, Yeliz; Mutlu, Hulya; Shahbazi, Reza; Ucar, Gulberk; Ulubayram, Kezban

    2015-01-01

    Targeted delivery of therapeutics is the favourable idea, whereas it is possible to distribute the therapeutically active drug molecule only to the site of action. For this purpose, in this study, catalase encapsulated poly(D,L-lactide-co-glycolide)-block-poly(ethylene glycol) (PLGA-b-PEG) nanoparticles were developed and an endothelial target molecule (anti-ICAM-1) was conjugated to this carrier system in order to decrease the oxidative stress level in the target site. According to the enzymatic activity results, initial catalase activity of nanoparticles was increased from 27.39 U/mg to up to 45.66 U/mg by adding 5 mg/mL bovine serum albumin (BSA). After 4 h, initial catalase activity was preserved up to 46.98% while free catalase retained less than 4% of its activity in proteolytic environment. Furthermore, FITC labelled anti-ICAM-1 targeted catalase encapsulated nanoparticles (anti-ICAM-1/CatNPs) were rapidly taken up by cultured endothelial cells and concomitantly endothelial cells were resistant to H2O2 induced oxidative impairment.

  13. IL-6 and sICAM-1 in seminal plasma relate to male immune infertility%免疫性不育男性精浆白细胞介素6和可溶性细胞黏附分子1分析

    Institute of Scientific and Technical Information of China (English)

    史波; 魏任雄; 崔云; 周俊; 张晓霞

    2014-01-01

    intedeukin-6 (IL-6) and soluble intercellular adhesion molecule-1 (sICAM-1) in the seminal plasma of infertile men and explore the role of inflammatory cytokines in male immune infertility.Methods:Based on the results of the sperm-bound antibody immunobead test,123 males with clinically suspected infertility were divided into an immune infertility group (n =41),other infertility group A (n =37),and other infertility group B (n =45).The immune infertility patients were further subdivided into a leukocyte-positive and a leukocyte-negative group according to the results of leukocyte peroxidase staining.The control group included 31 males confirmed to be fertile in the clinic.Statistical analyses were conducted on the differences in inflammatory cytokines expressions and main parameters in the seminal plasma among different groups.The seminal liquefaction time was measured by visual and microscopic observation,sperm concentration and motility detected using the computer-assisted sperm analysis system,sperm viability determined by hypotonic swelling assay,and the expression levels of IL-6 and sICAM-1 measured by ELISA.Results:The infertility groups showed significantly lowers perm viability (P < 0.05) and progressive motility (P < 0.01) than the fertile control,but no remarkable differences from the latter in sperm concentration (P >0.05) and semen liquefaction time (P > 0.05).No statistically significant differences were observed in seminal parameters between the immune infertility group and other infertility groups (P >0.05).The IL-6 and sICAM-1 levels in the seminal plasma were extremely significantly higher in the immune infertility group ([37.92 ± 17.01] ng/L and [89.15 ± 41.82] ng/ml),other infertility group A ([22.23 ± 13.77] ng/L and [67.81 ± 33.24] ng/ml),and other infertility group B ([18.75 ± 14.32] ng/L and [53.25 ± 27.09] ng/ml) than in the normal control group ([9.47 ± 5.76] ng/L and [19.46 ± 9.77] ng/ml) (P < 0.01),with remarkable differences

  14. Sulforaphane inhibits TNF-α-induced adhesion molecule expression through the Rho A/ROCK/NF-κB signaling pathway.

    Science.gov (United States)

    Hung, Chi-Nan; Huang, Hui-Pei; Wang, Chau-Jong; Liu, Kai-Li; Lii, Chong-Kuei

    2014-10-01

    Endothelial dysfunction is an early indicator of cardiovascular diseases. Increased stimulation of tumor necrosis factor-α (TNF-α) triggers the inflammatory mediator secretion of endothelial cells, leading to atherosclerotic risk. In this study, we investigated whether sulforaphane (SFN) affected the expression of intracellular adhesion molecule-1 (ICAM-1) in TNF-α-induced ECV 304 endothelial cells. Our data showed that SFN attenuated TNF-α-induced expression of ICAM-1 in ECV 304 cells. Pretreatment of ECV 304 cells with SFN inhibited dose-dependently the secretion of proinflammatory cytokines, such as interleukin (IL)-1β, IL-6, and IL-8. SFN inhibited TNF-α-induced nuclear factor-κB (NF-κB) DNA binding activity. Furthermore, SFN decreased TNF-α-mediated phosphorylation of IκB kinase (IKK) and IκBα, Rho A, ROCK, ERK1/2, and plasminogen activator inhibitor-1 (PAI-1) levels. Collectively, SFN inhibited the NF-κB DNA binding activity and downregulated the TNF-α-mediated induction of ICAM-1 in endothelial cells by inhibiting the Rho A/ROCK/NF-κB signaling pathway, suggesting the beneficial effects of SFN on suppression of inflammation within the atherosclerotic lesion.

  15. 过敏性紫癜患儿瘀血及黏附分子 sICAM-1、sVCAM-1表达水平的研究%Clinical research of blood stasis and the level of serous and urinary sICAM-1,sVCAM-1 in henoch-schonlein purpura

    Institute of Scientific and Technical Information of China (English)

    黄岩杰; 赵丽丽; 李玉蕊; 张建; 梅晓峰; 翟文生; 任献青; 丁樱

    2012-01-01

    Objective: We observed the expression of sICAM-1, sVCAM-1 in serum and urine in HSP, blood stasis and the relationship between blood stasis sICAM-1, sVCAM-1 in urine and kidney damage. Methods: 80 patients with HSP were divided into NO-HSPN (30 cases), hematuria group (23 cases) and proteinuria and hematuria group (27 cases), healthy children (10 cases) as normal group. Blood stasis was scored according to TCM symptoms for blood stasis. The concentration of sVCAM, sVCAM-1 in serum and urine was detected by enzyme linked immunosorbent assay (ELISA). Results: (DBlood stasis score in proteinuria and hematuria group was higher than NO-HSPN group(P<0.01). ㏒erous sICAM-1 was not obvious difference in each groups. Urinary sICAM-1 in proteinuria and hematuria group was higher than normal group and NO-HSPN group (P<0.05, f<0.01). 甋erous sVCAM-1 is not significant differences among all the groups. Urinary sVCAM-1 of proteinuria and hematuria group was significant higher than normal group, NO-HSPN group, hematuria group. 瓵 positive correlation can be found between urinary sVCAM-1 and sICAM-1 and blood stasis score in proteinuria and hematuria group. Conclusion: Blood stasis was involved in the renal lesion process in HSP. sICAM-1, sVCAM-1 in urine was increased in proteinuria and hematuria group, while those in serum was not changed compared with other group. These results suggested that blood stasis can increase the expression of sICAM, sVCAM-1 in kidney, and which triggered the cellular adhesion molecule-mediated inflammatory cells infiltration, followed up to increase renal lesion.%目的:观察过敏性紫癜(HSP)患儿可溶性细胞间黏附分子-1(sICAM-1)、可溶性血管细胞黏附分子-1 (sVCAM-1)表达水平及瘀血状态,分析瘀血与尿中黏附分子及肾脏损伤的关系.方法:HSP患儿80例分为无肾损( NO-HSPN)组、血尿组、血尿加蛋白尿组,正常组(健康儿童10名).根据中医瘀血症候积分表进行瘀血评分.ELISA法测定sICAM

  16. The effect of lidocaine on neutrophil CD11b/CD18 and endothelial ICAM-1 expression and IL-1beta concentrations induced by hypoxia-reoxygenation.

    LENUS (Irish Health Repository)

    Lan, W

    2012-02-03

    BACKGROUND: Lidocaine has actions potentially of benefit during ischaemia-reperfusion. Neutrophils and endothelial cells have an important role in ischaemia-reperfusion injury. METHODS: Isolated human neutrophil CD11b and CD18, and human umbilical vein endothelial cell (HUVEC) ICAM-1 expression and supernatant IL-1beta concentrations in response to hypoxia-reoxygenation were studied in the presence or absence of different concentrations of lidocaine (0.005, 0.05 and 0.5 mg mL(-1)). Adhesion molecule expression was quantified by flow cytometry and IL- 1beta concentrations by ELISA. Differences were assessed with analysis of variance and Student-Newman-Keuls as appropriate. Data are presented as mean+\\/-SD. RESULTS: Exposure to hypoxia-reoxygenation increased neutrophil CD11b (94.33+\\/-40.65 vs. 34.32+\\/-6.83 mean channel fluorescence (MCF), P = 0.02), CD18 (109.84+\\/-35.44 vs. 59.05+\\/-6.71 MCF, P = 0.03) and endothelial ICAM-1 (146.62+\\/-16.78 vs. 47.29+\\/-9.85 MCF, P < 0.001) expression compared to normoxia. Neutrophil CD18 expression on exposure to hypoxia-reoxygenation was less in lidocaine (0.005 mg mL(-1)) treated cells compared to control (71.07+\\/-10.14 vs. 109.84+\\/-35.44 MCF, P = 0.03). Endothelial ICAM-1 expression on exposure to hypoxia-reoxygenation was less in lidocaine (0.005 mg mL(-1)) treated cells compared to control (133.25+\\/-16.05 vs. 146.62+\\/-16.78 MCF, P = 0.03). Hypoxia-reoxygenation increased HUVEC supernatant IL-1beta concentrations compared to normoxia (3.41+\\/-0.36 vs. 2.65+\\/-0.21 pg mL(-1), P = 0.02). Endothelial supernatant IL-1beta concentrations in lidocaine-treated HUVECs were similar to controls. CONCLUSIONS: Lidocaine at clinically relevant concentrations decreased neutrophil CD18 and endothelial ICAM-1 expression but not endothelial IL-1beta concentrations.

  17. Studies Expression of intercellular adhesion molecule - 1 on Spinal Cord Ischemia/Reperfusion Injury%大鼠脊髓缺血 --再灌注损伤细胞间粘附分子表达研究

    Institute of Scientific and Technical Information of China (English)

    孙庆; 杨小玉; 朱庆三; 赵立君; 秦彦国; 段德生

    2003-01-01

    目的:探讨大鼠脊髓缺血-再灌注损伤细胞间粘附分子ICAM-1表达变化.方法:采用逆转录-聚合酶链反应、免疫组化及免疫荧光激光共聚焦扫描显微镜技术检测脊髓再灌注损伤血管内皮ICAM-1mRNA表达量.结果:正常组和单纯缺血组不引起细胞因子和粘附分子表达量的增加.而再灌注后缺血区粘附分子的表达及PMN的浸润先后发生了改变.再灌注4h明显升高,6h达到高峰,并持续到12h.ICAM-1 mRNA表达量于再灌注4h明显升高,再灌注12h其在单位微血管面积上的荧光强度约比单纯缺血组增加了二分之一,再灌注12h脊髓组织中MPO活性约为单纯缺血组的两倍.结论:再灌注损伤后脊髓内炎症反应是继发性脊髓损伤重要分子基础.

  18. Identification of Peptides Inhibiting Adhesion of Monocytes to the Injured Vascular Endothelial Cells through Phage-displaying Screening

    Institute of Scientific and Technical Information of China (English)

    Yu GUO; Jia ZHANG; Ji-Cheng WANG; Feng-Xiang YAN; Bing-Yang ZHU; Hong-Lin HUANG; Duan-Fang LIAO

    2005-01-01

    Using oxidized low-density lipoprotein (LDL)-injured vascular endothelial cells (ECs) as target cells, peptides specifically binding to the injured ECs were screened from a phage-displaying peptide library by using the whole-cell screening technique after three cycles of the "adsorption-elution-amplification"procedure. Positive phage clones were identified by ELISA, and the inserted amino acid sequences in the displaying peptides were deduced from confirmation with DNA sequencing. The adhesion rate of ECs to monocytes was evaluated by cell counting. The activity of endothelial nitric oxide synthase (eNOS), and the expression levels of caveolin- 1 and intercellular adhesion molecule- 1 (ICAM- 1) were determined by Western blotting. Six positive clones specifically binding to injured ECV304 endothelial cells were selected from fourteen clones. Interestingly, four phages had peptides with tandem leucine, and two of these even shared an identical sequence. Functional analysis demonstrated that the YCPRYVRRKLENELLVL peptide shared by two clones inhibited the expression of ICAM-1, increased nitric oxide concentration in the culture media, and upregulated the expression of caveolin-1 and eNOS. As a result, the adhesion rate of monocytes to ECV304 cells was significantly reduced by 12.1%. These data suggest that the anti-adhesion effect of these novel peptides is related to the regulation of the caveolin-1/nitric oxide signal transduction pathway, and could be of use in potential therapeutic agents against certain cardiovascular diseases initiated by vascular endothelial cell damage.

  19. The effect of lidocaine on in vitro neutrophil and endothelial adhesion molecule expression induced by plasma obtained during tourniquet-induced ischaemia and reperfusion.

    LENUS (Irish Health Repository)

    Lan, W

    2012-02-03

    BACKGROUND: Changes in neutrophil and endothelial adhesion molecule expression occur during perioperative ischaemia and reperfusion (I\\/R) injury. We investigated the effects of lidocaine on neutrophil-independent changes in neutrophil and endothelial adhesion molecule expression associated with tourniquet-induced I\\/R. METHODS: Plasma was obtained from venous blood samples (tourniquet arm) taken before (baseline), during, 15 min, 2 and 24 h following tourniquet release in seven patients undergoing elective upper limb surgery with tourniquet application. Isolated neutrophils from healthy volunteers (n = 7) were pretreated in the presence or absence of lidocaine (0.005, 0.05 and 0.5 mg mL(-1) for 1 h, and then incubated with I\\/R plasma for 2 h. Human umbilical vein endothelial cells (HUVECs) were pretreated in the presence or absence of lidocaine (0.005, 0.05 and 0.5 mg mL(-1)) for 1 h, and then incubated with the plasma for 4 h. Adhesion molecule expression was estimated using flow cytometry. Data were analysed using ANOVA and post hoc Student-Newman-Keuls tests. RESULTS: I\\/R plasma (withdrawn 15 min following tourniquet release) increased isolated neutrophil CD11b (P = 0.03), CD18 (P = 0.01) and endothelial intercellular adhesion molecule-1 (ICAM-1) (P = 0.008) expression compared to baseline. CD11b, CD18 and ICAM-1 expression on lidocaine (0.005 mg mL(-1)) treated neutrophils was similar to control. CD11b (P < 0.001), CD18 (P = 0.03) and ICAM-1 (P = 0.002) expression on lidocaine (0.05 mg mL(-1)) treated neutrophils and HUVECs was less than that on controls. CONCLUSION: Increased in vitro neutrophil and endothelial cell adhesion molecule expression on exposure to plasma obtained during the early reperfusion phase is diminished by lidocaine at greater than clinically relevant plasma concentrations.

  20. 血小板内皮细胞黏附分子-1(PECAM-1)与肿瘤关系研究进展%Platelet Endothelial Cell Adhesion Molecule-1 (PECAM-1) and Tumor

    Institute of Scientific and Technical Information of China (English)

    袁梅琴; 钟海均

    2016-01-01

    Platelet endothelial cell adhesion molecule-1 ( PECAM-1 ) is one of the immunoglobulin superfamily cell adhesion molecules, and is the key factor involved in platelet adhesion and aggregation.The gene and protein structure of PECAM-1 has been already studied.The studies have found that adhesion effect mediated by PECAM-1 including cells and cells,cells and extracellular matrix is closely related to a variety of physiological reaction;and PE-CAM-1 also have the vital significance in inflammation,wound healing and angiogenesis and so on;A variety of disea-ses,especially cardiovascular diseases such as atherosclerosis disease,are closely related to PECAM-1,and PECAM-1 gene polymorphism may affect the function of PECAM-1.Further studies indicate that PECAM-1 plays an important role in tumor growth as an adhesion factor,but its roles in different tumors,the methods and mechanisms of PECAM-1 are still not clear,and need further exploration.Treatments of anti-PECAM-1 have greatly inspired us.In this pa-per,the relationships between PECAM-1 and tumors,and associated research progress have been reviewed as follows.%血小板内皮细胞粘附分子-1(PECAM-1)是免疫球蛋白超家族细胞粘附分子中的一种,是参与血小板黏附和聚集的关键因子,对其基因及蛋白质结构已进行了较为深入的研究。研究发现,PECAM-1所介导的细胞与细胞、细胞与细胞外基质间黏附作用与多种生理反应密切相关;也在炎症反应、创伤愈合及血管生成等多方面均具有重要的意义;多种疾病尤其是心血管疾病如动脉粥样硬化等的发病与 PECAM-1也密切相关,且PECAM-1的基因多态性也会影响PECAM-1的功能。近期越来越多的研究已表明PECAM-1作为黏附因子在肿瘤生长中起着重要作用,但对其在不同肿瘤中的作用、作用方式及机制仍未明确,需要进一步探索。而抗 PECAM-1治疗的情况也很大程度上鼓舞了我们。本文就 PECAM

  1. sICAM-1、sE-selectin水平在肝癌诊疗中的价值①%The value of measurement of sICAM-1 and sE-selectin in hepatocellular carcinom a (HCC)

    Institute of Scientific and Technical Information of China (English)

    唐南洪; 陈燕凌; 李秀金; 王晓茜; 殷凤峙

    2001-01-01

    目的:探讨血清细胞间粘附分子-1(sICAM-1)、E-选择素(sE-selectin)在肝癌诊疗中的价值.方法:检测健康人、慢胜肝炎、肝硬化、肝癌者手术前后sICAM-1、sE-selectin水平变化.结果:79例各期肝癌者总体sICAM-1、SE-selectin水平明显高于慢性肝炎、肝硬化和健康对照组(P<0.01),但Ⅰ期肝癌组与慢性肝炎、肝硬化组比较无显著差异;各期肝癌术后sICAM1-1及Ⅰ、Ⅱ、Ⅲ期肝癌术后sE-selectin水平均较术前明显下降.结论:提示早期肝癌患者检测血清sICAM-1、sE-selectin无确诊意义 ,但可作为中、晚期肝癌者特别是AFP阴性患者的血清学确诊参考和预后的监测指标.

  2. 大肠癌PARP表达与P-selectin和ICAM-1表达的相关性%Correlation of PARP expression with P-selectin and ICAM-1 expression in colorectal carcinoma

    Institute of Scientific and Technical Information of China (English)

    郝兰香; 王娅兰; 李圆圆

    2006-01-01

    目的 初步探讨聚腺苷二磷酸核糖聚合酶(PARP)与大肠癌侵袭转移的关系及其可能机制.方法 采用SP免疫组化法检测PAR(聚腺苷二磷酸核糖,系PARP产物)、P-selectin及ICAM-1的表达;并应用免疫荧光双标法检测PAR与P-selectin、ICAM-1的共表达.结果 大肠癌组织内PAR、P-selectin及ICAM-1的表达均明显高于对照肠黏膜(P<0.05);3种蛋白的表达仅与大肠癌转移有关(P<0.05),而与其他临床病理因素无关;PAR与P-selectin和ICAM-1的表达均呈正相关关系(P<0.05).结论 大肠癌组织内PARP活性增强,并可能通过上调P-selectin和ICAM-1的表达而有利于大肠癌侵袭转移,有望成为判断大肠癌转移的参考指标之一.

  3. Glossogyne tenuifolia Extract Inhibits TNF-α-Induced Expression of Adhesion Molecules in Human Umbilical Vein Endothelial Cells via Blocking the NF-kB Signaling Pathway.

    Science.gov (United States)

    Hsuan, Chin-Feng; Hsu, Hsia-Fen; Tseng, Wei-Kung; Lee, Thung-Lip; Wei, Yu-Feng; Hsu, Kwan-Lih; Wu, Chau-Chung; Houng, Jer-Yiing

    2015-09-17

    Chronic inflammation plays a pivotal role in the development of atherosclerosis, where the pro-inflammatory cytokine-induced expression of endothelial adhesion molecules and the recruitment of monocytes are the crucial events leading to its pathogenesis. Glossogyne tenuifolia ethanol extract (GTE) is shown to have potent anti-inflammatory and antioxidant activities. We evaluated the effects of GTE and its major components, luteolin (lut), luteolin-7-glucoside (lut-7-g), and oleanolic acid (OA) on TNF-α-induced expression of adhesion molecules in human umbilical vein endothelial cells (HUVECs). The results demonstrated that GTE, lut, and lut-7-g attenuated the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in TNF-α-activated HUVECs, and inhibited the adhesion of monocytes to TNF-α-activated HUVECs. The TNF-α-induced mRNA expression of ICAM-1 and VCAM-1 was also suppressed, revealing their inhibitory effects at the transcriptional level. Furthermore, GTE, lut, and lut-7-g blocked the TNF-α-induced degradation of nuclear factor-kB inhibitor (IkB), an indicator of the activation of nuclear factor-kB (NF-kB). In summary, GTE and its bioactive components were effective in preventing the adhesion of monocytes to cytokine-activated endothelium by the inhibition of expression of adhesion molecules, which in turn is mediated through blocking the activation and nuclear translocation of NF-kB. The current results reveal the therapeutic potential of GTE in atherosclerosis.

  4. Celastrol inhibits lung infiltration in differential syndrome animal models by reducing TNF-α and ICAM-1 levels while preserving differentiation in ATRA-induced acute promyelocytic leukemia cells.

    Directory of Open Access Journals (Sweden)

    Li-min Xu

    Full Text Available All-trans retinoic acid (ATRA is a revolutionary agent for acute promyelocytic leukemia (APL treatment via differentiation induction. However, ATRA treatment also increases cytokine, chemokine, and adhesive molecule (mainly ICAM-1 expression, which can cause clinical complications, including a severe situation known as differentiation syndrome (DS which can cause death. Therefore, it is of clinical significance to find a strategy to specifically blunt inflammatory effects while preserving differentiation. Here we report that the natural compound, celastrol, could effectively block lung infiltrations in DS animal models created by loading ATRA-induced APL cell line NB4. In ATRA-treated NB4 cells, celastrol could potently inhibit ICAM-1 elevation and partially reduce TNF-α and IL-1β secretion, though treatment showed no effects on IL-8 and MCP-1 levels. Celastrol's effect on ICAM-1 in ATRA-treated NB4 was related to reducing MEK1/ERK1 activation. Strikingly and encouragingly, celastrol showed no obvious effects on ATRA-induced NB4 differentiation, as determined by morphology, enzymes, and surface markers. Our results show that celastrol is a promising and unique agent for managing the side effects of ATRA application on APL, and suggest that hyper-inflammatory ability is accompanied by, but not necessary for, APL differentiation. Thus we offered an encouraging novel strategy to further improve differentiation therapy.

  5. Value of knee skin temperature measured by infrared thermography and soluble intercellular adhesion molecule-1 in the diagnosis of peri-prosthetic knee infection in Chinese individuals following total knee arthroplasty

    Institute of Scientific and Technical Information of China (English)

    Mumingjiang Yishake; Zhou Xindie; He Rongxin

    2014-01-01

    Background Total knee arthroplasty (TKA) is a successful and frequently performed procedure in orthopedic surgery.The diagnosis of peri-prosthetic joint infection following TKA remains challenging.The present study estimated the usefulness of knee skin temperature (measured by infrared thermography) and serum soluble intercellular adhesion molecule-1 (slCAM-1) in the diagnosis of post-operative knee peri-prosthetic infection.Methods Patients were divided into three groups:21 patients undergoing uncomplicated TKAs,seven with prosthesis infection,and three undergoing TKA revisions.The serum levels of interleukin-6 (IL-6),C-reactive protein (CRP),erythrocyte sedimentation rate (ESR),and slCAM-1 as well as the local knee skin temperature were measured preoperatively and on Days 1 and 7 and at 1,3,and 6 months post-operatively in Groups 1 and 3.The same parameters were measured in Group 2 at the time of prosthesis infection diagnosis.Results In Group 1,the levels of IL-6,CRP,ESR,and knee skin temperature were significantly elevated post-operatively,but returned to baseline levels within 6 months.The slCAM-1 levels were not significantly different.The mean differential temperature (MDT) and levels of siCAM-1,IL-6,CRP,and ESR differed significantly between Groups 1 and 2.The MDT had returned to normal in Group 3 by 6 months post-operatively.Conclusions Elevations in IL-6,CRP,ESR,and MDT in patients undergoing TKA could be a normal response to surgical trauma,but sustained elevations may be indicative of complications.The knee skin temperature and slCAM-1 may be used as indicators in the diagnosis of knee prosthesis infection following TKA.

  6. 细胞间粘附分子-1、E-选择素及肿瘤坏死因子和慢性阻塞性肺疾病的关系%The Relationship of Intercellular Adhesion Molecules-1,E-selectin with Chronic Obstructive Pulmonary Disease

    Institute of Scientific and Technical Information of China (English)

    马希刚; 曹相原

    2006-01-01

    目的研究细胞间黏附分子(ICAM-1)、E选择素(E-selectin)和肿瘤坏死因子(TNF-α)与慢性阻塞性肺疾病(COPD)发病之间的关系.方法采用酶联免疫吸附双抗体夹心法原理(ELISA),分别检测45例COPD急性加重期患者和20例健康体检者(对照组)血清可溶性ICAM-1(sICAM-1)、可溶性E-selectin(sE-selectin)和TNF-α的含量.结果 COPD急性加重期患者血清sICAM-1和sE-selectin的平均含量明显高于对照组(P<0.001),并随着阻塞程度的加重而升高(P<0.01);TNF-α与sICAM-1和sE-selectin呈正相关(r=0.899、0.781,P<0.001).结论 ICAM-1和E-selectin参与了COPD的发生和发展,TNF-α是COPD急性加重期诱导ICAM-1和E-selectin表达上调的重要细胞因子.

  7. Upregulation of endothelial cell adhesion molecules characterizes veins close to granulomatous infiltrates in the renal cortex of cats with feline infectious peritonitis and is indirectly triggered by feline infectious peritonitis virus-infected monocytes in vitro.

    Science.gov (United States)

    Acar, Delphine D; Olyslaegers, Dominique A J; Dedeurwaerder, Annelike; Roukaerts, Inge D M; Baetens, Wendy; Van Bockstael, Sebastiaan; De Gryse, Gaëtan M A; Desmarets, Lowiese M B; Nauwynck, Hans J

    2016-10-01

    One of the most characteristic pathological changes in cats that have succumbed to feline infectious peritonitis (FIP) is a multifocal granulomatous phlebitis. Although it is now well established that leukocyte extravasation elicits the inflammation typically associated with FIP lesions, relatively few studies have aimed at elucidating this key pathogenic event. The upregulation of adhesion molecules on the endothelium is a prerequisite for stable leukocyte-endothelial cell (EC) adhesion that necessarily precedes leukocyte diapedesis. Therefore, the present work focused on the expression of the EC adhesion molecules and possible triggers of EC activation during the development of FIP. Immunofluorescence analysis revealed that the endothelial expression of P-selectin, E-selectin, intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) was elevated in veins close to granulomatous infiltrates in the renal cortex of FIP patients compared to non-infiltrated regions and specimens from healthy cats. Next, we showed that feline venous ECs become activated when exposed to supernatant from feline infectious peritonitis virus (FIPV)-infected monocytes, as indicated by increased adhesion molecule expression. Active viral replication seemed to be required to induce the EC-stimulating activity in monocytes. Finally, adhesion assays revealed an increased adhesion of naive monocytes to ECs treated with supernatant from FIPV-infected monocytes. Taken together, our results strongly indicate that FIPV activates ECs to increase monocyte adhesion by an indirect route, in which proinflammatory factors released from virus-infected monocytes act as key intermediates.

  8. Sequential expression of adhesion and costimulatory molecules in graft-versus-host disease target organs after murine bone marrow transplantation across minor histocompatibility antigen barriers.

    Science.gov (United States)

    Eyrich, Matthias; Burger, Gudrun; Marquardt, Katja; Budach, Wilfried; Schilbach, Karin; Niethammer, Dietrich; Schlegel, Paul G

    2005-05-01

    Graft-versus-host disease (GVHD) is a potentially fatal complication after allogeneic bone marrow transplantation. However, few data exist thus far on the molecular signals governing leukocyte trafficking during the disease. We therefore investigated the sequential pattern of distinct adhesion, costimulatory, and apoptosis-related molecules in GVHD organs (ileum, colon, skin, and liver) after transplantation across minor histocompatibility barriers (B10.D2 --> BALB/c, both H-2d). To distinguish changes induced by the conditioning regimen from effects achieved by allogeneic cell transfer, syngeneic transplant recipients (BALB/c --> BALB/c) and irradiated nontransplanted mice were added as controls. Irradiation upregulated the expression of vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule (ICAM)-l, and B7-2 in ileum, as well as VCAM-1 and B7-2 in colon, on day 3 in all animals. Whereas in syngeneic mice these effects were reversed from day 9 on, allogeneic recipients showed further upregulation of VCAM-1, ICAM-1, B7-1, and B7-2 in these organs on day 22, when GVHD became clinically evident. Infiltration of CD4+ and CD8+ donor T cells was noted on day 9 in skin and liver and on day 22 in ileum and colon. Surprisingly, the expression of several other adhesion molecules, such as ICAM-2, platelet-endothelial cell adhesion molecule 1, E-selectin, and mucosal addressin cell adhesion molecule 1, did not change. Proapoptotic and antiapoptotic markers were balanced in GVHD organs with the exception of spleen, in which a preferential expression of the proapoptotic Bax could be noted. Our results indicate that irradiation-induced upregulation of VCAM-1, ICAM-1, and B7-2 provides early costimulatory signals to incoming donor T cells in the intestine, followed by a cascade of proinflammatory signals in other organs once the alloresponse is established.

  9. Family with sequence similarity 5, member C (FAM5C increases leukocyte adhesion molecules in vascular endothelial cells: implication in vascular inflammation.

    Directory of Open Access Journals (Sweden)

    Junya Sato

    Full Text Available Identification of the regulators of vascular inflammation is important if we are to understand the molecular mechanisms leading to atherosclerosis and consequent ischemic heart disease, including acute myocardial infarction. Gene polymorphisms in family with sequence similarity 5, member C (FAM5C are associated with an increased risk of acute myocardial infarction, but little is known about the function of this gene product in blood vessels. Here, we report that the regulation of the expression and function of FAM5C in endothelial cells. We show here that FAM5C is expressed in endothelial cells in vitro and in vivo. Immunofluorescence microscopy showed localization of FAM5C in the Golgi in cultured human endothelial cells. Immunohistochemistry on serial sections of human coronary artery showed that FAM5C-positive endothelium expressed intercellular adhesion molecule-1 (ICAM-1 or vascular cell adhesion molecule-1 (VCAM-1. In cultured human endothelial cells, the overexpression of FAM5C increased the reactive oxygen species (ROS production, nuclear factor-κB (NF-κB activity and the expression of ICAM-1, VCAM-1 and E-selectin mRNAs, resulting in enhanced monocyte adhesion. FAM5C was upregulated in response to inflammatory stimuli, such as TNF-α, in an NF-κB- and JNK-dependent manner. Knockdown of FAM5C by small interfering RNA inhibited the increase in the TNF-α-induced production of ROS, NF-κB activity and expression of these leukocyte adhesion molecule mRNAs, resulting in reduced monocyte adhesion. These results suggest that in endothelial cells, when FAM5C is upregulated in response to inflammatory stimuli, it increases the expression of leukocyte adhesion molecules by increasing ROS production and NF-κB activity.

  10. White blood cell deformation and firm adhesion

    Science.gov (United States)

    Szatmary, Alex; Eggleton, Charles

    2011-11-01

    For a white blood cell (WBC) to arrive at infection sites, it forms chemical attachments with activated endothelial cells. First, it bonds with P-selectin, which holds it to the wall, but weakly; this allows the WBC to roll under the shear flow of the blood around it. Later, the WBCs bond with the stronger intracellular adhesion molecule-1 (ICAM-1); it is these ICAM bonds that allow the WBCs to fully resist the flow and stop rolling, allowing them to crawl through the endothelial wall. We model this numerically. Our model uses the immersed boundary method to represent the interaction of the shear flow with the deformable cell membrane. Receptors are on the tips of microvilli-little fingers sticking off of the cell membrane. The microvilli also deform. The receptors stochastically form and break bonds with molecules on the wall. Using this method, the history of each microvillus and its bonds can be found, as well as the distribution of the adhesion traction forces and how all of these vary with the deformability of the white blood cell. At higher shear rates, the white blood cell membrane deforms more, increasing its contact area with the surface; this effect is larger for softer membranes. We investigate how the deformability of the WBC affects the ease with which it forms firm adhesion.

  11. Selected immunological changes in patients with Goeckerman's therapy TNF-alpha, sE-selectin, sP-selectin, sICAM-1 and IL-8

    Energy Technology Data Exchange (ETDEWEB)

    Borska, L.; Fiala, Z.; Krejsek, J.; Andrys, C.; Vokurkova, D.; Hamakova, K.; Kremlacek, J.; Ettler, K. [Charles University, Hradec Kralove (Czech Republic). Faculty of Medicine

    2006-07-01

    Psoriasis is one of the most frequent inflammatory skin diseases in which abnormal individual immune reactivity plays an important role. The aim of the present study was to describe selected immunological changes, concerning pro-inflammatory cytokines (TNF-alpha, IL-8) and adhesion molecules (sE-selectin, sP-selectin, sICAM-1), in 56 patients cured by Goeckerman's therapy (GT). GT includes dermal application of crude coal tar (containing polycyclic aromatic hydrocarbons) and exposure to UV radiation.

  12. HT-29肠癌细胞中E-selectin、Integrin β1及ICAM-1表达水平%Expression of E-Selectin, Integrin β1 and ICAM-1 in HT-29 Colon Carcinoma Cells

    Institute of Scientific and Technical Information of China (English)

    刘长宝; 凌志强

    2007-01-01

    目的:探讨HT-29肠癌细胞、正常肠上皮细胞及ECV-304血管内皮细胞中E-selectin、Integrin β1及ICAM-1的表达状态.方法:采用Nothern Blotting方法检测HT-29肠癌细胞、正常肠上皮细胞和ECV-304血管内皮细胞中E-selectin、Integrin β1及ICAM-1 mRNA表达水平,采用ELISA法定量分析其表达含量.结果:HT-29肠癌细胞、正常肠上皮细胞和ECV-304血管内皮细胞均有E-selectin、Integrin β1及ICAM-1基因表达.ELISA定量测定3个粘附分子表达水平,HT-29肠癌细胞均高于正常肠上皮细胞和ECV-304血管内皮细胞,分别存在显著性差异(P<0.05).结论:E-selectin、Integrin β1、ICAM-1可能与肿瘤细胞转移有关.

  13. E-selectin和sICAM-1在儿童肺炎支原体感染中的价值%Clinical value of E-selectin and sICAM-1 in diagnosis of children with Mycoplasma Pneumoniae infection

    Institute of Scientific and Technical Information of China (English)

    李苏亮; 叶芸

    2015-01-01

    目的 探讨E-选择素( E-selectin)与可溶性细胞间黏附分子-1 ( sICAM-1 )在儿童肺炎支原体感染中的应用价值.方法 选取本院儿科急性期肺炎支原体感染的患儿48例,恢复期患儿42例,选取同期体检的40例健康儿童做为对照组,采用ELISA法测定血浆E-selectin和sICAM-1水平. 用ROC曲线评价E-selectin和sICAM-1对急性期肺炎支原体感染的诊断效能;将急性期患儿血浆E-selectin与sICAM-1浓度进行相关性分析. 结果 急性期患儿血浆E-selectin和sICAM-1的水平明显高于恢复期及健康对照组,差异有统计学意义(P<0. 05);E-selectin诊断急性期肺炎支原体肺炎的AUC为0. 852(95%可信区间为0. 751-0. 952),其敏感度为80. 0%,特异度为78. 5%;sICAM-1 诊断急性期肺炎支原体肺炎的 AUC为0. 859 (95%可信区间为0. 764-0. 954),其敏感度为80. 5%,特异度为80. 0%. 急性期患儿E-selectin和sICAM-1水平呈明显正相关(r=0. 758,P<0. 01). 结论 急性期肺炎支原体感染患者血浆E-selectin和sICAM-1水平显著增高,可作为评价肺炎支原体感染病情程度以及治疗疗效观察的重要指标.%Objective To explore the diagnostic value of the E-selectin and sICAM-1 in children suffering from Mycoplasma pneumoniae infection. Methods Clinical data of 48 patients with acute Mycoplasma pneumoniae infection and 42 patients in recovery phase were reviewed, and 40 healthy children were chosen as control group. ELISA was used to detect the levels of E-selectin and sICAM-1, and the receiver operating characteristic(ROC) curve was used to evaluate the diagnosis efficiency of acute Mycoplasma pneumoniae infec-tion. The correlation between E-selectin and sICAM-1 was analyzed in patients with acute Mycoplasma pneumoniae infection. Results The levels of E-selectin and sICAM-1 were significantly higher in acute Mycoplasma pneumoniae infection than those in recovery phase(P<0. 05). The area under ROC curve of E-selectin was 0. 852(95%CI 0

  14. 双歧杆菌LTA上调ICAM-1表达及其在LAK抗肿瘤中的作用%Upregulation of ICAM-1 expression enhances cytotoxic sensitivity of tumor cells to LAK by LTA from bifidobacterium

    Institute of Scientific and Technical Information of China (English)

    蒋虹; 胡宏; 魏启欧

    2000-01-01

    目的 探讨双歧杆菌脂磷壁酸(lipoteichoic acid,LTA)作用于LoVo细胞后是否能增强LAK对该细胞的识别 阳杀伤,以及ICAM-1在其中的作用。方法 采用MTT方法观察了LAK对LoVo细胞的识别和杀伤作用,并用流式细胞仪和 ELISA的方法检测了LoVo细胞表面ICAM-1的表达。结果 50 μg/ml LTA作用3 d,LAK对LoVo细胞的粘附率由9.62%增 加到24.42%,LoVo细胞对LAK的杀伤敏感性增加了2倍。并且使表达ICAM-1的细胞数由2.42%增加到27.9%,LoVo细胞 上ICAM-1的表达量增加10倍。结论 LTA增强了LoVo细胞对LAK的杀伤敏感性,其机制可能在于LTA通过上调LoVo细 胞上ICAM-1的表达,增强了效靶细胞之间的识别和结合。LTA与LAK相结合可能增强对大肠癌的治疗效果。%Objective To investigate whether the recognizing and cytotoxic abilities of LAK can be intensified by bifi- dobacterial lipoteichoic acid(LTA) and the possible role of ICAM-1 in this process. Methods Standard MTT assay was used to evaluate the binding rate and cytotoxic capability of LAK to LoVo cells. Flow cytometric assay and ELISA were used to deter- mine the expression of ICAM-1 on these cells. Results LAK cells bound much easier to LoVo cells with an increase from 9. 62% to 24.42% as well as a double increase of the anti-tumor sensitivity of LoVo cells to LAK after challenge with 50 μg/ml LTA of Bifidobacterium bffidum 1101. Compared with the control group,both the percentage of ICAM-1 positive cells and the amount of ICAM-1 expression on LoVo cells were greatly increased directly after the challenge of LTA. Conclusion The pos- sible mechanism of the increase of antitumor activity lies in that Bifidobacterial LTA can intensify the binding and recognizing capability of LAK to tumor cells by promoting the expression of ICAM-1 on the surface of LoVo cells. The therapeutic effect on intestinal cancer may be enhanced by the combined treatment of bifidobacterial LTA and LAK.

  15. A Chinese Herbal Preparation Containing Radix Salviae Miltiorrhizae, Radix Notoginseng and Borneolum Syntheticum Reduces Circulating Adhesion Molecules

    Directory of Open Access Journals (Sweden)

    Kylie A. O’Brien

    2011-01-01

    Full Text Available Circulating adhesion molecules (CAMs, surface proteins expressed in the vascular endothelium, have emerged as risk factors for cardiovascular disease (CVD. CAMs are involved in intercellular communication that are believed to play a role in atherosclerosis. A Chinese medicine, the “Dantonic Pill” (DP (also known as the “Cardiotonic Pill”, containing three Chinese herbal material medica, Radix Salviae Miltiorrhizae, Radix Notoginseng and Borneolum Syntheticum, has been used in China for the prevention and management of CVD. Previous laboratory and animal studies have suggested that this preparation reduces both atherogenesis and adhesion molecule expression. A parallel double blind randomized placebo-controlled study was conducted to assess the effects of the DP on three species of CAM (intercellular cell adhesion molecule-1 (ICAM-1, vascular cell adhesion molecule-1 and endothelial cell selectin (E-selectin in participants with mild-moderate hypercholesterolemia. Secondary endpoints included biochemical and hematological variables and clinical effects. Forty participants were randomized to either treatment or control for 12 weeks. Treatment with DP was associated with a statistically significant decrease in ICAM-1 (9% decrease, P = .03 and E-Selectin (15% decrease, P = .004. There was no significant change in renal function tests, liver function tests, glucose, lipids or C-reactive protein levels and clinical adverse effects did not differ between the active and the control groups. There were no relevant changes in participants receiving placebo. These results suggest that this herbal medicine may contribute to the development of a novel approach to cardiovascular risk reduction.

  16. Regional gene expression of LOX-1, VCAM-1, and ICAM-1 in aorta of HIV-1 transgenic rats

    DEFF Research Database (Denmark)

    Hag, Anne Mette Fisker; Kristoffersen, Ulrik Sloth; Pedersen, Sune Folke

    2009-01-01

    was elevated in the HIV-1Tg rats compared to controls, but the ICAM-1 gene expression profile did not show any differences between the groups. CONCLUSIONS/SIGNIFICANCE: HIV-1Tg rats have gene expression patterns indicating endothelial dysfunction and accelerated atherosclerosis in aorta, suggesting that HIV...

  17. Monascus Adlay and Monacolin K Attenuates Arterial Thrombosis in Rats through the Inhibition of ICAM-1 and Oxidative Stress

    Directory of Open Access Journals (Sweden)

    An-Jan Tien

    2016-11-01

    Full Text Available Background/Aims: Monascus Adlay (MA prepared from fungal fermentation of Monascus purpureus inoculating with cooked adlay contains high content of monakolin K (MK and phenolic compounds. We explored whether MA and MK improve FeCl3-induced arterial thrombosis in rats. Methods: The rats were divided into control, FeCl3-treated rat carotid artery occlusion (TTO, TTO determined with one-week MA, and TTO determined with one-week MK. We compared MA or MK effects on oxidative stress by chemiluminescence amplification and immunohistochemistry, TTO by a transonic system, NFκB, ICAM-1, endoplasmic reticulum stress CHOP and Nrf2 signaling by western blotting. Results: MA or MK efficiently depressed O2-, H2O2 and HOCl levels, platelet activation and aggregation and H2O2-enhanced ICAM-1 and VCAM-1 expression in the endothelial cells. FeCl3 significantly increased NFκB p65, 3-nitrotyrosine, CHOP and ICAM-1 expression, and decreased nuclear Nrf2 translocation and induces arterial thrombus formation. MA or MK pretreatment significantly elongated the level of FeCl3-induced TTO compared to TTO group, significantly decreased proinflammatory NF-κB/ICAM-1 signaling, endoplasmic reticulum stress CHOP expression and decreased thrombotic area. MA or MK significantly preserved nuclear Nrf2 translocation. MA and MK exerted a similar protective effect in attenuating thrombus formation. Conclusions: We suggest MA is better than MK to improve FeCl3-induced arterial thrombosis.

  18. The effects of perfluorocarbon on ICAM-1 expression in LPS-induced A549 cells and the potential mechanism.

    Science.gov (United States)

    Cao, Lu; Li, Chun-Sun; Chang, Yan; Liang, Zhi-Xin; Chen, Liang-An

    2016-04-01

    PFC is able to attenuate ICAM-1 expression in LPS-induced A549 cells by increasing miR-17-3p expression.

  19. Differential roles for endothelial ICAM-1, ICAM-2, and VCAM-1 in shear-resistant T cell arrest, polarization, and directed crawling on blood-brain barrier endothelium.

    Science.gov (United States)

    Steiner, Oliver; Coisne, Caroline; Cecchelli, Roméo; Boscacci, Rémy; Deutsch, Urban; Engelhardt, Britta; Lyck, Ruth

    2010-10-15

    Endothelial ICAM-1 and ICAM-2 were shown to be essential for T cell diapedesis across the blood-brain barrier (BBB) in vitro under static conditions. Crawling of T cells prior to diapedesis was only recently revealed to occur preferentially against the direction of blood flow on the endothelial surface of inflamed brain microvessels in vivo. Using live cell-imaging techniques, we prove that Th1 memory/effector T cells predominantly crawl against the direction of flow on the surface of BBB endothelium in vitro. Analysis of T cell interaction with wild-type, ICAM-1-deficient, ICAM-2-deficient, or ICAM-1 and ICAM-2 double-deficient primary mouse brain microvascular endothelial cells under physiological flow conditions allowed us to dissect the individual contributions of endothelial ICAM-1, ICAM-2, and VCAM-1 to shear-resistant T cell arrest, polarization, and crawling. Although T cell arrest was mediated by endothelial ICAM-1 and VCAM-1, T cell polarization and crawling were mediated by endothelial ICAM-1 and ICAM-2 but not by endothelial VCAM-1. Therefore, our data delineate a sequential involvement of endothelial ICAM-1 and VCAM-1 in mediating shear-resistant T cell arrest, followed by endothelial ICAM-1 and ICAM-2 in mediating T cell crawling to sites permissive for diapedesis across BBB endothelium.

  20. Immunologic changes in TNF-alpha, sE-selectin, sP-selectin, sICAM-1, and IL-8 in pediatric patients treated for psoriasis with the Goeckerman regimen

    Energy Technology Data Exchange (ETDEWEB)

    Borska, L.; Fiala, Z.; Krejsek, J.; Andrys, C.; Vokurkova, D.; Hamakova, K.; Kremlacek, J.; Ettler, K. [Charles University of Prague, Hradec Kralove (Czech Republic). Faculty of Medicine

    2007-11-15

    Psoriasis is a chronic inflammatory skin disease which is often manifested during childhood. The present study investigated changes in the serum levels of proinflammatory cytokines and soluble forms of adhesion molecules in children with psoriasis. The observed patient group of 26 children was treated with the Goeckerman regimen. This therapy combines dermal application of crude coal tar with ultraviolet radiation. The Psoriasis Area Severity Index decreased significantly after treatment by with the Goeckerman regimen (p < 0.001). Serum levels of the proinflammatory cytokine TNF-alpha and adhesion molecules sICAM-1, sP-selectin and sE-selectin decreased after the Goeckerman regimen. The TNF-alpha and sICAM-1 decreased significantly (p < 0.05). Our findings support the complex role of these immune parameters in the immunopathogenesis of psoriasis in children. The serum level of IL-8 increased after the Goeckerman regimen. This fact indicates that the chemokine pathway of IL-8 activity could be modulated by this treatment, most likely by polycyclic aromatic hydrocarbons.

  1. Effect of detoxicating and promoting blood circulation to remove meridian obstruction compound drug serum to the mRNA expression of LOX-1, TNF-α, ICAM-1 in Huvecs%解毒活血通络中药复方含药血清对人脐静脉内皮细胞LOX-1、TNF-α、ICAM-1表达的影响

    Institute of Scientific and Technical Information of China (English)

    朱爱松; 郑洪新

    2012-01-01

    Objective: To find out the mechanism and the target of the detoxicating and promoting blood circulation to remove meridian obstruction compound in treating AS. Methods: 18 New Zealand albino rabbits were randomly divided into 3 groups: normal control group, Chinese herbal treating group and atorvastatin treating group. Rabbits got inlragastric administrated for 7 days, normal control group with NS, Chinese herbal treating group with detoxicating and promoting blood circulation to remove meridian obstruction compound, and atorvastatin treating group with aiorvastatin. Finally the blood was collected from heart and the serum was separated out of the blood, which were ready for vitro cultured ECUV after in stimulated by LPS. mRNA expression of LOX-1, TNF-α, ICAM-1 was measured by Ihe way of Real time PCR. Protein expression of LOX-1 is examined by Western Blotting. Results: Compared to blank controlling group, result of model group showed a significantly higher mRNA expression of LOX-1, TNF-α, ICAM-1 (P<0.01). Compared with model group, result of medical serum group was significantly depressed (P<0.01). Result of LOX-1 protein showed the same as that of mRNA. Conclusion: Detoxicating and promoting blood circulation to remove meridian obstruction compound can protect the HUVEC stimulated with LPS and the mechanism may be related to that it can inhibit the expression of LOX-1, TNF-α, ICAM-1 so as to deduce cell adhesion between MC and VEC.%目的:研究解毒活血通络中药复方防治动脉粥样硬化的作用机制及其效应靶点.方法:选取新西兰大耳白兔18只,随机分为3组,分别以生理盐水和解毒活血通络中药复方、阿托伐他汀连续灌胃7d,心脏采血,分离血清;体外培养人脐静脉内皮细胞,用脂多糖( LPS)刺激后,用含药血清干预,收集细胞,用Real-time PCR方法和Western Blot方法分别检测凝集素样氧化低密度脂蛋白受体-1(LOX-1) mRNA和蛋白表达、肿瘤坏死因子α(TNF

  2. Propofol protects against high glucose-induced endothelial adhesion molecules expression in human umbilical vein endothelial cells

    Directory of Open Access Journals (Sweden)

    Zhu Minmin

    2013-01-01

    Full Text Available Abstract Background Hyperglycemia could induce oxidative stress, activate transcription factor nuclear factor kappa B (NF-κB, up-regulate expression of endothelial adhesion molecules, and lead to endothelial injury. Studies have indicated that propofol could attenuate oxidative stress and suppress NF-κB activation in some situations. In the present study, we examined whether and how propofol improved high glucose-induced up-regulation of endothelial adhesion molecules in human umbilical vein endothelial cells (HUVECs. Methods Protein expression of endothelial adhesion molecules, NF-κB, inhibitory subunit of NF-κBα (IκBα, protein kinase Cβ2 (PKCβ2, and phosphorylation of PKCβ2 (Ser660 were measured by Western blot. NF-κB activity was measured by electrophoretic mobility shift assay. PKC activity was measured with SignaTECT PKC assay system. Superoxide anion (O2.- accumulation was measured with the reduction of ferricytochrome c assay. Human peripheral mononuclear cells were prepared with Histopaque-1077 solution. Results High glucose induced the expression of endothelial selectin (E-selectin, intercellular adhesion molecule 1 (ICAM-1, vascular cell adhesion molecule 1 (VCAM-1, and increased mononuclear-endothelial adhesion. High glucose induced O2.- accumulation, PKCβ2 phosphorylation and PKC activation. Further, high glucose decreased IκBα expression in cytoplasm, increased the translocation of NF-κB from cytoplasm to nuclear, and induced NF-κB activation. Importantly, we found these high glucose-mediated effects were attenuated by propofol pretreatment. Moreover, CGP53353, a selective PKCβ2 inhibitor, decreased high glucose-induced NF-κB activation, adhesion molecules expression, and mononuclear-endothelial adhesion. Conclusion Propofol, via decreasing O2.- accumulation, down-regulating PKCβ2 Ser660 phosphorylation and PKC as well as NF-κB activity, attenuated high glucose-induced endothelial adhesion molecules expression

  3. 胃癌患者血清可溶性P-选择素和细胞间黏附分子-1的表达%Expression of serum soluble P-selectin and intercellar adhesion molecule-1 in patients with gastric carcinoma

    Institute of Scientific and Technical Information of China (English)

    王程虎; 张健

    2006-01-01

    目的:探讨胃癌患者手术前后血清可溶性P-选择素(sP-selectin)、细胞间黏附分子-1(sICAM-1)的表达及临床意义.方法:采用ELISA法检测40例胃癌患者术前、术后15 d、术后30 d及20例对照的血清sP-selectin、sICAM-1水平.结果:胃癌患者血清sP-selectin、sICAM-1水平均高于对照组(P<0.01);术后15 d下降,仍高于对照组水平(P<0.05);术后30 d降至对照组水平(P>0.05).血清sP-selectin、sICAM-1水平与胃癌的淋巴结转移和临床分期相关(P<0.05),与患者年龄、性别、肿瘤大小及组织学分级无明显相关(P>0.05).结论:sP-selectin、sICAM-1参与了胃癌的发生发展,可成为判断预后的一个重要指标.

  4. 大肠癌患者血清可溶性E-选择素和细胞间黏附分子-1检测%Detection of serum soluble E-selectin and intercellar adhesion molecule-1 in patients with colorectal carcinoma

    Institute of Scientific and Technical Information of China (English)

    张健; 王程虎

    2007-01-01

    目的:探讨大肠癌患者血清可溶性E-选择素(sE-selectin)、细胞间黏附分子-1(sICAM-1)检测的意义.方法:采用ELISA检测40例大肠癌患者术前、术后15 d、术后30 d及20例对照(健康体检者)血清sE-selectin、sICAM-1水平.结果:大肠癌患者术前血清sE-selectin、sICAM-1水平高于对照组(P<0.05);术后15 d下降,但仍高于对照组(P<0.05);术后30 d降至对照组水平(P>0.05).大肠癌患者血清sE-selectin、sICAM-1水平与淋巴结转移和临床分期有关(P<0.05),与年龄、性别、肿瘤大小及组织学分级无关(P>0.05).结论:sE-selectin、sICAM-1可能参与了大肠癌侵袭转移过程,是反映大肠癌发生、发展及预后的重要指标.

  5. Expression of junctional adhesion molecule-1 in rat corneal tissue%接合黏附分子-1在大鼠角膜中的表达研究

    Institute of Scientific and Technical Information of China (English)

    王光洁; 蒋华

    2012-01-01

    背景 接合黏附分子-1(JAM-1)是新发现的跨膜蛋白,参与细胞紧密连接的结构组成和功能发挥.在眼组织方面,紧密连接对维持角膜的透明性十分重要,但是目前就JAM-1在角膜紧密连接结构和功能方面的研究较少. 目的 确定JAM-1在大鼠角膜上皮层、基质层和内皮层的构成.方法 选取4只SPF级Wistar大鼠,2只用于JAM-1基因在角膜组织中表达的逆转录聚合酶链反应(RT-PCR)检测,另2只用于免疫组织化学检测.动物过量麻醉处死后获得角膜组织并制备角膜上皮、基质和内皮标本,RT-PCR法检测角膜标本中JAM-1、occludin和claudin-1 mRNA的表达.反应产物行质量分数1.5%琼脂糖凝胶电泳并用凝胶成像系统进行分析.用兔抗鼠JAM-1单克隆抗体对角膜石蜡切片、上皮及内皮铺片行免疫组织化学检测,评估JAM-1蛋白在大鼠角膜组织各层的表达部位和表达强度. 结果 在大鼠角膜各层均可检测到JAM-1、occludin和claudin-1 mRNA的表达,PCR熔解曲线为清晰的单峰.角膜组织各层中JAM-1 mRNA表达水平与occludin mRNA相似,均高于claudin-1 mRNA.3种黏附分子均在上皮层表达最强,角膜基质层表达较弱.免疫组织化学检测显示,JAM-1蛋白在角膜各层均有明确的阳性染色,角膜上皮基底层的表达强于基质层和内皮层.角膜上皮、内皮铺片检测显示,JAM-1蛋白主要表达于上皮细胞和内皮细胞的连接部位,而角膜内皮中JAM-1蛋白的阳性染色广泛而弥散.结论 JAM-1作为细胞连接的构成成分,在角膜上皮层、内皮层和基质层均有表达,但其表达的形态和水平因组织层次的不同而不同.%Background Junctional adhesion molecule-1 (JAM-1) is intercellular transmembrane protein newly discovered and associated with the tight junction.Tight junction plays an important role in keeping the transparency of cornea,but there are few studies about JAM-1 in cornea tight junction. Objective

  6. Changes of soluble intercellular adhesion molecules-1 in children with juvenile rheumatoid arthritis%幼年型类风湿性关节炎患儿血清可溶性细胞间黏附分子-1变化

    Institute of Scientific and Technical Information of China (English)

    钱小青; 张冬玲; 赵乃琤; 曹黎明; 王大为

    2003-01-01

    目的研究可溶性细胞间黏附分子-1(sICAM-1)在幼年型类风湿性关节炎(JRA)患儿中的变化.方法用双抗体夹心ELISA方法检测38例(20 例全身型,8例多关节型和10例少关节型)活动期与缓解期JRA患儿和15例正常对照患儿血清sICAM-1水平.结果 1.活动期全身型、多关节型及少关节型JRA患儿血清sICAM-1水平均较正常对照明显增高(P<0.001),全身型较少关节炎型明显增高(P<0.05);2.治疗后全身型血清sICAM-1水平明显降低(P<0.001),但仍高于正常对照组,多关节型与少关节型治疗后sICAM-1水平较治疗前虽有下降,但无显著差异(P>0.05).结论 ICAM-1在JRA的发病机制中起一定作用,血清sICAM浓度与病变类型有关,但不适合作为病情缓解指标.

  7. Inflammation determines the pro-adhesive properties of high extracellular d-glucose in human endothelial cells in vitro and rat microvessels in vivo.

    Directory of Open Access Journals (Sweden)

    Verónica Azcutia

    Full Text Available BACKGROUND: Hyperglycemia is acknowledged as an independent risk factor for developing diabetes-associated atherosclerosis. At present, most therapeutic approaches are targeted at a tight glycemic control in diabetic patients, although this fails to prevent macrovascular complications of the disease. Indeed, it remains highly controversial whether or not the mere elevation of extracellular D-glucose can directly promote vascular inflammation, which favors early pro-atherosclerotic events. METHODS AND FINDINGS: In the present work, increasing extracellular D-glucose from 5.5 to 22 mmol/L was neither sufficient to induce intercellular adhesion molecule-1 (ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1 expression, analyzed by flow cytometry, nor to promote leukocyte adhesion to human umbilical vein endothelial cells (HUVEC in vitro, measured by flow chamber assays. Interestingly, the elevation of D-glucose levels potentiated ICAM-1 and VCAM-1 expression and leukocyte adhesion induced by a pro-inflammatory stimulus, such as interleukin (IL-1beta (5 ng/mL. In HUVEC, high D-glucose augmented the activation of extracellular signal-regulated kinase 1/2 (ERK 1/2 and nuclear transcription factor-kappaB (NF-kappaB elicited by IL-1beta, measured by Western blot and electromobility shift assay (EMSA, respectively, but had no effect by itself. Both ERK 1/2 and NF-kappaB were necessary for VCAM-1 expression, but not for ICAM-1 expression. In vivo, leukocyte trafficking was evaluated in the rat mesenteric microcirculation by intravital microscopy. In accordance with the in vitro data, the acute intraperitoneal injection of D-glucose increased leukocyte rolling flux, adhesion and migration, but only when IL-1beta was co-administered. CONCLUSIONS: These results indicate that the elevation of extracellular D-glucose levels is not sufficient to promote vascular inflammation, and they highlight the pivotal role of a pro-inflammatory environment in diabetes, as

  8. The effects of caveolin - 1/eNOS pathway in monocyte adhesion to endothelial cells induced by oxidative stress

    Institute of Scientific and Technical Information of China (English)

    LiaoDuan-fang

    2005-01-01

    Leukocyte adhesion to endothelial cells is the initiate event of atherosclerosis, which includes injury of endothelial cells, leukocyte rolling, adhesion and extravasation. Many adhesion molecules such as E-selectin, P-selectin,the adhesion process.ICAM-1, VCAM, L-selectin, CD18, PECAM, VLA and ECM participate in Many factors such as infection of pathogenic organism,

  9. Clematichinenoside inhibits VCAM-1 and ICAM-1 expression in TNF-α-treated endothelial cells via NADPH oxidase-dependent IκB kinase/NF-κB pathway.

    Science.gov (United States)

    Yan, Simin; Zhang, Xu; Zheng, Haili; Hu, Danhong; Zhang, Yongtian; Guan, Qinghua; Liu, Lifang; Ding, Qilong; Li, Yunman

    2015-01-01

    Proinflammatory cytokine TNF-α-induced adhesion of leukocytes to endothelial cells plays a critical role in the early stage of atherosclerosis. Oxidative stress and redox-sensitive transcription factors are implicated in the process. Thus, compounds that mediate intracellular redox status and regulate transcription factors are of great therapeutic interest. Clematichinenoside (AR), a triterpene saponin isolated from the root of Clematis chinensis Osbeck, was previously demonstrated to have anti-inflammatory and antioxidative properties. However, little is known about the exact mechanism underlying these actions. Thus we performed a detailed study on its effect on leukocytes-endothelial cells adhesion with TNF-α-stimulated human umbilical vein endothelial cells (HUVECs) and cell-free systems. First, we found that AR reduced TNF-α-induced VCAM-1 and ICAM-1 expression and their promoter activity, inhibited translocation of p65 and phosphorylation of IκBα, suppressed IκB kinase-β (IKK-β) activity, lowered O2(∙-) and H2O2 levels, tackled p47(phox) translocation, and decreased NOX4 NADPH oxidase expression. Second, we showed that AR exhibited no direct free radical scavenging ability in cell-free systems at concentrations that were used in intact cells. Besides, AR had no direct effect on the activity of IKK-β that was extracted from TNF-α-stimulated HUVECs. We also found that p47 translocation, NOX4 expression, and reactive oxygen species (ROS) levels were up-regulated before IκB phosphorylation in TNF-α-induced HUVECs. Moreover, TNF-α-enhanced IKK-β activity was also inhibited by (polyethylene glycol) PEG-catalase, N-acetylcysteine (NAC), and vitamin E. In conclusion, these results suggest that AR reduces VCAM-1 and ICAM-1 expression through NADPH oxidase-dependent IKK/NF-κB pathways in TNF-α-induced HUVECs, which finally suppress monocyte-HUVECs adhesion. This compound is potentially beneficial for early-stage atherosclerosis.

  10. Genome-wide association analysis of soluble ICAM-1 concentration reveals novel associations at the NFKBIK, PNPLA3, RELA, and SH2B3 loci.

    Directory of Open Access Journals (Sweden)

    Guillaume Paré

    2011-04-01

    Full Text Available Soluble ICAM-1 (sICAM-1 is an endothelium-derived inflammatory marker that has been associated with diverse conditions such as myocardial infarction, diabetes, stroke, and malaria. Despite evidence for a heritable component to sICAM-1 levels, few genetic loci have been identified so far. To comprehensively address this issue, we performed a genome-wide association analysis of sICAM-1 concentration in 22,435 apparently healthy women from the Women's Genome Health Study. While our results confirm the previously reported associations at the ABO and ICAM1 loci, four novel associations were identified in the vicinity of NFKBIK (rs3136642, P = 5.4 × 10(-9, PNPLA3 (rs738409, P  =  5.8 × 10(-9, RELA (rs1049728, P =  2.7 × 10(-16, and SH2B3 (rs3184504, P =  2.9 × 10(-17. Two loci, NFKBIB and RELA, are involved in NFKB signaling pathway; PNPLA3 is known for its association with fatty liver disease; and SH3B2 has been associated with a multitude of traits and disease including myocardial infarction. These associations provide insights into the genetic regulation of sICAM-1 levels and implicate these loci in the regulation of endothelial function.

  11. THE EFFECTS OF PROSTAGLANDIN E1 ON SERUM INTERCELLULAR ADHESION MOLECULE-1 AND COLLAGEN TYPE IV IN PATIENTS WITH DIABETIC NEPHROPATHY%PGE1对糖尿病肾病血清黏附因子和Ⅳ型胶原的影响

    Institute of Scientific and Technical Information of China (English)

    徐乐超; 李云英

    2007-01-01

    目的 探讨前列腺素E1 (PGE1)对早期糖尿病肾病血清黏附因子(sICAM-1)和Ⅳ型胶原(C-IV)的影响.方法 对136例早期糖尿病肾病,在常规治疗基础上,加用PGE110 μg+生理盐水 100 ml,每日 1 次,静脉注射,连续 14 d.观察治疗前后sICAM-1和C-IV的变化,并与对照组比较.结果 治疗后s ICAM-1、尿白蛋白排泄率(UAER)、C-IV的水平与对照组比较有显著差异(P<0.01,P<0.05).结论 PGE1可有效降低早期糖尿病肾病患者sICAM-1和C-IV.从而起到改善和保护肾脏功能的作用.

  12. 血管性假血友病因子和细胞间黏附分子-1在急性呼吸窘迫综合征中的动态变化及早期诊断的意义%Variations and early prediction of von willebrand factor and soluble intercellular adhesion molecule-1 in acute respiratory distress syndrome

    Institute of Scientific and Technical Information of China (English)

    李锐; 曹书华; 王今达

    2004-01-01

    目的检测血管性假血友病因子、可溶性细胞间黏附分子-1浓度变化,以研究其在ARDS早期诊断中的意义.方法以ELISA法检测非ARDS组和ARDS组于0、2、3、5和7d血浆vWF和sICAM-1浓度.结果ARDS组vWF和sICAM-1浓度高于非ARDS组,前四个时点的中性粒细胞活化计数ARDS组高于非ARDS组.血浆vWF和sICAM-1水平具有相关性.结论血浆vWF和sICAM-1浓度及中性粒细胞活化计数在ARDS的早期即升高,对ARDS早期诊断有预警作用.

  13. The influence of TNF-alpha on concentration of soluble adhesion molecules in cultures of HT-29 cells exposed to inositol hexaphosphate.

    Science.gov (United States)

    Parfiniewicz, Beata; Pendzich, Joanna; Kapral, Małgorzata; Bednarek, Ilona; Weglarz, Ludmiła

    2012-01-01

    The latest studies suggest that adhesion molecules are involved in the arising of malignant changes and in distant metastasis induction. The soluble forms of several adhesion molecules, have recently emerged as novel and potentially useful tumor markers. Among a number of identified, high interest wake soluble molecules similar to the immunoglobulin -- soluble intercellular adhesion molecules-1 (sICAM-1) and soluble E-cadherin (sE-cadherin). In the present work, the authors concentrate on one tumor type, colorectal carcinoma, in which distant metastases, are the main cause of failure, in spite of surgical curing of the primary tumor. It is known that TNF-alpha (tumor necrosis factor - alpha) serum concentration of patients with cancer is raised. The changes in soluble adhesion molecules concentrations in serum and others fluids, could be modulated by many different factors affecting cancer cells. In the case of colon cancer one of the factors is a high-fiber diet, containing an anti-cancer chemical, inositol hexaphosphate (IP6). The aim of this study was to estimate the influence of TNF-alpha on the concentration of sICAM-1 and sE-cadherin in the microenvironment of HT-29 malignant epithelial colorectal cells stimulated with IP6. Additonally, adhesive property of HT-29 human colorectal cancer cell line to collagen I was estimated. The HT-29 cells were treated with TNF-alpha (10 ng/mL and 100 ng/mL - estimation of sICAM and sE-cadherin concentration; 100 ng/mL - adhesion assay), IP6 (0.5 mM, 1.0 mM, 2.0 mM) and TNF-alpha in combination with IP6. The level of sICAM-1 and sE-cadherin in cultures of HT-29 cells was measured by enzyme-linked immunosorbent assay (R&D Systems), and adhesion of the cells to collagen I was investigated by Cyquant Proliferation Assay Kit. The present findings demonstrate that TNF-alpha and inositol hexaphosphate have an effect on the sICAM-1 and sE-cadherin concentration in cultures of HT-29 cells. IP6 at a concentration of 2.0 mM induced a

  14. 烟酸对p38丝裂原活化蛋白激酶信号通路介导的内皮细胞功能障碍的早期干预研究%Effects of niacin on cell adhesion and early atherogenesis:involvement of the p38 mitogen-activated protein kinases pathway

    Institute of Scientific and Technical Information of China (English)

    牛娜; 韩波; 孙书珍; 于永慧; 汪翼; 王立俊

    2013-01-01

    制有待进一步研究.%Objective To examine the effects of niacin on lysophosphatidylcholine (LPC)-induced intercellular adhesion molecule-1 (ICAM-1),and gained insight to the mechanisms.Method Human umbilical vein endothelial cell line was cultured using Medium 200 medium in incubator at 37 ℃ and 5% CO2 condition.Experimental groups:(1) the negative control group:medium; (2) LPC different time groups:the medium added with 20 μmol/L final concentration of LPC,were cultured for 10 min and 8 h,24 h; (3) LPC + p38-mitogen-activated protein kinase (p38MAPK) inhibitor (SB203580) group:the medium added with 10 μmol/L p38MAPK inhibitor (SB203580) was cultured for 1 h,then human umbilical vein endothelial cells (HUVECs) added with the LPC were cultured for 10 min,8 h and 24 h.(4) LPC + different niacin dose group:after separately adding with 0.25,0.5,1 mmol/L niacin,the cells were cultured for 18 h,then HUVECs added with the LPC were cultured for 10 min,8 h and 24 h.Cell concentration in each group was 5 × 105/ml,inoculated in 6-well plates,each well 1 ml.Detected by Western blot analysis of pp38MAPK,ICAM-1 protein content,real-time quantitative PCR to detect endothelial cell ICAM-1 mRNA expression,cell immunofluorescence to detect LPC-induced ICAM-1 protein expression.Result In LPC 24 h group,the expression of ICAM-1 protein was significantly increased 0.786 ± 0.02,the LPC + niacin group,ICAM-1 protein levels (0.487 ±0.015) was significantly lower than the LPC 24 h group (P <0.01),in LPC + SB203580 intervention group,ICAM-1 protein levels (0.461 ± 0.011) was significantly lower than that of the LPC 24 h group (P < 0.01),but did not reach the level of the control group.Adding LPC to culture for 10 min,phosphorylation of p38MAPK (pp38MAPK) reached its peak (0.47 ± 0.02),niacin could reduce the pp38MAPK (0.07 ± 0.02),SB203580 could also reduce its activity (0.11 ± 0.02).Adding LPC to culture for 8 h,ICAM-1 mRNA expression (8.16 ± 0.15) compared with the control group (1.00 ± 0.02) had a

  15. 外源性IL-10对小儿牙龈炎组织中IL-6和细胞间黏附分子-1表达的影响研究%Study on the effect of exogenous IL-10 on IL-6 and intercellular adhesion molecule-1 expressions in gingivitis tissue of children

    Institute of Scientific and Technical Information of China (English)

    牛兵; 姜瑞中; 王国芳

    2015-01-01

    目的 研究外源性IL-10对小儿牙龈炎组织中IL-6和细胞间黏附分子-1 (ICAM-1)表达的影响.方法 选取2012年5月~2014年6月在该院接受治疗的80例牙龈炎患儿和正常进行健康检查的儿童40名为研究对象.根据探诊深度及附着丧失实施分组,轻度牙龈炎组简称轻度组、重度牙龈炎组简称重度组,各40例,选取同期在该院进行健康检查的儿童40名为对照组.对比各组IL-6含量水平,各组ICAM-1含量水平,分析外源性IL-10与IL-6及ICAM-1的相关性.结果 重度组IL-6含量水平均高于其他两组,经过治疗后重度组及轻度组的IL-6含量水平均降低,但治疗7天后仍显著高于对照组的水平,差异均有统计学意义(均P<0.05).重度组的ICAM-1含量水平均分别显著高于轻度组和对照组,经过治疗后,重度组及轻度组的ICAM-1含量水平均降低,但治疗7天后仍显著高于对照组的水平,差异均有统计学意义(均P<0.05).通过Spearman法分析相关性可知,外源性IL-10与IL-6及ICAM-1均呈显著负相关.结论 外源性IL-10能够较好地降低小儿牙龈炎组织关于IL-6及ICAM-1的表达,值得临床进一步深入研究.

  16. 脑梗死患者血清可溶性血管细胞黏附分子1的变化%Variation of soluble vascular cell adhesion molecule-1 in serum of patients with cerebral infarction

    Institute of Scientific and Technical Information of China (English)

    李静; 周华东; 王延江

    2006-01-01

    平明显高于无感染(P<0.01).结论:可溶性血管细胞黏附分子1参与了脑梗死的病理变化过程,可作为脑梗死时病情变化的监测指标.阻断其生成和表达为改善脑梗死的预后提供了新的思路.%BACKGROUND: In subjects with different inflammatory and autoimmune diseases, soluble vascular cell adhesion molecule-1 (sVCAM-1) in sera increases, and its change may become an important monitoring index of immunological function, but its change rule has been unclear in acute cerebral infarction.OBJECTIVE: To observe the change of sVCAM-1 in sera of subjects with cerebral infarction and its clinical significance, and compare between the subjects with cerebral hemorrhage and normal population.DESIGN: A case controlled analysis.SETTING: Second Department of Brain, Research Institute of Surgery,Daping Hospital, Third Military Medical University of Chinese PLA.PARTICIPANTS: A total of 132 inpatients were selected from Second Department of Brain, Research Institute of Surgery, Daping Hospital, Third Military Medical University of Chinese PLA between May 2002 and April 2004. Among them, 89 subjects with cerebral infarction were classified into large infarction group (n=25,> 10 cm3), medium infarction group (n=31,4-10 cm3) and small infarction group (n=33, < 4 cm3) respectively according to the size of infarct focus. There were 43 subjects in cerebral hemorrhage group, and 30 healthy persons were as normal control group.METHODS: Blood samples were isolated from subjects with cerebral infarction at hour 24, days 3, 7 and 14 after onset of the disease, while the blood samples were extracted from subjects with cerebral hemorrhage at hour24 and day 14 after the onset of the disease. 4 mL venous blood was obtained from the three groups. The serum concentration of sVCAM-1 was determined with double antibody sandwich method (DASM) in all the examinees.MAIN OUTCOME MEASURES: ①Dynamic change of the serum concentration of sVCAM-1 in the course of acute cerebral

  17. Effects of isoflurane on ICAM-1 expression and neutrophils infiltration in rats with liver ischemia and reperfusion injury

    Institute of Scientific and Technical Information of China (English)

    Xu Guangmin; Tao Guocai

    2009-01-01

    Objective: To establish a rat model of warm partial hepatic ischemia-reperfusion (IR), and investigate the protective and anti-inflammatory effects of isoflurane on warm hepatic ischemia-reperfusion injury (IRI) in rats. Methods: Thirty-two female Sprague-Dawley rots were divided equally into 4 groups (n=8): PB-Sham group in which the rats were anesthetized by intraperitoneal injection of pentobarbital sodium (1.0%, 40 mg/kg, PB) and received a sham operation without occlusion of liver blood flow; PB-IR group whose rats underwent partial hepatic IR after anesthesia; Iso-Sham group in which inhalation of 1.0 MAC isoflurane and sham operation was performed; Iso-IR group in which 1.0 MAC isoflurane was inhaled for 4 h and IR was performed. Rat model of warm partial hepatic IR was established by clamping the hepatic arteries and hilar vessels distributing to the left and median lobes to induce partial hepatic ischemia (70%) for 60 min followed by reperfusion for 3 h. The rats were killed 3 h after declamping, and specimens of liver tissue and blood were obtained. The serum ALT and AST were detected as liver damage markers. Viability of myeloperoxidase (MPO) in liver was measured. The protein level of ICAM-1 in the liver was detected by immunohistochemistry and Western blotting. Results: Rats treated with 1.0 MAC isoflurane during warm partial (70%) hepatic ischemia 60 min and 3 h reperfusion had significantly lower serum ALT and AST compared with rats anesthetized with pentobarbital sodium subjected to hepatic IRI. The expression of ICAM-1 in hepatic tissue was significantly increased by hepatic IRI after pentobarbital sodium anesthesia. Isoflurane significantly inhibited protein expression of ICAM-1 in hepatic IR injury compared with pentobarbital sodium anesthesia. Viability of liver MPO was significantly increased by hepatic IRI after pentobarbital sodium anesthesia; Isoflurane can significantly inhibit MPO alteration in rat liver ischemia-reperfusion injury

  18. Cell adhesion markers are expressed by a stable human endothelial cell line transformed by the SV40 large T antigen under vimentin promoter control.

    Science.gov (United States)

    Vicart, P; Testut, P; Schwartz, B; Llorens-Cortes, C; Perdomo, J J; Paulin, D

    1993-10-01

    Markers of endothelium have been studied in a new endothelial cell line derived from human umbilical cord vein cells by microinjection of a recombinant gene that includes a deletion mutant of the human vimentin gene regulatory region controlling the large T and small t antigen coding region of the SV40 virus. In culture, this immortalized venous endothelial cell line (IVEC) demonstrated morphological characteristics of endothelium; uptake of acetylated low density lipoprotein and presence of the Factor VIII-related antigen. Treatment of IVEC cells with Interleukin-1 beta (IL-1 beta) at 10 U.ml-1 activates the expression of cell adhesion molecules such as endothelial leucocyte adhesion molecule (ELAM-1), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1), as observed in primary culture. Prostacyclin secretion was induced in the IVEC cells by 100 nM PMA treatment and thrombin at 0.5 U/ml. Angiotensin converting enzyme (ACE) activity detected in IVEC cells was present but lower than ACE activity in primary endothelial cells and was completely blocked by enalaprilat (1 microM), a specific ACE inhibitor. The presence of ACE mRNA was also demonstrated in IVEC cells by RT-PCR amplification. Our data demonstrate that endothelial cells immortalized by use of this recombinant gene retain the morphological organization and numerous differentiated properties of endothelium.

  19. LFA-1 and ICAM-1 expression induced during melanoma-endothelial cell co-culture favors the transendothelial migration of melanoma cell lines in vitro

    Directory of Open Access Journals (Sweden)

    Ghislin Stephanie

    2012-10-01

    Full Text Available Abstract Background Patients with metastatic melanoma have a poor median rate of survival. It is therefore necessary to increase our knowledge about melanoma cell dissemination which includes extravasation, where cancer cells cross the endothelial barrier. Extravasation is well understood during travelling of white blood cells, and involves integrins such as LFA-1 (composed of two chains, CD11a and CD18 expressed by T cells, while ICAM-1 is induced during inflammation by endothelial cells. Although melanoma cell lines cross endothelial cell barriers, they do not express LFA-1. We therefore hypothesized that melanoma-endothelial cell co-culture might induce the LFA-1/ICAM ligand/receptor couple during melanoma transmigration. Methods A transwell approach has been used as well as blocking antibodies against CD11a, CD18 and ICAM-1. Data were analyzed with an epifluorescence microscope. Fluorescence intensity was quantified with the ImageJ software. Results We show here that HUVEC-conditioned medium induce cell-surface expression of LFA-1 on melanoma cell lines. Similarly melanoma-conditioned medium activates ICAM-1 expression in endothelial cells. Accordingly blocking antibodies of ICAM-1, CD11a or CD18 strongly decrease melanoma transmigration. We therefore demonstrate that melanoma cells can cross endothelial monolayers in vitro due to the induction of ICAM-1 and LFA-1 occurring during the co-culture of melanoma and endothelial cells. Our data further suggest a role of LFA-1 and ICAM-1 in the formation of melanoma cell clumps enhancing tumor cell transmigration. Conclusion Melanoma-endothelial cell co-culture induces LFA-1 and ICAM-1 expression, thereby favoring in vitro melanoma trans-migration.

  20. 未受控制的高血糖对2型糖尿病患者粘附分子的影响%Effect of uncontrolled hyperglycemia on levels of adhesion molecules in patients with diabetes mellitus type 2

    Institute of Scientific and Technical Information of China (English)

    Barbara RUSZKOWSKA-CIASTEK; Alina SOKUP; Tomasz WERNIK; Zofia RUPRECHT; Barbara GRALCZYK; Krzysztof GRALCZYK; Grayna GADOMSKA; Danuta RO

    2015-01-01

    目的:评估可溶性血管细胞间黏附分子(sVCAM-1)、可溶性细胞间黏附分子(sICAM-1)、可溶性选择素E和可溶性血栓调节蛋白在血糖控制良好和不受控制的2型糖尿病患者中的水平。  创新点:对2型糖尿病患者的血管内皮炎症标记物进行评估。  方法:62例糖尿病患者分成两组:第一组包括35个血糖控制良好的糖尿病患者,第二组包括27个未控制血糖并伴有微蛋白尿的糖尿病患者。对照组由25名健康志愿者组成。测定血浆中sVCAM-1、sICAM-1、可溶性选择素E和可溶性血栓调节蛋白的浓度,同时测定血清肌酐及血浆中空腹血糖和糖化血红蛋白(HbA1c)的浓度。  结论:与血糖控制良好的糖尿病组相比,未控制血糖组具有相对低的ICAM-1水平和更高的VCAM-1水平。未控制血糖组中患者的糖化血红蛋白和ICAM-1之间呈正相关,肾小球滤过率和可溶性选择素E之间呈正相关,而肌酐和ICAM-1之间呈负相关。研究证实2型糖尿病的发病机理中炎症过程的出现与血管内皮功能受损有关。未受控制的高血糖对粘附分子的反向作用表明,在糖尿病的并发症中VCAM-1和ICAM-1具有不同功能。%Objective: Uncontrol ed diabetes has become a major cause of mortality and morbidity by reason of vascular angiopathy. The aim of this study was to evaluate the concentrations of soluble forms of vascular adhesion molecule-1 (sVCAM-1), intercel ular adhesion molecule-1 (sICAM-1), E-selectin, and thrombomodulin in patients with wel-control ed and uncontrol ed diabetes type 2. Methods: The study was conducted on 62 patients with diabetes. Group I consisted of 35 patients with wel-control ed diabetes. The second group included 27 patients with uncontrol ed diabetes with micro-albuminuria. A control group was made up of 25 healthy volunteers. The concentrations of sVCAM-1, sICAM-1, sE-selectin, and soluble

  1. Induction of Mast Cell Accumulation by Tryptase via a Protease Activated Receptor-2 and ICAM-1 Dependent Mechanism.

    Science.gov (United States)

    Liu, Xin; Wang, Junling; Zhang, Huiyun; Zhan, Mengmeng; Chen, Hanqiu; Fang, Zeman; Xu, Chiyan; Chen, Huifang; He, Shaoheng

    2016-01-01

    Mast cells are primary effector cells of allergy, and recruitment of mast cells in involved tissue is one of the key events in allergic inflammation. Tryptase is the most abundant secretory product of mast cells, but little is known of its influence on mast cell accumulation. Using mouse peritoneal model, cell migration assay, and flow cytometry analysis, we investigated role of tryptase in recruiting mast cells. The results showed that tryptase induced up to 6.7-fold increase in mast cell numbers in mouse peritoneum following injection. Inhibitors of tryptase, an antagonist of PAR-2 FSLLRY-NH2, and pretreatment of mice with anti-ICAM-1, anti-CD11a, and anti-CD18 antibodies dramatically diminished tryptase induced mast cell accumulation. On the other hand, PAR-2 agonist peptides SLIGRL-NH2 and tc-LIGRLO-NH2 provoked mast cell accumulation following injection. These implicate that tryptase induced mast cell accumulation is dependent on its enzymatic activity, activation of PAR-2, and interaction between ICAM-1 and LFA-1. Moreover, induction of trans-endothelium migration of mast cells in vitro indicates that tryptase acts as a chemoattractant. In conclusion, provocation of mast cell accumulation by mast cell tryptase suggests a novel self-amplification mechanism of mast cell accumulation. Mast cell stabilizers as well as PAR-2 antagonist agents may be useful for treatment of allergic reactions.

  2. Determination of soluble ICAM-1 and TNFalphaR in the cerebrospinal fluid and serum levels in a population of Brazilian patients with relapsing-remitting multiple sclerosis Determinação dos níveis de ICAM-1 e TNFalfaR solúvel no líquido cefalorraqueano e soro numa população de pacientes brasileiros com esclerose múltipla forma surto-remissão

    Directory of Open Access Journals (Sweden)

    Soniza Vieira Alves-Leon

    2001-03-01

    Full Text Available Cytokines and adhesion molecules have been implicated in the pathogenesis of multiple sclerosis (MS, a chronic inflammatory disease of the central nervous system. In this study we analyzed intrathecal (CSF and serum levels of soluble intercellular adhesion molecule (ICAM-1 and TNFalphaR (60kD from 20 patients with clinically definite MS during acute relapse or stable disease. Comparing to control groups of healthy individuals and patients with intervertebral herniated disc, MS patients showed increased levels (pCitocinas e moléculas de adesão estão implicadas na patogênese da esclerose múltipla (EM, uma doença inflamatória crônica do sistema nervoso central. Neste estudo, nós determinamos os níveis solúveis da molécula de adesão intercelular (sICAM-1 e TNFalfaR (60kD no soro e líquido cefalorraqueano (LCR de 20 pacientes com EM clinicamente definida durante surto ou remissão. Os pacientes com EM apresentaram, em comparação com os grupos controle formados por indivíduos sadios e com hérnia de disco intervertebral submetidos a mielografia, níveis significativamente (p< 0.001 elevados de sICAM-1 e TNFalfaR tanto no soro como no LCR. Independente do estágio da doença, nenhuma diferença significativa foi encontrada entre os pacientes durante o surto (657±124.9 ng/ml ou na remissão (627±36.2 ng/ml. Um aumento consistente dos níveis de TNFalfaR no soro e LCR, apontam para a existência de processo inflamatório continuado no tecido cerebral dos pacientes com EM, a despeito da ausência de sinais clínicos de doença em atividade.

  3. Mechanism of sphingosine 1-phosphate- and lysophosphatidic Acid-induced up-regulation of adhesion molecules and eosinophil chemoattractant in nerve cells.

    LENUS (Irish Health Repository)

    Costello, Richard W

    2012-02-01

    The lysophospholipids sphingosine 1-phosphate (S1P) and lysophosphatidic acid (LPA) act via G-protein coupled receptors S1P(1-5) and LPA(1-3) respectively, and are implicated in allergy. Eosinophils accumulate at innervating cholinergic nerves in asthma and adhere to nerve cells via intercellular adhesion molecule-1 (ICAM-1). IMR-32 neuroblastoma cells were used as an in vitro cholinergic nerve cell model. The G(i) coupled receptors S1P(1), S1P(3), LPA(1), LPA(2) and LPA(3) were expressed on IMR-32 cells. Both S1P and LPA induced ERK phosphorylation and ERK- and G(i)-dependent up-regulation of ICAM-1 expression, with differing time courses. LPA also induced ERK- and G(i)-dependent up-regulation of the eosinophil chemoattractant, CCL-26. The eosinophil granule protein eosinophil peroxidase (EPO) induced ERK-dependent up-regulation of transcription of S1P(1), LPA(1), LPA(2) and LPA(3), providing the situation whereby eosinophil granule proteins may enhance S1P- and\\/or LPA- induced eosinophil accumulation at nerve cells in allergic conditions.

  4. Mechanism of sphingosine 1-phosphate- and lysophosphatidic Acid-induced up-regulation of adhesion molecules and eosinophil chemoattractant in nerve cells.

    LENUS (Irish Health Repository)

    Costello, Richard W

    2011-05-01

    The lysophospholipids sphingosine 1-phosphate (S1P) and lysophosphatidic acid (LPA) act via G-protein coupled receptors S1P(1-5) and LPA(1-3) respectively, and are implicated in allergy. Eosinophils accumulate at innervating cholinergic nerves in asthma and adhere to nerve cells via intercellular adhesion molecule-1 (ICAM-1). IMR-32 neuroblastoma cells were used as an in vitro cholinergic nerve cell model. The G(i) coupled receptors S1P(1), S1P(3), LPA(1), LPA(2) and LPA(3) were expressed on IMR-32 cells. Both S1P and LPA induced ERK phosphorylation and ERK- and G(i)-dependent up-regulation of ICAM-1 expression, with differing time courses. LPA also induced ERK- and G(i)-dependent up-regulation of the eosinophil chemoattractant, CCL-26. The eosinophil granule protein eosinophil peroxidase (EPO) induced ERK-dependent up-regulation of transcription of S1P(1), LPA(1), LPA(2) and LPA(3), providing the situation whereby eosinophil granule proteins may enhance S1P- and\\/or LPA- induced eosinophil accumulation at nerve cells in allergic conditions.

  5. Structure and Function of Human Carcinoembryonic Antigen-related Cellular Adhesion Molecule 1%人体癌胚抗原相关细胞黏附分子1的结构与功能

    Institute of Scientific and Technical Information of China (English)

    叶秋芳

    2012-01-01

    人癌胚抗原相关细胞黏附分子1(CEACAMl)是广泛表达于中性粒细胞、巨噬细胞、内皮细胞、上皮细胞及淋巴细胞表面的Ⅰ型跨膜糖蛋白,属癌胚抗原家族免疫球蛋白超家族分子,胞膜外区有Ig样结构域,CEACAM1-L型具有两个免疫受体酪氨酸抑制性基序,其生物学功能包括免疫调节、促进血管形成、调节血管重构、参与细胞凋亡调控、促进腺体管腔形成及调控胰岛素的清除,同时CEACAM1也是致病微生物的黏着受体.%Human carcinoembryonic antigen-related cellular adhesion molenile l( CEACAM1 )is a member of the carcinoembryonir antigen iamily(CEA )whirh is a type I-transmembrane glycoprotein broadly expressed on the surface oi cells including: macrophages, neutrophilic granulocyte, lymphocyte, epithelial, and endothelial cells. It is an adhesion molecule oi immunoglobulin superfamily. The extiacellulai' domain oi CEACAM 1 contains IgG-like stmctuie. The long form oi CEACAM1 protein has two immunoieceptoi tinosine-based inhibitoiy motiis( ITIMs )that have crucial roles in immu no-regulation, vascular neogenesis, vascular remolding, cell apoptosis regulation, gland lumen formation and insulin clearance. CEACAM1 is also a receptor for pathogenic bacteria and viruses.

  6. The influences of ulinastatin on serum levels of IL-Iβ and sICAM- 1 in acute cerebral hemorrhage patients%乌司他丁对脑出血患者急性期血清IL-1β和sICAM-1的影响

    Institute of Scientific and Technical Information of China (English)

    李改丽; 汪丙昂; 王晓湘; 胡健; 王建; 张汝

    2011-01-01

    Objective To investigate the influences of ulinastatin on serum levels of IL??(inter-leukin條? and sICAM?(soluble intercellular adhesion molecule?). Methods 140 cerebral hemor-rhage patients were collected in 4 years (July in 2006 to July in 2010) from neurology and neurosurgery departments in the General Hospital of Chengdu Military Region were randomly divided into two groups : control group and treatment group. The treatment group was treated with ulinastatin 14 days i. v.. Blood samples were collected at three time points:day 2,day 7 and day 14 after admission to hospital. Se-rum levels of IL - 1?and sICAM - 1 were determined with double antibody ABC - ELISA. Results Compared with controls, the levels of two inflammatory mediators of cerebral hemorrhage pa-tients in acute stage were significantly reduced by ulinastatin. All patients showed no obvious side effects. Conclusions The ulinastatin may be one of alternative medicines inhibiting the inflammatory re-sponse after intracerebral hemorrhage.%目的 观察鸟司他丁对脑出血患者血清IL-1β和可溶性细胞间黏附分子水平的影响.方法 对我院2006年7月~2010年7月神经内、外科的脑出血患者140例进行研究,随机分为对照组和治疗组两组,治疗组静滴鸟司他丁14 d,分别在入院第2,7,14天采用双抗体夹心ABC- ELISA法观察患者血清IL-1β和sICAM-1的水平.结果 和对照组相比,乌司他丁可以降低脑出血患者急性期这两种交性介质的水平,全部病例未出现明显副作用.结论 乌司他丁可能可以作为抑制脑出血后炎性反应的备选药物之一.

  7. The RhoA guanine nucleotide exchange factor, LARG, mediates ICAM-1-dependent mechanotransduction in endothelial cells to stimulate transendothelial migration.

    Science.gov (United States)

    Lessey-Morillon, Elizabeth C; Osborne, Lukas D; Monaghan-Benson, Elizabeth; Guilluy, Christophe; O'Brien, E Timothy; Superfine, Richard; Burridge, Keith

    2014-04-01

    RhoA-mediated cytoskeletal rearrangements in endothelial cells (ECs) play an active role in leukocyte transendothelial cell migration (TEM), a normal physiological process in which leukocytes cross the endothelium to enter the underlying tissue. Although much has been learned about RhoA signaling pathways downstream from ICAM-1 in ECs, little is known about the consequences of the tractional forces that leukocytes generate on ECs as they migrate over the surface before TEM. We have found that after applying mechanical forces to ICAM-1 clusters, there is an increase in cellular stiffening and enhanced RhoA signaling compared with ICAM-1 clustering alone. We have identified that leukemia-associated Rho guanine nucleotide exchange factor (LARG), also known as Rho GEF 12 (ARHGEF12) acts downstream of clustered ICAM-1 to increase RhoA activity, and that this pathway is further enhanced by mechanical force on ICAM-1. Depletion of LARG decreases leukocyte crawling and inhibits TEM. To our knowledge, this is the first report of endothelial LARG regulating leukocyte behavior and EC stiffening in response to tractional forces generated by leukocytes.

  8. The Effect of Dehydroepiandrosterone on the Expression of AT1 receptor and TNF-induced ICAM-1 in Vascular Smooth Muscle Cells

    Institute of Scientific and Technical Information of China (English)

    Wu Saizhu; Wang Zidong; Zhou Zhongjiang; Zhou Kexiang; Wu Yanxian; Sun Fei; Rong Zhiyi; Ma Rui; Wei Heming

    2005-01-01

    Objectives To further investigate the molecular mechanism of vasoprotective role of dehydroepiandrosterone (DHEA), we examined DHEA on AT1 receptor and ICAM-1 gene expression in vascular smooth muscle cells (VSMCs). Methods RT-PCR and Western Blot was used to determine the change of the expressions of mRNA and protein of AT1 and ICAM-1 when given various concentration dehydroepiandrosterone. Results 1.AT1 was abundant under the basal condition. The expression of AT1 mRNA and protein decreased after stimulated by DHEA (at 10-10mol/L , 10-8 mol/L, 10-6 mol/L), and the effects of DHEA on AT1 protein was dose-dependent. ER inhibitor Tamoxifen and AR inhibitor Flutamide enhanced AT1 protein expression, but did not influence the mRNA expression. 2. The exp-ression of ICAM-1 gene was low under the basal condition. It increased when induced by TNF-α,but decreased when induced by DHEA (at l0-10 mol/L, 10-8 mol/L, 10-6 mol/L) ,and the effects of DHEA on ICAM-1 gene expression were dose-dependent. Conclusions These findings suggest that DHEA modulates AT1 and inflammatory factor induced ICAM-1 gene expression in VSMC, but further studies are necessary in the mecha-nism of DHEA action.

  9. Bi-directional induction of matrix metalloproteinase-9 and tissue inhibitor of matrix metalloproteinase-1 during T lymphoma/endothelial cell contact: implication of ICAM-1.

    Science.gov (United States)

    Aoudjit, F; Potworowski, E F; St-Pierre, Y

    1998-03-15

    The mechanisms that lead to the expression of matrix metalloproteinases (MMP) and tissue inhibitors of MMP (TIMPs) during the invasive process of normal and transformed T cells remain largely unknown. Since vascular cells form a dynamic tissue capable of responding to local stimuli and activating cells through the expression of cytokine receptors and specific cell adhesion molecules, we hypothesized that the firm adhesion of T lymphoma cells to endothelial cells is a critical event in the local production of MMP and TIMP. In the present work, we show that adhesion of lymphoma cells to endothelial cells induced a transient and reciprocal de novo expression of MMP-9 mRNA and enzymatic activity by both cell types. Up-regulation of MMP-9 in T lymphoma cells was concomitant to that of TIMP-1, and required direct contact with endothelial cells. Induction of MMP-9, but not of TIMP-1, was blocked by anti-LFA-1 and anti-intercellular adhesion molecule-1 Abs, indicating that induction of MMP-9 and TIMP-1 in lymphoma cells required direct, yet distinct, intercellular contact. In contrast, the induction of MMP-9 in endothelial cells by T lymphoma cells did not necessitate direct contact and could be achieved by exposure to IL-1 and TNF, or to the supernatant of T lymphoma cell culture. Together, these results demonstrate that firm adhesion of T lymphoma cells to endothelial cells participates in the production of MMP-9 in both cell types through bi-directional signaling pathways, and identify intercellular adhesion molecule-1/LFA-1 as a key interaction in the up-regulation of MMP-9 in T lymphoma cells.

  10. 脓毒症大鼠肺含水量、ICAM-1和E-选择素表达的变化及谷氨酰胺对其作用的研究%The Change of Pulmonary Water Content,ICAM-1 and E-selectin and Study of the Role of Glutamine in Sepsis Rats

    Institute of Scientific and Technical Information of China (English)

    何志捷; 邹子俊

    2009-01-01

    Objective To observe the changes and significance of pulmonary water content,ICMA-1 and E-selectin in sepsis rats and exploring its role in glutamine.Methods 56 SD rats were randomly divided into 3 groups:the control group,the sepsis group and the treatment group.The expression of ICMA-1 and E-selectin was detected.Pulmonary water content was detected,and the morphological changes were observed.Results Compared with the control group and the treatment group in 24 h,the water content of the sepsis group was significantly increased(P<0.05).Compared with the control group and the treatment group,the expression of ICMA-1 was significantly increased in the sepsis group(P<0.05).The expression of E-selectin of the sepsis group and the treatment group was achieved the peak value at 6 h and decreased gradually at 24 h.Light microscopy examination of the sepsis group revealed pulmonary edema,RBC and neutrophil infiltration.Conclusion The expression of ICMA-1 and E-selectin in sepsis rat was significantly increased,probably leading to the necrosis and apoptosis of pulmonary VEC,as well as the occurrence of acute lung injury(ALI) and acute respiratory distress syndrome(ARDS).Glutamine had protective effect to pulmonary VEC.%目的 观察脓毒症大鼠肺组织肺含水量、细胞间黏附分子-1(intercellular adhesion-1,ICAM-1)和E-选择素(E-selectin,E-sel)的变化特点,并探讨谷氨酰胺(glutamine,Gln)对其的作用.方法 56只SD大鼠随机分成对照组、脓毒症组和治疗组.测定肺组织含水量,采用ICAM-1和E-SEL的表达;在光镜下观察肺组织形态学改变.结果 脓毒症组24h亚组大鼠肺组织含水量高于治疗组和对照组,差异有统计学意义(P<0.05).脓毒症组大鼠肺ICAM-1的表达与治疗组和对照组比较明显增加(P<0.05).脓毒症组和治疗组E-SEL的表达6h达高峰,以后逐渐下降.肺组织光镜检查发现脓毒症组肺间质水肿,红细胞及中性粒细胞浸润.结论

  11. 细胞间黏附分子-1及肿瘤坏死因子-α在糖尿病大鼠肾内的表达%Expression of intercellular adhesion molecule-1 and tumor necrosis factor-alpha in the kidney of diabetic rats

    Institute of Scientific and Technical Information of China (English)

    吴学平; 金晓梅; 彭彦霄; 伍雪芳; 贾雪梅

    2011-01-01

    目的:观察糖尿病大鼠肾内细胞间黏附分子-1(ICAM-1)及肿瘤坏死因子-α(TNF-α)的表达.方法:SD雄性大鼠用链脲佐菌素复制糖尿病动物模型,分别于4周、12周后测体质量、尿蛋白、血糖、尿素氮及肌酐,H-E染色观察肾形态学变化,免疫组织化学方法检测ICAM-1和TNF-α蛋白表达变化及TUNEL法观察大鼠肾皮质细胞凋亡情况.结果:与正常对照组比较,糖尿病组大鼠尿蛋白、血糖、尿素氮及血肌酐增高.4周糖尿病组大鼠肾小球体积增大,12周组肾小球萎缩,肾小管上皮细胞空泡样变.糖尿病组大鼠肾小管上皮细胞ICAM-1和TNF-α表达随病程延长增强.细胞凋亡检测结果显示,4周时凋亡细胞增多,多数在远曲肾小管,12周远曲肾小管及近曲肾小管均可见凋亡细胞.结论:ICAM-1及TNF-α表达随糖尿病病程延长而增强,引起细胞凋亡增加,导致肾功能异常,这可能是糖尿病肾病的重要发病机制.%Objective: To observe ICAM-1 and TNF-α expression in the kidney of diabetic rats. Methods: The Sprague-Daw-ley diabetic rats model was induced by injection of streptozotocin. After 4 and 12 weeks, the rats were killed for assaying weight, urine protein, blood glucose, blood urine nitrogen and serum creatinine. The change of the renal morphology was observed by H-E staining. ICAM-1 and TNF-a expression and apoptosis of renal cells was determinated by immunocyto-chemistry and TUNEL methods. Results: Compared with the normal control group, urine protein, blood glucose, blood u-rine nitrogen and serum creatinine in the diabetic group were higher. Renal glomerulus of 4 weeks diabetic rats increased in size, and that of 12 weeks showed glomerular atrophy, vacuolar degeneration in renal tubular epithelial cells. ICAM-1 and TNF-a immunopositive cells in the kidney showed an ascending tendency with the progression of the disease. Apoptosis tests showed that apoptotic cells increased most in the distal

  12. Mapping the binding site of a cross-reactive Plasmodium falciparum PfEMP1 monoclonal antibody inhibitory of ICAM-1 binding

    DEFF Research Database (Denmark)

    Lennartz, Frank; Bengtsson, Anja; Olsen, Rebecca W

    2015-01-01

    of domain cassette 4 PfEMP1s. 24E9 Fab fragments bind DBLβ3_D4 with nanomolar affinity and inhibit ICAM-1 binding of domain cassette 4-expressing IE. The antigenic regions targeted by 24E9 Fab were identified by hydrogen/deuterium exchange mass spectrometry and revealed three discrete peptides......-resolution structure of the DBLβ3_D4::24E9 Fab complex derived from small-angle x-ray scattering. The convex surface of DBLβ3_D4 has previously been shown to contain the ICAM-1 binding site of DBLβ domains, suggesting that the mAb acts by occluding the ICAM-1 binding surface. Conserved epitopes, such as those targeted...

  13. sICAM-1的表达在实验性重症急性胰腺炎肺损伤中的作用

    Institute of Scientific and Technical Information of China (English)

    郭建红; 余崇林

    2011-01-01

    目的观察血清可溶性细胞间粘附分子-1(sICAM-1)的水平变化与重症急性胰腺炎(SAP)肺损伤(ALI)的关系,并观察二硫代氨基甲酸吡(pyrrolidine dithiocarbamate,PDTC)对SAP ALI的保护作用。方法对SD大鼠采用逆行胰胆管注射5%牛磺胆酸钠(0.1ml/100g)的方法制作SAP模型和PDTC干扰组模型,取3h、6h、9h、12h不同时点的血清进行sICAM-1检测,同时检测血清淀粉酶的浓度。结果制模3h后,血清sICAM-1的水平开始持续上升,肺部组织损伤程度逐渐加重,且血清淀粉酶浓度持续上升,血清sICAM-1与血清淀粉酶的水平之间有相关性。PDTC干预组血清sICAM-1的水平较低,肺部损伤也较轻。结论重症急性胰腺炎肺损伤时血清sICAM-1的水平变化与肺部损伤程度密切相关。

  14. TNF-alpha and 9-cis-retinoic acid synergistically induce ICAM-1 expression: evidence for interaction of retinoid receptors with NF-kappa B.

    Science.gov (United States)

    Chadwick, C C; Shaw, L J; Winneker, R C

    1998-03-15

    TNF-alpha and 9-cis-retinoic acid (9-cis-R) synergistically enhance ICAM-1 protein expression in immortalized human aortic endothelial cells (HAECTs). At a TNF-alpha concentration of 0.1 ng/ml, 1 microM 9-cis-R enhanced ICAM-1 protein expression 4-fold. Treatment with 1 microM 9-cis-R alone caused no induction of ICAM-1 expression. Functional analysis of human ICAM-1 promoter-luciferase constructs revealed that the synergism was attributable to transcriptional regulation. Expression of a luciferase reporter vector containing a 311-bp fragment of the ICAM-1 promoter (-252 to + 59 bp relative to the transcriptional start site) was increased 2.9- and 4.9-fold by treatment with 9-cis-R and TNF-alpha, respectively, while cotreatment with 9-cis-R and TNF-alpha induced expression to 19.9-fold. Mutation studies revealed that RARE and NF-kappa B sites located respectively at -226 and -188 bp relative to the transcription start site are essential for the synergistic control of promoter activity. Mutation of either the RARE or the NF-kappa B site eliminated the synergistic enhancement of promoter activity. Moreover, mutation of the RARE abrogated promoter activity induced by treatment with TNF-alpha alone and mutation of the NF-kappa B site eliminated promoter activity induced by treatment with 9-cis-R alone. We conclude that retinoid receptors and NF-kappa B act in concert at the promoter level to facilitate ICAM-1 expression in endothelial cells.

  15. 糖尿病视网膜病变患者血清E-selectin和sICAM-1检测及意义探讨

    Institute of Scientific and Technical Information of China (English)

    王绪山; 徐桂玲; 王敏; 宋凤英

    2014-01-01

    目的:探讨糖尿病视网膜病变患者血清中E选择素(E-selectin)、可溶性细胞间黏附分子-1(sICAM-1)的水平及其临床意义。方法将70例2型糖尿病确诊患者分为糖尿病无视网膜病变组(NDR组)33例,糖尿病并发非增殖期视网膜病变组(NPDR组)20例,糖尿病并发增殖期视网膜病变组(PDR组)17例。同期选取32例健康体检者作为正常对照组(NC组)。采用酶联免疫吸附试验(ELISA)检测血清中 E-selectin、sICAM-1水平,并将各组的检测结果进行比较。结果 PDR组、NPDR组、NDR组血清中E-selectin和sICAM-1水平明显高于NC组,差异有统计学意义(P<0.01);PDR组血清中E-selectin、sICAM-1水平明显高于NPDR组和NDR组,差异有统计学意义(P<0.01);NPDR组血清中E-selectin、sICAM-1水平明显高于 NDR组,差异有统计学意义(P<0.01)。E-selectin水平与 sICAM-1水平呈明显正相关(r=0.756,P<0.01)。结论 E-selectin、sICAM-1参与了糖尿病视网膜病的形成与发展。早期检测血清中E-selectin、sICAM-1水平有助于保护糖尿病患者的血管内皮细胞,减少和预防动脉硬化的发生。

  16. Expression of myeloperoxidase, soluble intercellular adhesion molecule-1 and pentraxin-3 in the gingival crevicular fluid during maxillary canine distal movement%上颌尖牙远中移动过程中龈沟液内中性粒细胞浸润炎症相关因子的表达

    Institute of Scientific and Technical Information of China (English)

    许桓溪; 邢洪波; 苗芳; 李宁; 邱静怡; 李娟

    2016-01-01

    BACKGROUND:To dynamicaly monitor the varying levels of inflammatory factors in the gingival crevicular fluid is helpful to assess the early effect of orthodontic tooth movement. Myeloperoxidase, soluble intercelular adhesion molecule-1, pentraxin 3 are proven to be closely related to inflammation, but it is unclear about the levels of these three kinds of inflammatory factors as wel as association of these three kinds of inflammatory factors with orthodontic tooth. OBJECTIVE:To detect the expression levels of myeloperoxidase, soluble intercelular adhesion molecule-1 and pentraxin-3 in the gingival crevicular fluid during maxilary canine distal movement and to assess their correlation with periodontal disease, canine movement distance and orthodontic force. METHODS:Twenty-one orthodontic patients were enroled and assigned into 150 g (n=12) or 100 g (n=9) groups according to orthodontic force. The gingival crevicular fluid samples of orthodontic patients were colected before and at 4, 12, 24 hours, 7, 14 days after maxilary canine distal movement. Levels of myeloperoxidase, soluble intercelular adhesion molecule-1 and pentraxin-3 in the gingival crevicular fluid were measured and analyzed using ELISA assay. RESULTS AND CONCLUSION: During the distal movement of maxilary canine, under orthodontic force, the level of myeloperoxidase was peaked at 4 hours and then decreased, while the expression level of soluble intercelular adhesion molecule-1 was peaked at 12 hours, and then decreased. Both myeloperoxidase and soluble intercelular adhesion molecule-1 levels returned to normal at 7 days under orthodontic force. The expression level of pentraxin-3 was increased significantly under orthodontic force, peaked at 24 hours, and then decreased gradualy to the normal level at 7 days. In addition, the expression levels of myeloperoxidase, soluble intercelular adhesion molecule-1 and pentraxin-3 in the gingival crevicular fluid were significantly higher under 150 g force than

  17. Effect of 5-Aminoisoquinolinone on the Adhesion of Colon Carcinoma

    Institute of Scientific and Technical Information of China (English)

    WANG Ya-lan; HAO Lan-xiang

    2007-01-01

    Objective: 5-Aminoisoquinolinone, a water-soluble, potent inhibitor of the activity of poly (adenosine 5'-diphosphate ribose) polymerase, plays an important role in the tissue injury associated with ischaemia-reperfusion injury and inflammation by inhibiting the activity of poly (adenosine 5'-diphosphate ribose) polymerase and the expression of cell adhesion molecules such as ICAM-1, P-selectin et al. But how about it in the tumor is not clear. The aim of the present study was to study the effects of 5-Aminoisoquinolinon on the adhesion of colon carcinoma line HT-29 cells to human umbilical vein endothelial cells; and the effects of 5-Aminoisoquinolinon on the expression of ICAM-1, P-selectin and the activity of poly (adenosine 5'-diphosphate ribose) polymerase in colon carcinoma HT-29 cells. Methods: The adhesion of HT-29 cells to human umbilical vein endothelial cells was detected by adhesive experiment. Immunocytochemically Streptavidin-Peroxidase method was used to investigate the expression of ICAM-1, P-selectin and Poly (adenosine 5'-diphosphate ribose)( the product of poly (adenosine 5'-diphosphate ribose) polymerase activation). Results: the results of the adhesion assay of HT-29 cells to HUVEC showed that the OD570 value in each 5-AIQ-treated group was significant lower than that in the control group (5-AIQ-untreated) in a dose-dependent manner. The expression of ICAM-1, P-selectin and Poly (adenosine 5'-diphosphate ribose) was significant lower in 5-Aminoisoquinolinone-treated HT-29 cell group than that in 5-Aminoisoquinolinone- untreated groups. Conclusion: The data suggest that 5-Aminoisoquinolinone can inhibit the adhesion of HT-29 cells to human umbilical vein endothelial cells. 5-Aminoisoquinolinone also can inhibit poly (adenosine 5'-diphosphate ribose) polymerase activation and the expressions of ICAM-1 and P-selectin in HT-29 cells. 5-Aminoisoquinolinone probably contributes to the prevention of tumor cell metastasis. Further study is needed.

  18. Manganese supplementation increases adiponectin and lowers ICAM-1 and creatinine blood levels in Zucker type 2 diabetic rats, and downregulates ICAM-1 by upregulating adiponectin multimerization protein (DsbA-L) in endothelial cells.

    Science.gov (United States)

    Burlet, Elodie; Jain, Sushil K

    2017-01-13

    Blood and tissue levels of manganese (Mn) are lower in type 2 diabetic and atherosclerosis patients compared with healthy subjects. Adiponectin has anti-diabetic and anti-atherogenic properties. Impairment in Disulfide bond A-like protein (DsbA-L) is associated with low adiponectin levels and diabetes. This study investigates the hypothesis that the beneficial effects of Mn supplementation are mediated by adiponectin and DsbA-L. At 6 weeks of age, Male Zucker diabetic fatty rats (ZDF) were randomly divided into two groups: diabetic controls and Mn-supplemented diabetic rats. Each rat was supplemented with Mn (D+Mn, 16 mg/kg BW) or water (placebo, D+P) daily for 7 weeks by oral gavage. For cell culture studies, Human Umbilical Vein Endothelial Cells (HUVEC) or 3T3L1 adipocytes were pretreated with Mn (0-10 µM MnCl2) for 24 h, followed by high glucose (HG, 25 mM) or normal glucose (5 mM) exposure for another 24 h. Mn supplementation resulted in higher adiponectin (p = 0.01), and lower ICAM-1 (p = 0.04) and lower creatinine (p = 0.04) blood levels compared to those in control ZDF rats. Mn-supplemented rats also caused reduced oxidative stress (ROS) and NADPH oxidase, and higher DsbA-L expression in the liver (p = 0.03) of ZDF rats compared to those in livers of control rats; however, Fe levels in liver were lower but not significant (p = 0.08). Similarly, treatment with high glucose (25 mM) caused a decrease in DsbA-L, which was prevented by Mn supplementation in HUVEC and adipocytes. Mechanistic studies with DsbA-L siRNA showed that the beneficial effects of Mn supplementation on ROS, NOX4, and ICAM-1 expression were abolished in DsbA-L knock-down HUVEC. These studies demonstrate that DsbA-L-linked adiponectin mediates the beneficial effects observed with Mn supplementation and provides evidence for a novel mechanism by which Mn supplementation can increase adiponectin and reduce the biomarkers of endothelial dysfunction in diabetes.

  19. Patterns of nucleotide sequence variation in ICAM1 and TNF genes in twelve ethnic groups of India: roles of demographic history and natural selection

    Indian Academy of Sciences (India)

    Sanghamitra Sengupta; Shabana Farheen; Neelanjana Mukherjee; Partha P. Majumder

    2007-12-01

    We have studied DNA sequence variation in and around the genes ICAM1 and TNF, which play functional and correlated roles in inflammatory processes and immune cell responses, in 12 diverse ethnic groups of India, with a view to investigating the relative roles of demographic history and natural selection in shaping the observed patterns of variation. The total numbers of single nucleotide polymorphisms (SNPs) detected at the ICAM1 and TNF loci were 29 and 12, respectively. Haplotype and allele frequencies differed significantly across populations. The site frequency spectra at these loci were significantly different from those expected under neutrality, and showed an excess of intermediate-frequency variants consistent with balancing selection. However, as expected under balancing selection, there was no significant reduction of $F_{ST}$ values compared to neutral autosomal loci. Mismatch distributions were consistent with population expansion for both loci. On the other hand, the phylogenetic network among haplotypes for the TNF locus was similar to expectations under population expansion, while that for the ICAM1 was as expected under balancing selection. Nucleotide diversity at the ICAM1 locus was an order of magnitude lower in the promoter region, compared to the introns or exons, but no such difference was noted for the TNF gene. Thus, we conclude that the pattern of nucleotide variation in these genes has been modulated by both demographic history and selection. This is not surprising in view of the known allelic associations of several polymorphisms in these genes with various diseases, both infectious and noninfectious.

  20. House dust mite allergen Der p 1 elevates the release of inflammatory cytokines and expression of adhesion molecules in co-culture of human eosinophils and bronchial epithelial cells.

    Science.gov (United States)

    Wong, Chun K; Li, Mandy L Y; Wang, Cheng B; Ip, Wai K; Tian, Ya P; Lam, Christopher W K

    2006-08-01

    House dust mite (HDM) is a common allergen of allergic asthma. Eosinophils are principal effector cells of allergic inflammation and their adhesion onto human bronchial epithelial cells is mediated by a CD18-intracellular adhesion molecule-1 (ICAM-1)-dependent interaction. We studied the effects of HDM Dermatophagoides pteronyssinus (Der p) 1 on the activation of eosinophils and bronchial epithelial BEAS-2B cells. Cytokines and adhesion molecules were measured using flow cytometry. Transcription factor nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1) and signaling molecule p38 mitogen-activated protein kinase (MAPK) were analyzed using electromobility shift assay and western blot, respectively. Der p 1 protein was found to potently induce the release of IL-1beta, IL-6, IL-10, tumor necrosis factor (TNF)-alpha and granulocyte macrophage colony-stimulating factor from eosinophils. Such induction was further up-regulated for IL-6 and IL-10, and down-regulated for TNF-alpha and IL-1beta in eosinophil-BEAS-2B cells co-culture. Surface expression of CD18 and ICAM-1 on eosinophils was greatly increased by Der p 1; such inductive effect on ICAM-1 was also found to be more prominent on BEAS-2B cells from the co-culture than BEAS-2B cells alone. Der p 1 was found to activate NF-kappaB and AP-1 activity in eosinophils alone and in co-culture and BEAS-2B cells in co-culture. Moreover, Der p 1 could activate p38 MAPK in BEAS-2B cells and eosinophils alone and in co-culture. Selective inhibition of NF-kappaB, AP-1 and p38 MAPK resulted in differential suppression of the Der p 1-induced cytokine release and adhesion molecule expression. As an allergen, HDM could therefore induce the release of inflammatory cytokines and expression of adhesion molecules from the interaction of human eosinophils and bronchial epithelial cells.

  1. Cooperative inhibitory effects of antisense oligonucleotide of cell adhesion molecules and cimetidine on cancer cell adhesion

    Institute of Scientific and Technical Information of China (English)

    Nan-Hong Tang; Yan-Ling Chen; Xiao-Qian Wang; Xiu-Jin Li; Feng-Zhi Yin; Xiao-Zhong Wang

    2004-01-01

    AIM: To explore the cooperative effects of antisense oligonucleotide (ASON) of cell adhesion molecules and cimetidine on the expression of E-selectin and ICAM-1 in endothelial cells and their adhesion to tumor cells.METHODS: After treatment of endothelial cells with ASON and/or cimetidine and induction with TNF-α, the protein and mRNA changes of E-selectin and ICAM-1 in endothelial cells were examined by flow cytometry and RT-PCR,respectively. The adhesion rates of endothelial cells to tumor cells were measured by cell adhesion experiment.RESULTS: In comparison with TNF-α inducing group, lipoASON and lipo-ASON/cimetidine could significantly decrease the protein and mRNA levels of E-selectin and ICAM-1 in endothelial cells, and lipo-ASON/cimetidine had most significant inhibitory effect on E-selectin expression (from 36.37±1.56% to 14.23±1.07%, P<0.001). Meanwhile,cimetidine alone could inhibit the expression of E-selectin (36.37±1.56% vs 27.2±1.31%, P<0.001), but not ICAM-1 (69.34±2.50% vs68.07±2.10%,P>O.05)and the two kinds of mRNA, either. Compared with TNF-αα inducing group, the rate of adhesion was markedly decreased in lipo-E-selectin ASON and lipo-E-selectin ASON/cimetidine treated groups(P<0.05),and Jipo-E-selectin ASON/cimetidine worked better than lipo-E-selectin ASON alone except for HepG2/ECV304 group(P<0.05). However, the decrease of adhesion was not significant in lipo-ICAM-1 ASON and lipo-ICAM-1 ASON/cimetidine treated groups except for HepG2/ECV304 group (P >0.05).CONCLUSION: These data demonstrate that ASON in combination with cimetidine in vitro can significantly reduce the adhesion between endothelial cells and hepatic or colorectal cancer cells, which is stronger than ASON or cimetidine alone. This study provides some useful proofs for gene therapy of antiadhesion.

  2. 糖尿病合并脑梗死患者血清sICAM-1和sE-selectin水平的变化

    Institute of Scientific and Technical Information of China (English)

    张弘

    2004-01-01

    目的检测糖尿病合并脑梗死患者血清可溶性细胞间黏附因子-1(sICAM-1)可溶性E-选择素(sE-selectin)的水平,探讨其在糖尿病合并脑血管病变发病机制中的作用.方法采用ELISA和酶法分别检测31例糖尿病合并脑梗死患者,58例无并发症的糖尿病患者,31例对照组血清sICAM-1、sE-selectin、空腹血糖(BS)、总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C),用Friedewald公式计算低密度脂蛋白胆固醇(LDL-C).结果血清sICAM-1、sE-selectin水平糖尿病合并脑梗死组>无并发症糖尿病组>对照组,血清sICAM-1与sE-selectin水平呈现显著正相关(r=0.68,P0.05).结论 ICAM-1与E-selectin可能参与糖尿病脑血管并发症的发生,并在其发展中起促进作用.

  3. 卵巢癌患者围手术期血清sICAM-1和P-Selectin检测的临床意义%Clinical significance of serum sICAM-1 and P-selectin in patients with ovarian cancer at perioperative period

    Institute of Scientific and Technical Information of China (English)

    王旭平; 郭丽娜; 杨海英

    2010-01-01

    目的 探讨卵巢癌患者围手术期血清可溶性细胞黏附分子-1(sICAM-1)和P-选择素(P-Selectin)的变化及其临床意义.方法 72例卵巢癌患者根据病情分为根治性手术组和姑息性手术组,采用酶联免疫法(ELISA)测定手术前后血清sICAM-1和P-Selectin的水平,并与对照组比较.结果 卵巢癌组治疗前血清sICAM-1和P-Selectin均增高,与对照组比较差异有统计学意义(P0.05).结论 卵巢癌患者血清sICAM-1和P-Selectin的水平与肿瘤的浸润转移和病程有关,检测卵巢癌患者血清sICAM-1和P-Selectin的变化,有助于了解患者的预后.

  4. Age dependency of the composition of immunocompetent cells and the expression of adhesion molecules in rat laryngeal mucosa.

    Science.gov (United States)

    Jecker, P; Ptok, M; Pabst, R; Westermann, J

    1996-06-01

    Clinical evidence shows that laryngeal infections in infants differ significantly from those in adults. Therefore, the composition of the mucosal immune system (granulocytes, macrophages, dendritic cells, natural killer cells, and T and B lymphocytes) and the epithelial expression of class II-MHC molecules and adhesion molecules ICAM-1, VCAM-1, and E-selectin were studied in the larynx of newborn, 5-week-old, and 3-year-old rats. With the exception of macrophages, the immunocompetent cells began to immigrate into the laryngeal mucosa after birth, indicating that the laryngeal mucosa in newborn rats is immature. In contrast, ICAM-1 was already expressed. The number of immunocompetent cells and the expression of epithelial class II-MHC and ICAM-1 increased with age. Immunocompetent cells and epithelial class II-MHC and ICAM-1 expression were mainly detected in the subglottic region, but were almost absent in the vocal fold region.

  5. Identifying the rules of engagement enabling leukocyte rolling, activation, and adhesion.

    Science.gov (United States)

    Tang, Jonathan; Hunt, C Anthony

    2010-02-19

    The LFA-1 integrin plays a pivotal role in sustained leukocyte adhesion to the endothelial surface, which is a precondition for leukocyte recruitment into inflammation sites. Strong correlative evidence implicates LFA-1 clustering as being essential for sustained adhesion, and it may also facilitate rebinding events with its ligand ICAM-1. We cannot challenge those hypotheses directly because it is infeasible to measure either process during leukocyte adhesion following rolling. The alternative approach undertaken was to challenge the hypothesized mechanisms by experimenting on validated, working counterparts: simulations in which diffusible, LFA1 objects on the surfaces of quasi-autonomous leukocytes interact with simulated, diffusible, ICAM1 objects on endothelial surfaces during simulated adhesion following rolling. We used object-oriented, agent-based methods to build and execute multi-level, multi-attribute analogues of leukocytes and endothelial surfaces. Validation was achieved across different experimental conditions, in vitro, ex vivo, and in vivo, at both the individual cell and population levels. Because those mechanisms exhibit all of the characteristics of biological mechanisms, they can stand as a concrete, working theory about detailed events occurring at the leukocyte-surface interface during leukocyte rolling and adhesion experiments. We challenged mechanistic hypotheses by conducting experiments in which the consequences of multiple mechanistic events were tracked. We quantified rebinding events between individual components under different conditions, and the role of LFA1 clustering in sustaining leukocyte-surface adhesion and in improving adhesion efficiency. Early during simulations ICAM1 rebinding (to LFA1) but not LFA1 rebinding (to ICAM1) was enhanced by clustering. Later, clustering caused both types of rebinding events to increase. We discovered that clustering was not necessary to achieve adhesion as long as LFA1 and ICAM1 object

  6. Identifying the rules of engagement enabling leukocyte rolling, activation, and adhesion.

    Directory of Open Access Journals (Sweden)

    Jonathan Tang

    2010-02-01

    Full Text Available The LFA-1 integrin plays a pivotal role in sustained leukocyte adhesion to the endothelial surface, which is a precondition for leukocyte recruitment into inflammation sites. Strong correlative evidence implicates LFA-1 clustering as being essential for sustained adhesion, and it may also facilitate rebinding events with its ligand ICAM-1. We cannot challenge those hypotheses directly because it is infeasible to measure either process during leukocyte adhesion following rolling. The alternative approach undertaken was to challenge the hypothesized mechanisms by experimenting on validated, working counterparts: simulations in which diffusible, LFA1 objects on the surfaces of quasi-autonomous leukocytes interact with simulated, diffusible, ICAM1 objects on endothelial surfaces during simulated adhesion following rolling. We used object-oriented, agent-based methods to build and execute multi-level, multi-attribute analogues of leukocytes and endothelial surfaces. Validation was achieved across different experimental conditions, in vitro, ex vivo, and in vivo, at both the individual cell and population levels. Because those mechanisms exhibit all of the characteristics of biological mechanisms, they can stand as a concrete, working theory about detailed events occurring at the leukocyte-surface interface during leukocyte rolling and adhesion experiments. We challenged mechanistic hypotheses by conducting experiments in which the consequences of multiple mechanistic events were tracked. We quantified rebinding events between individual components under different conditions, and the role of LFA1 clustering in sustaining leukocyte-surface adhesion and in improving adhesion efficiency. Early during simulations ICAM1 rebinding (to LFA1 but not LFA1 rebinding (to ICAM1 was enhanced by clustering. Later, clustering caused both types of rebinding events to increase. We discovered that clustering was not necessary to achieve adhesion as long as LFA1 and

  7. Expression of ICAM-1, P-selectin, D-dimer in placental tissue and matemal plasm of preeclampsia patients%ICAM-1、P-selectin、D-dimer在子痫前期胎盘和血浆表达研究

    Institute of Scientific and Technical Information of China (English)

    岳永飞; 许多

    2014-01-01

    目的 探讨细胞间黏附分子(ICAM-1)、p-选择素(P-selectin)、D二聚体(D-dimer)在子痫前期发生发展中的作用.方法 随机选取子痫前期患者39例为研究组,37例正常妊娠孕妇为对照组,采用免疫组织化学技术检测两组胎盘组织中ICAM-l、P-selectin的表达情况;采用酶联免疫吸附法(ELISA)检测两组血浆ICAM-1、P-selectin和D-dimer的表达水平.结果 子痫前期组胎盘ICAM-1、P-selectin的表达明显高于对照组(P<0.05);两组血浆均有ICAM-1、P-selectin和D-dimer的表达,子痫前期组的血浆ICAM-1、P-selectin和D-dimer表达明显高于对照组(P<0.05).结论 子痫前期患者ICAM-1、P-selectin和D-dimer表达升高可能与子痫前期的发生发展有关,监测这些指标对病情判断及指导治疗具有重要意义.

  8. Changes of serum soluble intercellular adhesion molecule-1 in children patients with bronchial asthma by Pediatric Cough and Asthma Relieving Gel%小儿止咳平喘露的平喘作用及其对外周血可溶性细胞黏附分子-1的影响

    Institute of Scientific and Technical Information of China (English)

    宋慧珠

    2013-01-01

    Objective To investigate the antiasthmatic effect of Pediatric Cough and Asthma Relieving Gel and its effect on peripheral blood soluble cell adhesion molecule-1. Methods 236 children with cough and asthma were selected in the hospital from October 2010 to March 2012,who were divided into two groups randomly. 118 children used cough syrup in the treatment as the control group. 118 children used Pediatric Cough and Asthma Relieving Gel in the treatment as the observation group. All children underwent observation of cough induced by histamine,observation of cough induced by citric acid,sputum eosinophil cells count,detection of peripheral blood soluble cell adhesion molecule-1. Clinical indexes were compared between two groups. Results Cough latency induced by histamine in the observation group [(81.4±16.5)s] was significantly longer than that in the control group [(52.7±12.0)s]. Cough latency induced by citric acid in the observation group [(48.3±12.6)s] was significantly longer than that in the control group [(30.1±9.2)s]. Sputum eosinophil cells count in the observation group [(1.3±0.6)x106/mL] was significantly lower than that in the control group [(2.1±1.0)×106/mL]. Peripheral blood soluble cell adhesion molecule-1 in the observation group [(42.7±13.8)μg/L] was significantly lower than that in the control group [(59.2±17.5) μg/L]. The difference was statistically significant (P < 0.05). Conclusion Pediatric Cough and Asthma Relieving Gel can obvious relieve cough and asthma,which not only can reduce the induced sputum in children with eosinophilic,but also can effectively reduce level of peripheral blood soluble cell adhesion molecule-1 of children.%目的 探讨小儿止咳平喘露的平喘作用及其对外周血可溶性细胞黏附分子-1的影响.方法选取本院2010年10月~2012年3月收治的咳喘患儿236例,随机分为两组,采用小儿止咳糖浆治疗患儿118例为对照组,采用小儿止咳平喘露治疗患儿118例为观察

  9. Multifunctional interleukin-1beta promotes metastasis of human lung cancer cells in SCID mice via enhanced expression of adhesion-, invasion- and angiogenesis-related molecules.

    Science.gov (United States)

    Yano, Seiji; Nokihara, Hiroshi; Yamamoto, Akihiko; Goto, Hisatsugu; Ogawa, Hirohisa; Kanematsu, Takanori; Miki, Toyokazu; Uehara, Hisanori; Saijo, Yasuo; Nukiwa, Toshihiro; Sone, Saburo

    2003-03-01

    We examined whether interleukin-1 (IL-1), a multifunctional proinflammatory cytokine, progresses or regresses metastasis of lung cancer. Exogenous IL-1beta enhanced expression of various cytokines (IL-6, IL-8, and vascular endothelial growth factor (VEGF)) and intracellular adhesion molecule-1 (ICAM-1) by A549, PC14, RERF-LC-AI, and SBC-3 cells expressing IL-1 receptors. A549 cells transduced with human IL-1beta-gene with the growth-hormone signaling-peptide sequence (A549/IL-1beta) secreted a large amount of IL-1beta protein. Overexpression of IL-1beta resulted in augmentation of expression of the cytokines, ICAM-1, and matrix metalloproteinase-2 (MMP-2). A549/IL-1beta cells intravenously inoculated into severe combined immunodeficiency (SCID) mice distributed to the lung more efficiently and developed lung metastasis much more rapidly than did control A549 cells. Treatment of SCID mice with anti-IL-1beta antibody inhibited formation of lung metastasis by A549/IL-1beta cells. Moreover, A549/IL-1beta cells inoculated in the subcutis grew more rapidly, without necrosis, than did control A549 cells, which produced smaller tumors with central necrosis, suggesting involvement of angiogenesis in addition to enhanced binding in the high metastatic potential of A549/IL-1beta cells. Histological analyses showed that more host-cell infiltration, fewer apoptotic cells, more vascularization, and higher MMP activity were observed in tumors derived from A549/IL-1beta cells, compared with tumors derived from control A549 cells. These findings suggest that IL-1beta facilitates metastasis of lung cancer via promoting multiple events, including adhesion, invasion and angiogenesis.

  10. Increase in IL-6, TNF-a, and MMP-9, but not sICAM-1, concentrations depends on exercise duration

    DEFF Research Database (Denmark)

    Reihmane, Dace; Jurka, Antra; Tretjakovs, Peteris

    2013-01-01

    -α, and MMP-9 returned to pre-exercise levels. Competitive HM and M races induce significant increases in IL-6, TNF-α, sICAM-1, and MMP-9 concentrations. As HM and M runners performed the competition with similar absolute intensity, the difference in response between the groups suggests that exercise duration...... is of importance in the regulation of IL-6, TNF-α, and MMP-9, but not sICAM-1 concentrations in response to prolonged running.......It has been suggested that exercise intensity is of importance in the regulation of increase in pro-inflammatory molecules, but there is still a debate about the effect of duration on these molecules. Therefore, the effect of exercise duration on the serum concentrations of interleukin-6 (IL-6...

  11. The candidate genes TAF5L, TCF7, PDCD1, IL6 and ICAM1 cannot be excluded from having effects in type 1 diabetes

    Directory of Open Access Journals (Sweden)

    Vella Adrian

    2007-11-01

    Full Text Available Abstract Background As genes associated with immune-mediated diseases have an increased prior probability of being associated with other immune-mediated diseases, we tested three such genes, IL23R, IRF5 and CD40, for an association with type 1 diabetes. In addition, we tested seven genes, TAF5L, PDCD1, TCF7, IL12B, IL6, ICAM1 and TBX21, with published marginal or inconsistent evidence of an association with type 1 diabetes. Methods We genotyped reported polymorphisms of the ten genes, nonsynonymous SNPs (nsSNPs and, for the IL12B and IL6 regions, tag SNPs in up to 7,888 case, 8,858 control and 3,142 parent-child trio samples. In addition, we analysed data from the Wellcome Trust Case Control Consortium genome-wide association study to determine whether there was any further evidence of an association in each gene region. Results We found some evidence of associations between type 1 diabetes and TAF5L, PDCD1, TCF7 and IL6 (ORs = 1.05 – 1.13; P = 0.0291 – 4.16 × 10-4. No evidence of an association was obtained for IL12B, IRF5, IL23R, ICAM1, TBX21 and CD40, although there was some evidence of an association (OR = 1.10; P = 0.0257 from the genome-wide association study for the ICAM1 region. Conclusion We failed to exclude the possibility of some effect in type 1 diabetes for TAF5L, PDCD1, TCF7, IL6 and ICAM1. Additional studies, of these and other candidate genes, employing much larger sample sizes and analysis of additional polymorphisms in each gene and its flanking region will be required to ascertain their contributions to type 1 diabetes susceptibility.

  12. 糖肾安对糖尿病肾病大鼠的保护作用及对肾脏ICAM-1的影响

    Institute of Scientific and Technical Information of China (English)

    张书征; 杨巧红; 苏俊芳; 赵自明; 刘向国; 钟毅; 李永胜; 连至诚

    2011-01-01

    目的:探讨糖肾安对糖尿病肾病(DN)大鼠肾脏损害的保护作用及其机制。方法:采用链脲佐菌素(STZ)腹腔注射建立糖尿病(DM)大鼠模型,将SD大鼠随机分为正常对照组、模型组、辛伐他汀组、糖肾安组。治疗30周。观察治疗期间及治疗后大鼠的一般状况、血糖、肾质量/体质量(LKW)、内生肌酐清除率(CCr)和24小时尿蛋白改变;用免疫组化法检测细胞间黏附分子-1(ICAM-1)在DN大鼠肾小球及肾小管中的表达。结果:模型组LKW、CCr、24小时尿蛋白均高于正常对照组(P<0.01);肾小管中ICAM-1有明显表达,肾小球未见明显ICAM-1表达。糖肾安组血糖、LKW、CCr、24小时尿蛋白降低(P<0.01),ICAM-1表达明显下降。结论:糖肾安对糖尿病肾病有一定的保护作用。

  13. The therapeutic effects of XueZHiKang on unstable angina in patients with coronary heart disease and its effects on soluble intercellular adhesion molecule-1%血脂康对冠心病不稳定性心绞痛的疗效及对可溶性细胞间黏附分子-1的影响

    Institute of Scientific and Technical Information of China (English)

    姜丽萍; 张伟强; 刘长山

    2002-01-01

    目的观察血脂康对冠心病不稳定性心绞痛(UA)的疗效并探讨其治疗作用的机制.方法80例UA患者随机分为血脂康加常规组(治疗组)和常规治疗组(对照组),疗程8周,治疗前后观察2组患者临床症状、心电图缺血变化及可溶性细胞间黏附分子-1(sICAM-1)浓度的改变.结果①治疗后治疗组、对照组心绞痛的发作次数分别为1.4±2.5和3.7±3.2,硝酸甘油日用量分别为0.3±0.5和0.9±0.4,差别均有显著性(p<0.05).②治疗组症状疗效有效率为95%,对照组有效率为82.5%,治疗组心电图疗效有效率为62.5%,对照组有效率为42.5%,两组差别均有显著性(p<0.05).③治疗后两组sICAM-1水平均明显下降,而以治疗组下降更为明显(p<0.05).结论血脂康可降低UA患者sICAM-1水平,从而消除炎症、稳定斑块,进而改善UA患者临床症状及心电图缺血改变.

  14. LFA-1/ICAM-1 Ligation in Human T Cells Promotes Th1 Polarization through a GSK3β Signaling-Dependent Notch Pathway.

    Science.gov (United States)

    Verma, Navin K; Fazil, M H U Turabe; Ong, Seow Theng; Chalasani, Madhavi Latha S; Low, Jian Hui; Kottaiswamy, Amuthavalli; P, Praseetha; Kizhakeyil, Atish; Kumar, Sunil; Panda, Aditya K; Freeley, Michael; Smith, Sinead M; Boehm, Bernhard O; Kelleher, Dermot

    2016-07-01

    In this study, we report that the integrin LFA-1 cross-linking with its ligand ICAM-1 in human PBMCs or CD4(+) T cells promotes Th1 polarization by upregulating IFN-γ secretion and T-bet expression. LFA-1 stimulation in PBMCs, CD4(+) T cells, or the T cell line HuT78 activates the Notch pathway by nuclear translocation of cleaved Notch1 intracellular domain (NICD) and upregulation of target molecules Hey1 and Hes1. Blocking LFA-1 by a neutralizing Ab or specific inhibition of Notch1 by a γ-secretase inhibitor substantially inhibits LFA-1/ICAM-1-mediated activation of Notch signaling. We further demonstrate that the Notch pathway activation is dependent on LFA-1/ICAM-1-induced inactivation of glycogen synthase kinase 3β (GSK3β), which is mediated via Akt and ERK. Furthermore, in silico analysis in combination with coimmunoprecipitation assays show an interaction between NICD and GSK3β. Thus, there exists a molecular cross-talk between LFA-1 and Notch1 through the Akt/ERK-GSK3β signaling axis that ultimately enhances T cell differentiation toward Th1. Although clinical use of LFA-1 antagonists is limited by toxicity related to immunosuppression, these findings support the concept that Notch inhibitors could be attractive for prevention or treatment of Th1-related immunologic disorders and have implications at the level of local inflammatory responses.

  15. T-cell-receptor engagement and tumor ICAM-1 up-regulation are required to by-pass low susceptibility of melanoma cells to autologous CTL-mediated lysis.

    Science.gov (United States)

    Anichini, A; Mortarini, R; Alberti, S; Mantovani, A; Parmiani, G

    1993-04-01

    Tumor-specific and non-specific CD3+, TcR alpha beta+, CD8+ cytotoxic T-cell (CTL) clones, isolated from tumor-infiltrating lymphocytes (TIL) or peripheral blood lymphocytes (PBL) of a melanoma patient and allogeneic LAK cells, were used to investigate the requirements for bypassing the low lysability of some melanoma clones derived from an s.c. metastasis from which highly lysable clones were also obtained. Cytofluorimetric analysis showed that all melanoma clones expressed ICAM-1, although to different extents, reaching a 10-fold difference in fluorescence units, while HLA class-I antigens were similarly expressed. The differences in expression of ICAM-1 among tumor clones correlated with differences in lysability, by both specific and non-specific CTL, but were not large enough to affect lymphocyte-tumor conjugate formation. Cytokine- or gene-transfer-mediated up-regulation of ICAM-1 did not induce de novo lysis of ICAM-1low tumor cells; however, it markedly enhanced a low level of killing of the same cells by tumor-specific, TcR-dependent and HLA-restricted CTL clones but not by non-specific, TcR-independent effectors. In addition, lysis of melanoma clones by any effector was similarly inhibited by anti-ICAM-1 and anti-LFA-1 antibodies. This indicates that by-pass of low lysability of ICAM-1low melanoma clones by CTL clones, after ICAM-1 up-regulation, is possible only if simultaneous LFA-1 and TcR engagement takes place. In addition, these results suggest that the constitutive high level of expression of ICAM-1 on the subset of ICAM-1high melanoma cells must be only one of the factors contributing to the high lysability of these cells by any effector.

  16. 复方丹参滴丸对老年不稳定性心绞痛患者内皮素、一氧化氮和可溶性细胞间粘附分子-1的影响%Effects of Composite Salvia Pill on Endothelin, Nitric Oxide and Soluble Intercellular Adhesion Molecule-1 in Elderly Patients with Unstable Angina Pectoris

    Institute of Scientific and Technical Information of China (English)

    周益伟; 马长松; 赵晓燕; 孙杰

    2012-01-01

    目的:探讨复方丹参滴丸对不稳定性心绞痛(UAP)患者血浆内皮素(ET)、一氧化氮(NO)和可溶性细胞间粘附分子-1 (sICAM-1)水平的影响及作用机制.方法:将90例UAP患者随机分成两组,每组45例.2个月的疗程结束后,观察患者心绞痛及心电图改善情况,比较治疗前后血浆ET、NO和sICAM -1水平的变化.结果:治疗组治疗后ET、sICAM -1均明显降低且低于对照组(P<0.01),NO明显升高且高于对照组(P<0.01).结论:复方丹参滴丸是一种有效的治疗UAP的中成药,其作用可能是通过降低血浆ET、sICAM -1和升高血浆NO而实现的.

  17. Adhesion molecule expression stimulated by Bacteroides thetaiotaomicron cell-surface antigens.

    Science.gov (United States)

    Rokosz, A; Meisel-Mikołajczyk, F; Malchar, C; Nowaczyk, M; Górski, A

    1999-01-01

    Bacteroides thetaiotaomicron, a Gram-negative anaerobic rod belonging to the Bacteroides fragilis group (BFG), is involved in many systemic and local, most frequently suppurative infections in man. The cell envelope of these rods is composed of two carbohydrate-containing antigens: lipopolysaccharide (LPS) and capsular polysaccharide (CPS). Adhesion molecules ICAM-1, VCAM-1 and E-selectin (ELAM-1) are induced on the endothelial cells by mediators of inflammation. The aim of this study was to assay the ability of B. thetaiotaomicron surface antigens to induce adhesion molecule expression on the endothelial cells. The influence of LPS and CPS on the expression of adhesion molecules on HMEC-1 cell line was examined in an ELISA test. ELISA was performed with monoclonal mouse anti-human: ICAM-1, VCAM-1 and E-selectin antibodies of the IgG class. B. thetaiotaomicron lipopolysaccharides revealed the ability to induce ICAM-1, VCAM-1 and E-selectin expression on the endothelial cells. Their activities were similar, but lower than the activity of Eschericha coli LPS. ICAM-1 was the most stimulated adhesion molecule. The strongest activation by LPS was achieved at the concentrations of 10.0 and 1.0 micrograms/ml. The ability of capsular polysaccharide to induce the expression of adhesion molecules was considerably weaker.

  18. 眼部蠕形螨寄居患者结膜上皮ICAM-1和HLA-DR的表达和意义%Expression of ICAM-1 and HLA-DR in conjunctival epithelium of patients with ocular Demodex

    Institute of Scientific and Technical Information of China (English)

    范春梅; 高莹莹; 许锻炼; 戴炳发; 李静

    2011-01-01

    目的:探讨眼部蠕形螨寄居患者结膜上皮ICAM-1和HLA-DR的表达和意义.方法:选择痤疮、脂溢性皮炎以及类固醇皮炎眼部蠕形螨检查为阳性的患者共58例为蠕形螨寄居组,另选50例无面部疾病眼部蠕形螨检查阴性的健康成人,作为正常对照组.用流式细胞术联合印迹细胞学检测细胞表面分子的方法检测结膜上皮细胞ICAM-1和HLA-DR的表达阳性率及荧光强度.结果:与正常对照组相比,蠕形螨寄居组患者结膜上皮细胞中ICAM-1和HLA-DR的阳性率和荧光强度均明显提高,差异具有统计学意义(P<0.05).结论:眼部蠕形螨寄居患者结膜上皮中ICAM-1和HLA-DR的表达增强.%AIM: Expression of ICAM-1 and HLA-DR in conjunctival epithelium of patients with ocular Demodex was investigation.METHODS: Acne, seborrheic dermatitis and facial steroid dermatitis, skin diseases, and conduct inspections of Demodex total of 58 cases of patients with Demodex stranger group, the other selected 50 patients with non-facial disease in healthy adults as normal control group without Demodex.Flow cytometry combined with blot-cytology was used to detect the expression of HLA-DR.RESULTS: Compared with the normal control group, Demodex sojoum the positive rate and fluorescence intensity in conjunctival epithelial cells of patients with Demodex of ICAM-1 and HLADR were significantly increased ( P < 0.05 ).DISCUSSION:ICAM-1 and HLA-DR expression is increased in the eye inflammation with Demodex.

  19. 辛伐他汀预处理对脓毒症大鼠心肌细胞 ICAM-1表达的影响及意义%Effect and significance of simvastatin pretreatment on ICAM-1 expression in myocardial cells of rats with sepsis

    Institute of Scientific and Technical Information of China (English)

    张立涛; 于织波; 赵鹤龄

    2013-01-01

    目的观察心肌细胞间粘附分子-1(ICAM-1)在脓毒症大鼠心肌细胞的表达,同时探讨辛伐他汀预处理对其表达的影响及意义。方法雌性Wistar大鼠60只随机分为正常组、脓毒症组和辛伐他汀组,每组20例,应用盲肠结扎穿孔法制造脓毒症模型。辛伐他汀组喂养辛伐他汀20 mg/kg,1次/d,共2周。2周后辛伐他汀组与脓毒症组大鼠行盲肠结扎穿孔术。术后48 h取各组大鼠心肌组织制成石蜡切片,采用免疫组织化学染色方法观察心肌细胞ICAM-1的蛋白表达。结果免疫组织化学染色显示脓毒症组大鼠心肌细胞ICAM-1蛋白表达于术后48 h较正常组明显增加( P <0铑.05),辛伐他汀组大鼠心肌细胞ICAM-1蛋白表达与脓毒症组比较明显减弱( P <0.05),与正常组比较差异有统计学意义( P <0.05)。%Objective To observe the expressions of ICAM-1 in myocardial cells of rats with sepsis ,and to explore the effect and significance of simvastatin pretreatment on ICAM-1 expression .Methods Sixty female Wistar rats were randomly divided into three groups:control group ( n =20 ) , sepsis group ( n =20 ) and simvastatin group ( n =20 ) .The animal models with sepsis were established by cecal ligation and puncture (CLP).The rats in simvastatin group were treated with simvastatin ,20mg/kg,once a day for two weeks before CLP.After teo weeks the rats both simvastatin group and sepsis group underwent CLP ,then 48h after operation the myocardium tissues of rats in three groups were collected to be made paraffin section , and the expressions of ICAM-1 protein in myocardial cells were detected by immunohistochemistry ( IH ) staining.Results Immunohistochemistry staining showed that the expression levels of ICAM-1 in sepsis group were significantly higher than those in control group at 48h after CLP ( P <0.05),however,which in simvastatin group were significantly decreased,as ompared with those in

  20. Human carcinoembryonic antigen-related cellular adhesion molecules 1 mediated susceptibility of Neisseria gonorrhoeae to mouse%人癌胚抗原相关细胞黏附分子1介导的小鼠淋病奈瑟菌易感性

    Institute of Scientific and Technical Information of China (English)

    李国才; 季明春; 杜庆辉; 王晓红; 王劲松; 于峰; 刘双喜; 解如山; 焦红梅; 严华

    2011-01-01

    Objective To develop a transgenic mouse model for N.gonorrhoeae researches.Methods Human carcinoembryonic antigen-related cellular adhesion molecules 1 (hCEACAM1) eukaryotic expression vector,pCDPGICAM1,was used to generate transgenic mice by microinjection.The funder mice were screened by PCR,sequence analysis,Western blot and fluorescence-activated cell sorting analysis,respectively.The transgenic mice expressing hCEACAM1 were inoculated with N.gonorrhoeae intravaginally.Adhesion and infection of gonococci to mice were analyzed by bacteria culture and microscopy.Results Four (lines 50,53,54,and 59) of the 22 F0 generation transgenic mice were found to carry the transgene.The hCEACAM1 protein was expressed on the cell membrane of various tissues in the line 53 transgenic mouse.Compared with normal mice,N.gonorrhoeae can successfully infect and cause inflammation in the transgenic mice.Conclusion The hCEACAM1 transgenic mouse can be used as an animal model for gonococcal infections.%目的 研究制备淋病奈瑟菌感染人癌胚抗原相关细胞黏附分子1(hCEACAM1)转基因小鼠模型的可行性.方法 用hCEACAM1真核表达载体pCDPGICEA1,通过显微注射法制备转基因小鼠,PCR及序列分析法检测目的基因在小鼠基因组中的整合,Western blot及FACS技术检测目的基因的表达,镜检及培养法检查淋病奈瑟菌对转基因小鼠的感染.结果 产生的22只F0代小鼠中4只为转基因整合阳性,其中1只可表达hCEACAM1蛋白,且目的蛋白表达在细胞膜上.淋病奈瑟菌可在转基因小鼠中形成感染.结论 hCEACAM1转基因小鼠可作为淋病奈瑟菌感染研究的转基因动物模型.

  1. Human β-Defensin 3 Reduces TNF-α-Induced Inflammation and Monocyte Adhesion in Human Umbilical Vein Endothelial Cells

    Directory of Open Access Journals (Sweden)

    Tianying Bian

    2017-01-01

    Full Text Available The aim of this study was to investigate the role of human β-defensin 3 (hBD3 in the initiation stage of atherosclerosis with human umbilical vein endothelial cells (HUVECs triggered by tumor necrosis factor- (TNF- α. The effects of hBD3 on TNF-α-induced endothelial injury and inflammatory response were evaluated. Our data revealed that first, hBD3 reduced the production of interleukin-6 (IL-6, IL-8, monocyte chemoattractant protein-1 (MCP-1, and macrophage migration inhibitory factor (MIF in HUVECs in a dose-dependent manner. In addition, hBD3 significantly prevented intracellular reactive oxygen species (ROS production by HUVECs. Second, western blot analysis demonstrated that hBD3 dose-dependently suppressed the protein levels of intracellular adhesion molecule-1 (ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1 in TNF-α-induced HUVECs. As a result, hBD3 inhibited monocyte adhesion to TNF-α-treated endothelial cells. Additionally, hBD3 suppressed TNF-α-induced F-actin reorganization in HUVECs. Third, hBD3 markedly inhibited NF-κB activation by decreasing the phosphorylation of IKK-α/β, IκB, and p65 subunit within 30 min. Moreover, the phosphorylation of p38 and c-Jun N-terminal protein kinase (JNK in the mitogen-activated protein kinase (MAPK pathway were also inhibited by hBD3 in HUVECs. In conclusion, hBD3 exerts anti-inflammatory and antioxidative effects in endothelial cells in response to TNF-α by inhibiting NF-κB and MAPK signaling.

  2. Human β-Defensin 3 Reduces TNF-α-Induced Inflammation and Monocyte Adhesion in Human Umbilical Vein Endothelial Cells

    Science.gov (United States)

    Bian, Tianying; Li, Houxuan; Zhou, Qian; Ni, Can; Zhang, Yangheng

    2017-01-01

    The aim of this study was to investigate the role of human β-defensin 3 (hBD3) in the initiation stage of atherosclerosis with human umbilical vein endothelial cells (HUVECs) triggered by tumor necrosis factor- (TNF-) α. The effects of hBD3 on TNF-α-induced endothelial injury and inflammatory response were evaluated. Our data revealed that first, hBD3 reduced the production of interleukin-6 (IL-6), IL-8, monocyte chemoattractant protein-1 (MCP-1), and macrophage migration inhibitory factor (MIF) in HUVECs in a dose-dependent manner. In addition, hBD3 significantly prevented intracellular reactive oxygen species (ROS) production by HUVECs. Second, western blot analysis demonstrated that hBD3 dose-dependently suppressed the protein levels of intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in TNF-α-induced HUVECs. As a result, hBD3 inhibited monocyte adhesion to TNF-α-treated endothelial cells. Additionally, hBD3 suppressed TNF-α-induced F-actin reorganization in HUVECs. Third, hBD3 markedly inhibited NF-κB activation by decreasing the phosphorylation of IKK-α/β, IκB, and p65 subunit within 30 min. Moreover, the phosphorylation of p38 and c-Jun N-terminal protein kinase (JNK) in the mitogen-activated protein kinase (MAPK) pathway were also inhibited by hBD3 in HUVECs. In conclusion, hBD3 exerts anti-inflammatory and antioxidative effects in endothelial cells in response to TNF-α by inhibiting NF-κB and MAPK signaling.

  3. Expression of ICAM-1,LFA-1 and VEGFR-3 In Brest Cancer and its Relationship with Lymphatical Metastasis%人乳腺癌组织中ICAM-1、LFA-1和VEGFR-3的表达与癌淋巴转移关系的研究

    Institute of Scientific and Technical Information of China (English)

    郑辉; 潘辑

    2009-01-01

    目的 观察不同时期,不同转移阶段的人乳腺癌组织中细胞间黏附分子(ICAM-1)和淋巴细胞功能相关抗原1(LFA-1)的表达,探讨ICAM-1和LFA-1对乳腺癌淋巴道转移的影响,为乳腺癌淋巴道转移的分子机制提供理论依据.方法 根据不同病变阶段的手术患者切除的乳腺癌标本进行HE染色和免疫组化染色,观察ICAM-1、LFA-1在乳腺癌组织和ICAM-1、LFA-1、VEGFR-3在癌旁组织淋巴管内皮的表达情况.结果 随着临床分期的增高和淋巴结转移的发生,ICAM-1和LFA-1在乳腺癌癌细胞和癌巢中的表达阳性率逐渐增高,同时ICAM-1、LFA-1和VEGFR-3在癌旁组织淋巴管内皮细胞的表达阳性率也逐渐增高,具有正相关性,并且ICAM-1和LFA-1在癌旁组织淋巴管内皮细胞的表达之间具有正相关性(P<0.01).同时发现无论是在乳腺癌癌细胞、癌巢还是在癌旁组织淋巴管内皮细胞,ICAM-1和LFA-1表达的高低都与癌的分化程度、性别、年龄不具有相关性,差异无统计学意义(P>0.05).结论 ICAM-1和LFA-1与乳腺癌的淋巴道转移有关,并且通过两者的协同作用促进了乳腺癌的淋巴道转移.两者在癌组织及癌旁组织淋巴管内皮细胞表达的高低,可以作为数据指标对乳腺癌淋巴道转移的预防和治疗起到一定的指导作用.随着肿瘤的进展,乳腺癌癌旁组织中的淋巴管数量随之增加,可能与乳腺癌的淋巴道转移有关.VEGFR-3在淋巴管内皮细胞的表达具有较高的特异性,可以作为淋巴管内皮细胞的特异性标志物来标志淋巴管.

  4. Effect of vitamin D supplementation in early life on the expression of interleukin-10 and intercellular adhesion molecule-1 in rat asthma model%生命早期补充维生素D对哮喘大鼠白细胞介素10和细胞间黏附分子1表达的影响

    Institute of Scientific and Technical Information of China (English)

    张巧玲; 周小建; 洪建国

    2009-01-01

    目的 研究生命早期补充维生素D对大鼠哮喘模型的影响与机制.方法选用性成熟的雌性Wistar大鼠32只.随机分为4组:对照组、低、中、高剂量组各8只.于受孕第7天起隔天以灌胃的方式给予各组大鼠不同剂量的1,25(OH)_2D_3,对照组以DMSO-PBS代替.子代大鼠离乳后,从每组中随机取出8只制备哮喘模型.HE染色肺组织切片;ELISA法检测血清及肺泡灌洗液(BALF)中IL-10浓度;免疫组化法检测细胞间黏附分子I(ICAM-1)在肺组织中的表达.结果 (1)肺组织病理变化:低剂量组和中剂量组气道炎症和嗜酸性细胞浸润均低于对照组,高剂量组则明显高于对照组.(2)血清及BALF中IL-10浓度:血清中,低剂量组[(30.2±2.8)pg/ml]和中剂量组[(51.5±6.6)pg/ml]IL-10浓度均高于对照组[(18.7±4.7)pg/ml](P0.05);BALF中,与对照组[(59.1±14.4)pg/ml]相比,低剂量组[(58.1±3.4)pg/ml]无显著性变化(P>0.05),中剂量组[(90.0±14.3)pg/ml]IL-10浓度高于对照组(P0.05);中剂量组低于对照组(P0.05], whereas in the high dose group [(45.3±6.5) pg/ml, P0.05). The expression of ICAM-1 was significantly decreased in the medium dose group (P0.05). Conclusion Adequate intervention with 1,25 (OH)_2D_3 in the early life could alleviate the inflammation in the lung tissues, reduces eosinophil cell infiltration in rat asthma model. However, overdose might play a detrimental role. Its mechanism may be associated with the effect of 1,25 (OH)_2D_3 on IL-10 secretion and the expression of ICAM-1.

  5. Experimental Study of Changes of Skin Blister Fluid NPY, IL-12, sICAM-1 and GM-CSF Levels in Patients with Vitiligo in Progressive Stage%白癜风进展期患者皮肤疱液中NPY、sICAM-1、IL-12和GM-CSF水平变化的实验研究

    Institute of Scientific and Technical Information of China (English)

    毕鸣晔; 黄海峰

    2011-01-01

    目的:探讨白癜风病患者的发病、进展与免疫学机制的关系.方法:将确诊为进展期白癜风的80例患者分为寻常型(54例),节段型(26例)组.各以白斑处和非白斑处2组的疱液中的研究指标水平进行比较.疱液NPY和GM-CSF采用RIA;IL-12、sICAM-1水平均采用ELISA.结果:本文测定的患者疱液NPY水平显示,寻常型白癜风患者白斑处与非白斑处无显著差异(P>0.05),节段型白癜风患者白斑处与非白斑处比较则呈显著性差异(P0.05).结论:白癜风病患者的发病及病情进展与疱液NPY、IL-12、sICAM-1和GM-CSF四项指标的变化关系密切,其测定有助于了解其病因及病理学机制.%Objective To explore the significance of changes of skin blister fluid NPY, IL-12, sICAM-1 and GM-CSF levels in patients with vitiligo in progressive stage. Methods 80 patients with vitiligo in progressive stage were divided into two groups (vulgar-is vitiligo groups; n = 54, segmental vitiligo groups: n = 26) Their blister fluid levels of NPY and GM-CSF were determined by radioim-munoassay (RIA ) , and IL-12 and sICAM-1 were determined by enzyme immunoassay . Results The levels of skin blister fluid NPY were definitely higher in vitilignous skin than those in non- vitilignous patches in segmental vitiligo groups (P 0. 05) . The levels of skin blister fluid IL-12,sICAM-1 and GM-CSF were all obviously higher in vitilignous skin than that in non- vitilignous patches in vulgaris vitiligo groups (P 0. 05) . Conclusion The changes of skin blister fluid NPY, IL-12, sICAM-1 and GM-CSF levels in vitilignous skin may be closely related to development of difference type vitiligo patients with vitiligo, determination of 4 indexes might be helpful for studying the pathogenesis and clinical diagnosis of vitiligo.

  6. Serum inflammatory cytokine and adhesion molecule content in patients with coronary heart disease and their value for disease severity diagnosis

    Institute of Scientific and Technical Information of China (English)

    Wei Hu; Li-juan Fu; Jiang-Qiao Hu; Peng Liang; Lin Pi; Gui-Hua Li

    2016-01-01

    Objective:To detect inflammatory cytokine and adhesion molecule content in patients with coronary heart disease and analyze their value for disease severity diagnosis.Methods:A total of 113 patients with coronary heart disease and 107 healthy subjects were included in the study and further divided into mild group (n=40), moderate group (n=52) and severe group (n=21) according to the severity of coronary heart disease. Serum inflammatory cytokine and adhesion molecule content of all subjects were detected, and the value of inflammatory cytokine and adhesion molecule content for judging the severity of coronary heart disease was further analyzed.Results:Serum CRP, TNF-α and YKL-40 levels of coronary heart disease group were higher than those of healthy control group while IL-35 level was lower than that of healthy control group (P<0.05); serum E-selectin, ICAM-1, VCAM-1 and sICAM-1 levels of coronary heart disease group were higher than those of healthy control group (P<0.05); serum CRP, TNF-α, YKL-40, E-selectin, ICAM-1, VCAM-1 and sICAM-1 levels of mild group were lower than those of moderate group and severe group, IL-35 level was higher than those of moderate group and severe group (P<0.05), and with the aggravation of coronary heart disease, CRP, TNF-α, YKL-40, E-selectin, ICAM-1, VCAM-1 and sICAM-1 levels increased while IL-35 level decreased (P<0.05).Conclusions: Serum inflammatory cytokine and adhesion molecule content change significantly in patients with coronary heart disease, are directly correlated with the severity of coronary heart disease and can be used as the reliable means to assess the condition and prognosis of patients with coronary heart disease.

  7. Postprandial lipaemia and endothelial adhesion molecules in preand postmenopausal Spanish women Lipemia postprandial y moléculas de adhesión endotelial en mujeres españolas premenopáusicas y postmenopáusicas

    Directory of Open Access Journals (Sweden)

    S. Schoppen

    2010-04-01

    Full Text Available Background: Postprandial hyperlipaemia is an independent risk factor for atherosclerosis. Objectives: To compare postprandial lipaemia and fasting adhesion molecules levels in healthy young premenopausal(PrW and postmenopausal (PoW Spanish women. Subjects and methods: Twenty healthy PrW and 18 healthy PoW participated in a postprandial 7-hour intervention study. All participants were given a fat-rich standard meal (11.8% saturated, 39.7% monounsaturated, and 6.6% polyunsaturated after a 12 h fast. Blood samples were taken at baseline and at 60, 120, 240, 360 and 420 min after eating. Triacylglycerols (TAG, total cholesterol (Chol, soluble intercellular adhesion molecule-1 (sICAM-1 and soluble vascular adhesion molecule-1 (sVCAM-1 were determined in fasting serum samples and TAG andtotal Chol postprandial levels were measured. Results: Anthropometric data, serum lipid and sICAM-1 presented significant higher values in PoW compared to PrW, but sVCAM-1 did not significantly differ between groups. Postprandial TAG and Chol concentrations in PoW were significantly higher than in PrW (p Introducción: La hiperlipemia postprandial es un factor independiente de riesgo de aterosclerosis. Objetivos: Comparar la lipemia postprandial y concentraciones en ayunas de moléculas de adhesión en mujeres sanas, jóvenes premenopáusicas (PrW y postmenopáusicas (PoW. Sujetos y métodos: 20 PrW y 18 PoW participaron en un estudio de intervención postprandial de 7 horas. Tras 12 horas de ayuno, las participantes tomaron una comida estándar rica en grasa (11,8% saturada, 39,7% monoinsaturada y 6,6% poliinsaturada. Se tomaron muestras de sangre basal y a los 60, 120, 240, 360 y 420 min después de comer. En las muestras en ayunas se determinaron triglicéridos (TAG, colesterol total (Chol, moléculas solubles de adhesión intercelular-1 (sICAM-1 y moléculas solubles de adhesión vascular-1 (sVCAM-1. Asimismo se determinaron TAG y Chol postprandiales. Resultados

  8. 布地奈德直肠给药对远端溃疡性结直肠炎患者P-选择素、ICAM-1表达影响%The impact of topical administration of budesonide on P-selectin, ICAM-1 expression in distal ulcerative colitis or proctitis

    Institute of Scientific and Technical Information of China (English)

    文政伟; 余洁梅; 晏洁影; 陈创杰

    2015-01-01

    [目的]探讨布地奈德直肠给药治疗远端溃疡性结直肠炎患者的临床疗效及对P-选择素、ICAM-1表达影响.[方法]选取我院收治的82例远端溃疡性结直肠炎患者为研究对象,采用随机数字表法分为观察组和对照组各41例,观察组采用布地奈德混悬液保留灌肠,对照组采用地塞米松保留灌肠.比较2组治疗效果、P-选择素(P-sel)、ICAM-1表达水平及免疫组化结果.[结果]观察组治疗疗效明显高于对照组(92.68%vs.80.49%);P-sel、ICAM-1明显低于对照组[(18.65+3.12) vs.(24.34+4.05),(230.12+16.45)vs.(286.65+20.14)]ng/L;P-sel(++)表达强度明显低于对照组.[结论]布地奈德直肠给药有助于下调组织中黏附分子P-sel、ICAM-1表达水平,缓解炎症反应,提高治疗效果.

  9. Graves病患者血清IL-4、IL-12、IL-13及ICAM-1、CRP、TNF-α水平变化研究%The study of the level changes on the serum IL-4,IL-12,IL-13 and ICAM-1,CRP,TNF-α in the patients with Graves disease

    Institute of Scientific and Technical Information of China (English)

    王晓书

    2010-01-01

    目的 探讨Graves病患者血清IL-4、IL-12、IL-13及ICAM-1、CRP、TNF-α水平变化规律.方法 选取2008年11月~2010年7月于笔者所在医院进行治疗的60例Graves病患者为研究对象,将其设为观察组,同时选取同期的60名健康人为对照组,对两组人员的血清IL-4、IL-12、IL-13及ICAM-1、CRP、TNF-α水平进行检测及比较.结果 经研究比较发现,观察组的血清IL-4、IL-12、IL-13及ICAM-1、CRP、TNF-α水平均明显高于对照组,同时随着疾病的加重水平也呈现增高趋势,经比较有显著性差异或有非常显著性差异(P<0.05或P<0.01).结论 Graves病患者血清IL-4、IL-12、IL-13及ICAM-1、CRP、TNF-α水平变化对于了解疾病的严重程度及发展转归均有积极的意义.

  10. Immuno-histochemical study of the expression of ICAM-1 in the skin of mice under the effect of exposure to ultra violet rays type-B, before and after topical Retinoic acid

    Directory of Open Access Journals (Sweden)

    Somaya H. Mohamed*, Fouad M. Badr*, Howayda Abed El-Aal,Rushdy W

    2003-12-01

    Full Text Available The exposure to ultraviolet radiations (UVR become a medical problem, not just cosmetics or aesthetic concern, but for their skin photoaging and photodamage. The naturally and synthetic derivatives of vitamin A (Retinoids may have a role in treatment and prophylaxis against skin photodamage. The current work studied the effect of ultraviolet-B rays on the ICAM-1 expression of mice's skin, before and after topical retinoids acid. Thirty-six mice were subjected to ultraviolet-B rays in dose of 1.4J/cm2 for 15minutes every other day for 10weeks. The mice were subdivided into 3 equal groups; Radiated, Prophylactic, Treated, besides the non-exposed skin samples, which considered as control group. The prophylactic mice were subjected to topical Retinoic acid one day before UVR exposure, the mice of treated groups were subjected to topical Retinoic acid after the last UVR exposure 3times weekly for 10weeks. Paraffin sections slides were prepared and stained with Hematoxylin and eosin stains for study the morphology. The immuno-histochemical study for detection of ICAM-1 expression was performed using labeled streptavidin biotin technique (Dako with the monoclonal antibody {ICAM-1 (G-5}. The ICAM-1 expression was evaluated as optical density, and the obtained data was statistically analyzed by using student's t-test. The study revealed a clinical signs of photodamaged skin only in radiated group mice. Histologically epidermal thickness associated with keratinocytic atypia, and necrotic cells were observed in radiated group mice. There was a statistically significant increase in the optical density of ICAM-1 expression in radiated and prophylactic groups mice (p<0.001 and p< 0.005 respectively.. The study concluded that retinoic acid given after UVB completely reversed the morphological, histological and ICAM-1 expression changes induced by UVB exposure and retinoic acid given before UVB prevented some of the morphological, histological and ICAM-1

  11. Nonmuscle myosin heavy chain IIA mediates integrin LFA-1 de-adhesion during T lymphocyte migration.

    Science.gov (United States)

    Morin, Nicole A; Oakes, Patrick W; Hyun, Young-Min; Lee, Dooyoung; Chin, Y Eugene; Chin, Eugene Y; King, Michael R; Springer, Timothy A; Shimaoka, Motomu; Tang, Jay X; Reichner, Jonathan S; Kim, Minsoo

    2008-01-21

    Precise spatial and temporal regulation of cell adhesion and de-adhesion is critical for dynamic lymphocyte migration. Although a great deal of information has been learned about integrin lymphocyte function-associated antigen (LFA)-1 adhesion, the mechanism that regulates efficient LFA-1 de-adhesion from intercellular adhesion molecule (ICAM)-1 during T lymphocyte migration is unknown. Here, we show that nonmuscle myosin heavy chain IIA (MyH9) is recruited to LFA-1 at the uropod of migrating T lymphocytes, and inhibition of the association of MyH9 with LFA-1 results in extreme uropod elongation, defective tail detachment, and decreased lymphocyte migration on ICAM-1, without affecting LFA-1 activation by chemokine CXCL-12. This defect was reversed by a small molecule antagonist that inhibits both LFA-1 affinity and avidity regulation, but not by an antagonist that inhibits only affinity regulation. Total internal reflection fluorescence microscopy of the contact zone between migrating T lymphocytes and ICAM-1 substrate revealed that inactive LFA-1 is selectively localized to the posterior of polarized T lymphocytes, whereas active LFA-1 is localized to their anterior. Thus, during T lymphocyte migration, uropodal adhesion depends on LFA-1 avidity, where MyH9 serves as a key mechanical link between LFA-1 and the cytoskeleton that is critical for LFA-1 de-adhesion.

  12. CD40-CD40 ligand (CD154) engagement is required but not sufficient for modulating MHC class I, ICAM-1 and Fas expression and proliferation of human non-small cell lung tumors.

    Science.gov (United States)

    Yamada, M; Shiroko, T; Kawaguchi, Y; Sugiyama, Y; Egilmez, N K; Chen, F A; Bankert, R B

    2001-05-15

    To determine the possible functional significance of CD40 expression on human non-small cell lung carcinomas and to assess the potential of CD40 as a therapeutic target, 18 lung tumor cell lines were established from biopsy tissues and were monitored for phenotypic changes on the cell surface and alterations in tumor cell proliferation after the ligation of CD40 with a trimeric fusion protein complex of CD40 ligand (CD40Lt). CD40 cross-linking resulted in up to a 6-fold increase in the surface expression of major histocompatibility complex (MHC) class I, Fas and intracellular adhesion molecule (ICAM)-1 in a subset of tumors expressing the highest levels of CD40. Suppression of tumor proliferation was seen after the ligation of CD40 on CD40Lt-responsive cell lines. The suppression was dose dependent, reversible and resulted from a delay of the tumor cells entering S-phase. No change in the cell phenotype or in proliferation were observed in CD40-negative tumors or in tumors expressing moderate-to-low levels of CD40 after incubation with CD40Lt. CD40-negative tumors transfected with the CD40 gene expressed high levels of CD40 on their surface, but were also unresponsive to CD40Lt cross-linking of CD40. Our data establish that CD40 is required (but not sufficient) for transducing a signal that results in phenotypic changes in human lung tumors and suppression in their proliferation. We conclude that CD40 on non-small cell lung tumors may represent a potential therapeutic target, but only on a subset of the CD40+ tumors.

  13. Adhesion molecules and chemokines: relation to anthropometric, body composition, biochemical and dietary variables

    OpenAIRE

    2014-01-01

    Introduction: Among the inflammatory mediators involved in the pathogenesis of obesity, the cell adhesion molecules P-selectin, E-selectin, VCAM-1, ICAM-1 and the chemokine MCP-1 stand out. They play a crucial role in adherence of cells to endothelial surfaces, in the integrity of the vascular wall and can be modulated by body composition and dietary pattern. Objectives: To describe and discuss the relation of these cell adhesion molecules and chemokines to anthropometric, body composition, d...

  14. Adhesion molecules and chemokines : relation to anthropometric, body composition, biochemical and dietary variables.

    OpenAIRE

    Vieira, Renata Adrielle Lima; Freitas,Renata Nascimento; Volp, Ana Carolina Pinheiro

    2014-01-01

    Introduction: Among the inflammatory mediators involved in the pathogenesis of obesity, the cell adhesion molecules Pselectin, E-selectin, VCAM-1, ICAM-1 and the chemokine MCP-1 stand out. They play a crucial role in adherence of cells to endothelial surfaces, in the integrity of the vascular wall and can be modulated by body composition and dietary pattern. Objectives: To describe and discuss the relation of these cell adhesion molecules and chemokines to anthropometric, body composition, di...

  15. Rhein lysinate inhibits monocyte adhesion to human umbilical vein endothelial cells by blocking p38 signaling pathway.

    Science.gov (United States)

    Lin, Yajun; Zhen, Yongzhan; Liu, Jiang; Wei, Jie; Tu, Ping; Hu, Gang

    2013-11-01

    The objective of this study was to investigate the effect of rhein lysinate (RHL) on monocyte adhesion and its mechanism. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to determine the growth inhibition by drugs. The monocyte chemoattractant protein (MCP)-1 levels were assayed using MCP-1 ELISA. The expression of proteins was detected by Western blotting analysis. The results indicated that RHL inhibited monocyte adhesion in a dose- and time-dependent manner. RHL (<20 μmol/L) and lipopolysaccharide (LPS) had no effect on viability of human umbilical vein endothelial cells. Therefore, 20 μmol/L RHL was selected for this study. RHL inhibited secretion of MCP-1 induced by LPS and expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1. In the meantime, both RHL and p38 inhibitor (SB203580) inhibited phosphorylation of p38 and mitogen-activated protein kinase-activated protein kinase-2 (MAPKAPK-2) and transcription and expression of ICAM-1 and VCAM-1. In conclusion, RHL inhibits the transcription and expression of ICAM-1 and VCAM-1 by the p38/MAPKAPK-2 signaling pathway, and the effect of RHL on transcription and expression of ICAM-1 and VCAM-1 is similar to p38 inhibitor. RHL could be a prophylactic drug for atherosclerosis.

  16. Group a Pfemp1 functional domains bind icam1 and induce cross-reactive and adhesion inhibitory antibodies during malaria infections

    DEFF Research Database (Denmark)

    Bengtsson, A.; Jørgensen, L.; Rask, Thomas Salhøj

    2012-01-01

    The Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) plays an important role in antigenic variation and pathogenesis of malaria. PfEMP1 proteins encoded by group A var genes appear to be involved in the pathogenesis of severe disease and have been suggested as attractive candidates f...

  17. 苍白二陈汤对代谢综合征大鼠血脂水平和主动脉ICAM1表达的影响%Therapeutic Effect of Cangbai Erchen Decoction on Aorta ICAM1 in Metabolic Syndrome Rats

    Institute of Scientific and Technical Information of China (English)

    王志宏; 季旭明; 吴智春; 于华芸

    2013-01-01

    目的:观察健脾燥湿经典方苍白二陈汤对代谢综合征(MS)大鼠主动脉ICAM1表达的影响,探讨其降低动脉粥样硬化风险的可能分子机制.方法:以高糖高脂高盐饲料长期喂饲建立MS大鼠模型.将21只MS大鼠随机分为模型组、西药组和中药组,分别予蒸馏水、洛伐他汀和苍白二陈汤灌胃.4周后,测血脂(TG、TC、LDLc、HDLc和ox-LDL),计算动脉粥样硬化指数(AI),免疫组化法检测主动脉ICAM1表达.结果:与模型组相比,中药组大鼠血清TG、TC、LDLc和ox-LDL水平,AI及主动脉ICAM1表达量(以平均光密度表示)均显著降低(P<0.05).结论:苍白二陈汤可以调节代谢综合征模型大鼠的血脂,降低AI,抑制主动脉ICAM1的表达,具有抗动脉粥样硬化作用.%Objective:To observe the effect of Cangbai Erchen decoction on aorta ICAM1 in metabolic syndrone(MS) rats and the possible mechanism which would reduce risk for atherosclerosis.Method:Models of metabolic syndrome rats were made by feeding high fat,high salt and high glucose diet.Twenty-one MS rats were randomly divided into model group,TCM group and Western medicine group.The TCM group was administered by Cangbai Erchen decoction and the Western medicine group by Lovastatin.Blood lipid levels (TG,TC,LDLc,ox-LDL and HDLc) of the rats were measured,and atherosclerosis index (AI) was calculated,and expression of ICAM in aorta was inspected by immunohistochemistry after four weeks.Result:In TCM group,the levels of TG and TC,AI and the expression of ICAM1 in aorta were significantly lower than those in modle group (P < 0.05).Conclusion:Cangbai Erchen decoction can regulate the blood lipid level in diet-induced MS rats,reduce AI and ox-LDL level,inhibit the expression of ICAM1,and can effectively stop the form of atherosclerosis.

  18. Roles of phosphatidylinositol 3-kinase and NF-kappaB in human cytomegalovirus-mediated monocyte diapedesis and adhesion: strategy for viral persistence.

    Science.gov (United States)

    Smith, M Shane; Bivins-Smith, Elizabeth R; Tilley, A Michael; Bentz, Gretchen L; Chan, Gary; Minard, Jessica; Yurochko, Andrew D

    2007-07-01

    Infected peripheral blood monocytes are proposed to play a key role in the hematogenous dissemination of human cytomegalovirus (HCMV) to tissues, a critical step in the establishment of HCMV persistence and the development of HCMV-associated diseases. We recently provided evidence for a unique strategy involved in viral dissemination: HCMV infection of primary human monocytes promotes their transendothelial migration and differentiation into proinflammatory macrophages permissive for the replication of the original input virus. To decipher the mechanism of hematogenous spread, we focused on the viral dysregulation of early cellular processes involved in transendothelial migration. Here, we present evidence that both phosphatidylinositol 3-kinase [PI(3)K] and NF-kappaB activities were crucial for the HCMV induction of monocyte motility and firm adhesion to endothelial cells. We found that the beta(1) integrins, the beta(2) integrins, intracellular adhesion molecule 1 (ICAM-1), and ICAM-3 were upregulated following HCMV infection and that they played a key role in the firm adhesion of infected monocytes to the endothelium. The viral regulation of adhesion molecule expression is complex, with PI(3)K and NF-kappaB affecting the expression of each adhesion molecule at different stages of the expression cascade. Our data demonstrate key roles for PI(3)K and NF-kappaB signaling in the HCMV-induced cellular changes in monocytes and identify the biological rationale for the activation of these pathways in infected monocytes, which together suggest a mechanism for how HCMV promotes viral spread to and persistence within host organs.

  19. Reduced immunohistochemical expression of adhesion molecules in vitiligo skin biopsies.

    Science.gov (United States)

    Reichert Faria, Adriane; Jung, Juliana Elizabeth; Silva de Castro, Caio César; de Noronha, Lucia

    2017-03-01

    Because defects in adhesion impairment seem to be involved in the etiopathogenesis of vitiligo, this study aimed to compare the immunohistochemical expression of several adhesion molecules in the epidermis of vitiligo and non lesional vitiligo skin. Sixty-six specimens of lesional and non lesional skin from 33 volunteers with vitiligo were evaluated by immunohistochemistry using anti-beta-catenin, anti-E-cadherin, anti-laminin, anti-beta1 integrin, anti-collagen IV, anti-ICAM-1 and anti-VCAM-1 antibodies. Biopsies of vitiligo skin demonstrated a significant reduction in the expression of laminin and integrin. The average value of the immunohistochemically positive reaction area of the vitiligo specimens was 3053.2μm(2), compared with the observed value of 3431.8μm(2) in non vitiligo skin (p=0.003) for laminin. The immuno-positive area was 7174.6μm(2) (vitiligo) and 8966.7μm(2) (non lesional skin) for integrin (p=0.042). A reduction in ICAM-1 and VCAM-1 expression in the basal layer of the epidermis in vitiligo samples was also observed (p=0.001 and pskin. Our results suggest that an impairment in adhesion exists in vitiligo skin, which is supported by the diminished immunohistochemical expression of laminin, beta1 integrin, ICAM-1 and VCAM-1.

  20. 种植窗口期子宫内膜中MMP-9、TIMP-1及ICAM-1的表达与体外受精-胚胎移植妊娠结局的关系%The relationship between expression of MMP-9/TIMP-1 and ICAM-1 in the implantation window and the outcome of In Vitro Fertilization and Embryo Transfer

    Institute of Scientific and Technical Information of China (English)

    盛敏; 任春娥; 韩海艳; 乔鹏云; 姜爱芳; 王桂丽

    2012-01-01

    目的:探讨种植窗口期子宫内膜中MMP-9、TIMP-1和ICAM-1的表达及其与体外受精-胚胎移植妊娠结局的关系.方法:收集40例拟行IVF/ICSI-ET妇女前1周期黄体中期的子宫内膜组织,分别检测妊娠组与非妊娠组中MMP-9、TIMP-1及ICAM-1的表达.结果:与妊娠组相比,非妊娠组中MMP-9、TIMP-1及ICAM-1的表达显著降低,差异有显著性(P<0.05).结论:种植窗口期子宫内膜中MMP-9、TIMP-1及ICAM-1表达降低,影响胚胎的着床,降低妊娠率,可作为预测IVF/ICSI-ET妊娠结局的指标之一.%Objective:To investigate the expression of MMP -9, TIMP - 1 and ICAM - 1 in the planting window of endometrial tissue and the relationship with the pregnancy in IVF. Methods: The midluteal endometrial tissue of the first cycle from 40 women undergoing IVF/ICSI - ET were collected for detecting the expression of MMP - 9, TIMP - 1 and ICAM -1. The women were divided into two groups, pregnancy group and non - pregnant group Re-sults : The expression of MMP - 9, TIMP - 1 and ICAM - 1 in non - pregnant group was lower than that in pregnant group, and there was significant difference between the two groups(P <0. 05) . Conclusion: The lower expression of MMP - 9 , TIMP - 1 and ICAM - 1 in the endometrial tissue of planting window can affect the implantation of em-bryo and cause the failure of the pregnancy in IVF. So the expression of MMP - 9, TIMP - 1 and ICAM - 1 in the endometrial tissue of planting window can be used as one of the indicators of pregnancy in the IVF/ICSL - ET.

  1. Effect of sevoflurane on pulmonary ICAM-1 and TNF-α after acute lung injury induced by endotoxin in rats%七氟烷对内毒素致急性肺损伤鼠肺组织ICAM-1和TNF-α的影响

    Institute of Scientific and Technical Information of China (English)

    孙艳红; 崔湧; 王俊科; 裴凌

    2011-01-01

    目的:考察七氟烷对内毒素致大鼠急性肺损伤肺组织细胞间黏附分子-1(ICAM-1)和肿瘤坏死因子-α(TNF-α)表达的影响.方法:48只雄性Wistar大鼠(200~290 S)随机分为对照组,内毒素组,七氟烷低(1.0 MAC)、高浓度(1.5 MAC)组,每组12只,分别予以股静脉注射生理盐水1.2 mL后机械通气2h,股静脉注射内毒素5 mg· kg-1后机械通气2h,股静脉注射内毒素5 mg·kg-1后机械通气分别吸入1.0,1.5倍肺泡气最低有效浓度(minimal alveolar concentration,MAC)七氟烷2h的处理.处死大鼠,取肺组织,采用免疫组化和RT-PCR法测定ICAM-1和TNF-α的蛋白及mRNA表达水平.结果:与对照组相比,内毒素组ICAM-1和TNF-α的蛋白及mRNA表达水平明显升高(P<0.01或0.05);与内毒素组相比,七氟烷低、高浓度组ICAM-1和TNF-α的蛋白及mRNA表达水平明显降低(P<0.05).结论:吸入1.0或1.5倍MAC的七氟烷2h可下调内毒素所致大鼠急性肺损伤后肺部ICAM-1和TNF-α的蛋白及mRNA表达,在一定程度上减轻了内毒素所致大鼠急性肺损伤的炎性反应.%Objective: To investigate the effect of sevoflurane on pulmonary ICAM-1 and TNF-α after acute lung injury induced by endotoxin in rats. Methods: Forty-eight Wistar rats weighing bewteen 200 to 290 g were randomly divided into four groups as control group, endotoxin group, low-dose sevoflurane group (1.0 MAC) and high-dose sevoflurane group (1.5 MAC) , 12 rats for each group. The rats in the control group were intravenously injected Normal Saline 1.2 mL through femoral vein, while other three active groups were intravenously injected endotoxin 5 mg·kg-1 at the same time. All rats were conducted in mechanical ventilation for 2 hour, in which sevoflurane groups were maintained with sevoflurane 1. 0 MAC ( minimal alveolar concentration, MAC ) in low-dose group and 1.5 MAC in high-dose group, respectively. Then lungs were isolated to detect the levels of protein and mRNA expression of

  2. A subpopulation of large granular von Willebrand Ag negative and CD105 positive endothelial cells, isolated from abdominal aortic aneurysms, overexpress ICAM-1 and Fas antigen.

    Science.gov (United States)

    Páez, Araceli; Archundia, Abel; Méndez Cruz, René; Rodríguez, Emma; López Marure, Rebeca; Masso, Felipe; Aceves, José Luis; Flores, Leopoldo; Montaño, Luis F

    2002-01-01

    The aim of this work was to determine whether there is a pre-established basal condition of the endothelial cells isolated from aortic abdominal aneurysm that might augment immune effector mechanisms and thus provide us an insight into the possible causes of aneurysm rupture. Endothelial cells isolated from saccular aortic aneurysm fragments were analyzed by cytofluorometry for the expression of different immune response-related molecules. Our results showed that there is a subpopulation of granule-rich, CD105 positive and von Willebrand antigen negative endothelial cells that have an enhanced basal expression of ICAM-1, and Fas antigen, but, interestingly, no apoptotic bodies were detected. Control endothelial cells derived from healthy areas of the same abdominal aortas did not show such enhanced expression. We conclude that in the endothelium that lines abdominal aorta aneurysms there is, at least, one endothelial cell subpopulation with an apparent inhibition of programmed cell death and in a proinflammatory activation status.

  3. 沙鼠脑缺血再灌注损伤后细胞间黏附分子1及降钙素基因相关肽变化与阿司匹林的干预效应%Effect of aspirin on the expressions of intercellular adhesion molecule 1 and calcitonin-gene-related peptide in gerbils with ischemic reperfusion injury

    Institute of Scientific and Technical Information of China (English)

    刘爽; 李义召; 张涛

    2006-01-01

    carotid artery was not occluded; IRI group: The unfolded bilateral carotid artery was occluded by bulldog clamp for 7 minutes, and then the blood circulation was recovered by removing the clamp. Aspirin group: Before the operation,50 mg/kg enteric-coated aspirin was infused via gastric canal. And the same procedures as IRI group were performed. The gastric infusion of aspirin was given daily until the gerbils were executed at 24 hours, 3 days and 7 days after IRI for brain tissue examinations. The immunohistochemistry SABC method was applied to detect the changes of ICAM 1 and CGRP expressions as well as the influence of aspirin on the two.MAIN OUTCOME MEASURES: The expressions of ICAM and CGRP in brain tissues.RESULTS: A total of 63 gerbils were involved in the result analysis.①Changes of ICAM expression: In IRI group, the expression of ICAM began to increase at 24 hours after IRI,enhanced remarkably at 3 days and maintained at high levels at 7 days,with the significant difference compared with sham group [IRI group: (3.36±2.26)%, (5.68±3.13)%, (4.98±2.10)%; Sham group: (1.53±1.07)%, (1.56±1.23)%, (1.62±1.33)%, P < 0.05];However,the ICAM expression was significantly lower in aspirin group than in IRI group at different time points [(0.96±0.83)%, (2.76±2.10)%,(1.96±1.09)%, P < 0.05].②Changes of CGRP expression: At the different time points after IRI,the CGRP expression was weakly positive in IRI group [(3.12±2.26)%, (2.68±2.04)%, (2.57±1.97)%], but strongly positive in aspirin group [(4.98±2.47)%, (5.97±2.35)%, (6.04±2.40)%].CONCLUSION: IRI can increase the ICAM 1 expression while inhibit the CGRP expression; Aspirin can make great impacts on brain protection by inhibiting ICAM 1 expression and reinforcing the CGRP expression.

  4. 电针对OLETF大鼠sICAM-1、sVCAM-1及PAI-1表达的影响%Effect of Electroacupuncture on Plasma Levels of sICAM-1, sVCAM-1 and PAI-1 in OLETF Rats

    Institute of Scientific and Technical Information of China (English)

    蓝丹纯; 易玮; 许能贵; 孙健; 陈婧; 李知行; 张弘弢

    2016-01-01

    目的:探讨电针对自发性胰岛素抵抗模型大鼠血浆中细胞间黏附分子(sICAM-1)及血管间黏附分子(sVCAM-1)、纤溶酶原激活物抑制物-1(PAI-1)的影响.方法:以8只雄性LETO大鼠(Long-Evans Tokushima rats)作为空白组,将16只雄性OLETF大鼠(Otsuka Long-Evans Tokushima Fatty rats)随机分为两组,即电针组及模型组,每组8只.空白组及模型组进行正常饲养,不给予其他处理.电针组针刺双侧内关、三阴交、足三里及肾俞,并予双侧足三里及三阴交加电.1次/d,每次20 min,持续4周.治疗结束后,禁食12 h,次晨眼眶静脉窦采血.检测各组大鼠空腹血糖(FPG)、空腹胰岛素(FINS)、sICAM-1及sVCAM-1、PAI-1.HE染色观察主动脉病理变化.结果:模型组的FPG、FINS、HOMA-IR、C-P及sICAM-1、sVCAM-1、PAI-1水平相比空白组显著升高(P<0.01).电针组的FPG、FINS和HOMA-IR与空白组相比,差异无统计学意义(P>0.05).电针组的FPG、FINS、C-P及sICAM-1、sVCAM-1及PAI-1水平较模型组显著降低(P<0.01).HOMA-IR与大鼠血浆sICAM-1、sVCAM-1及PAI-1均成正相关关系.光镜显示,电针干预能总体病理损伤有不同程度的改善.结论:电针能改善胰岛素抵抗水平,控制血浆中过高的sICAM-1、sVCAM-1及PAI-1水平,对糖尿病血管并发症的防治有良性作用.

  5. Inhibitory effects of muscone on PMNs adherence to HUVEC and the expression of ICAM-1,VCAM-1 and CD44 of HUVEC%麝香酮抑制血管内皮细胞与中性粒细胞黏附及其表面ICAM-1、VCAM-1和CD44表达

    Institute of Scientific and Technical Information of China (English)

    何秀娟; 李萍; 邱全瑛; 盛巡; 王芳; 娄金丽

    2006-01-01

    目的:从中性粒细胞与血管内皮细胞黏附的角度探讨麝香对创伤愈合的作用基础.方法:以TNF处理体外培养的人脐静脉内皮细胞(HUVEC)为模型,应用MTT法、虎红法、荧光免疫组化法研究麝香酮对人外周血中性粒细胞(PMN)与HUVEC黏附及HUVEC表面黏附分子表达的影响.结果:TNF处理HUVEC 12小时,能明显增强PMN与HUVEC黏附(P<0.01),并能明显促进HUVEC表面ICAM-1、VCAM-1和CD44表达(P<0.05).75~150 μg/ml麝香酮作用于TNF活化的HUVEC,明显抑制PMN与HUVEC黏附(P<0.01),仅150 μg/ml时降低HUVEC表面ICAM-1表达(P<0.05),37.5 μg/ml和150 μg/ml时减少其表面VCAM-1表达(P<0.05),75~150 μg/ml时抑制其表面CD44表达(P<0.05或P<0.01).结论:麝香酮通过降低HUVEC表面ICAM-1、VCAM-1和CD44表达而抑制中性粒细胞与血管内皮细胞黏附,可能是麝香促进慢性创面愈合的机制之一.

  6. Altered Clathrin-Independent Endocytosis in Type A Niemann-Pick Disease Cells and Rescue by ICAM-1-Targeted Enzyme Delivery.

    Science.gov (United States)

    Rappaport, Jeff; Manthe, Rachel L; Garnacho, Carmen; Muro, Silvia

    2015-05-04

    Pharmaceutical intervention often requires therapeutics and/or their carriers to enter cells via endocytosis. Therefore, endocytic aberrancies resulting from disease represent a key, yet often overlooked, parameter in designing therapeutic strategies. In the case of lysosomal storage diseases (LSDs), characterized by lysosomal accumulation of undegraded substances, common clinical interventions rely on endocytosis of recombinant enzymes. However, the lysosomal defect in these diseases can affect endocytosis, as we recently demonstrated for clathrin-mediated uptake in patient fibroblasts with type A Niemann-Pick disease (NPD), a disorder characterized by acid sphingomylinase (ASM) deficiency and subsequent sphingomyelin storage. Using similar cells, we have examined if this is also the case for clathrin-independent pathways, including caveolae-mediated endocytosis and macropinocytosis. We observed impaired caveolin-1 enrichment at ligand-binding sites in NPD relative to wild type fibroblasts, corresponding with altered uptake of ligands and fluid-phase markers by both pathways. Similarly, aberrant lysosomal storage of sphingomyelin induced by pharmacological means also diminished uptake. Partial degradation of the lysosomal storage by untargeted recombinant ASM led to partial uptake enhancement, whereas both parameters were restored to wild type levels by ASM delivery using model polymer nanocarriers specifically targeted to intercellular adhesion molecule-1. Carriers also restored caveolin-1 enrichment at ligand-binding sites and uptake through the caveolar and macropinocytic routes. These results demonstrate a link between lysosomal storage in NPD and alterations in clathrin-independent endocytosis, which could apply to other LSDs. Hence, this study shall guide the design of therapeutic approaches using viable endocytic pathways.

  7. Novel strategies for the treatment of inflammatory bowel disease: Selective inhibition of cytokines and adhesion molecules

    Institute of Scientific and Technical Information of China (English)

    Kazuhiko Nakamura; Kuniomi Honda; Takahiro Mizutani; Hirotada Akiho; Naohiko Harada

    2006-01-01

    The etiology of inflammatory bowel disease (IBD) has not yet been clarified and immunosuppressive agents which non-specifically reduce inflammation and immunity have been used in the conventional therapies for IBD. Evidence indicates that a dysregulation of mucosal immunity in the gut of IBD causes an overproduction of inflammatory cytokines and trafficking of effector leukocytes into the bowel, thus leading to an uncontrolled intestinal inflammation. Such recent advances in the understanding of the pathogenesis of IBD created a recent trend of novel biological therapies which specifically inhibit the molecules involved in the inflammatory cascade. Major targets for such treatment are inflammatory cytokines and their receptors, and adhesion molecules. A chimeric anti-TNF-α monoclonal antibody, infliximab, has become a standard therapy for CD and it is also likely to be beneficial for UC. Several anti-TNF reagents have been developed but most of them seem to not be as efficacious as infliximab. A humanized anti-TNF monoclonal antibody, adalimumab may be useful for the treatment of patients who lost responsiveness or developed intolerance to infliximab.Antibodies against IL-12 p40 and IL-6 receptor could be alternative new anti-cytokine therapies for IBD. Antiinterferon-γ and anti-CD25 therapies were developed,but the benefit of these agents has not yet been established. The selective blocking of migration of leukocytes into intestine seems to be a nice approach.Antibodies against α4 integrin and α4β7 integrin showed benefit for IBD. Antisense oligonucleotide of intercellular adhesion molecule 1 (ICAM-1) may be efficacious for IBD. Clinical trials of such compounds have been either recently reported or are currently underway. In this article, we review the efficacy and safety of such novel biological therapies for IBD.

  8. Papel de las moléculas de adhesión ICAM-1 Y LFA-1 en la patogénesis de la Paracoccidioidomicosis pulmonar experimental

    Directory of Open Access Journals (Sweden)

    Luz Elena Cano

    2000-02-01

    Full Text Available

    Introducción: La Paracoccidioidomicosis (PCM, micosis sistémica común en América Latina, es una enfermedad crónica progresiva, causada por la inhalación de las conidias del hongo dimórfico térmico Paracoccidiodes brasiliensis (Pb. La infección pulmonar inicial se caracteriza por una importante respuesta inflamatoria aguda, posteriormente se observa una respuesta inflamatoria crónica y finalmente se desencadena un proceso fibrótico, secuela que se presenta en el 60 - 80 % de los pacientes. El proceso de adhesión de los leucocitos al endotelio se considera un evento temprano y es requisito indispensable para que se produzca la respuesta inflamatoria. Este proceso de adherencia es mediado por moléculas de adhesión como la molécula de adhesión intercelular-1 (ICAM-1 presente en el endotelio que se une a una b-2 integrina presente en el leucocito (LFA-1. Dichas moléculas no solo son necesarias para la adhesión de los leucocitos sino también, para su migración y activación. Su importancia ha sido demostrada en otras micosis como la candidiasis, criptococosis, aspergilosis y pneumocistosis. El objetivo del presente estudio es evaluar la expresión a nivel pulmonar de ICAM-1 y LFA-1 en un modelo murino de PCM experimental, establecer su relación con la respuesta inflamatoria observada y determinar el papel que jugarían estas moléculas en la patogénesis de la micosis.

    Metodología: se utilizan ratones machos isogénicos BALB/c de 6 semanas de edad, los cuales son inoculados intranasalmente (i.n. con 4 x 10

  9. Mast cells play a key role in Th2 cytokine-dependent asthma model through production of adhesion molecules by liberation of TNF-α.

    Science.gov (United States)

    Chai, Ok Hee; Han, Eui-Hyeog; Lee, Hern-Ku; Song, Chang Ho

    2011-01-31

    Mast cells are well recognized as key cells in allergic reactions, such as asthma and allergic airway diseases. However, the effects of mast cells and TNF-α on T-helper type 2 (Th2) cytokine-dependent asthma are not clearly understood. Therefore, an aim of this study was to investigate the role of mast cells on Th2 cytokine-dependent airway hyperresponsiveness and inflammation. We used genetically mast cell-deficient WBB6F1/J-Kitw/Kitw-v (W/Wv), congenic normal WBB6F1/J-Kit+/Kit+ (+/+), and mast cell-reconstituted W/Wv mouse models of allergic asthma to investigate the role of mast cells in Th2 cytokine-dependent asthma induced by ovalbumin (OVA). And we investigated whether the intratracheal injection of TNF-α directly induce the expression of ICAM-1 and VCAM-1 in W/Wv mice. This study, with OVA-sensitized and OVA-challenged mice, revealed the following typical histopathologic features of allergic diseases: increased inflammatory cells of the airway, airway hyperresponsiveness, and increased levels of TNF-α, intercellular adhesion molecule (ICAM)-1, and vascular cellular adhesion molecule (VCAM)-1. However, the histopathologic features and levels of ICAM-1 and VCAM-1 proteins in W/Wv mice after OVA challenges were significantly inhibited. Moreover, mast cell-reconstituted W/Wv mice showed restoration of histopathologic features and recovery of ICAM-1 and VCAM-1 protein levels that were similar to those found in +/+ mice. Intratracheal administration of TNF-α resulted in increased ICAM-1 and VCAM-1 protein levels in W/Wv mice. These results suggest that mast cells play a key role in a Th2 cytokine-dependent asthma model through production of adhesion molecules, including ICAM-1 and VCAM-1, by liberation of TNF-α.

  10. Effects of N2 O on the content of FHb and ICAM-1 in HIFU treatment patients%氧化亚氮对HIFU治疗患者FHb及ICAM-1含量的影响

    Institute of Scientific and Technical Information of China (English)

    陈佳; 但伶; 田泽丹; 黄燕; 周瑜; 张昭莉

    2014-01-01

    Objective To observe the effect of nitrous oxide (N2O) on the content of serum free hemoglobin ,and intercellular adhesion molecule‐1 (ICAM‐1) of patients with HIFU Therapy ,and investigate its action of tissue damage mechanism .Methods 50 patients with primary liver cancer undergoing HIFU surgery (ASA Ⅰ - Ⅱ class) were randomly divided into control group (group C) and experimental group(group N) ,25 patients of each group .General anesthesia method was used in both two groups , group C was by total intravenous anesthesia ,group N was adopted intravenous‐inhalation anesthesia .both two groups was adopted the same anesthesia induction method .anesthesia maintain of group N was joined N2 O on the basis of group C .both two groups were draw blood from the radial artery at the points of before anesthesia (T1 ) ,before operation (T2 ) ,1 h (T3 ) ,2 h (T4 ) ,3 h (T5 ) after intraoperative ,and 24 h after operation (T6 ) ,peroxidase reaction test and double antibody sandwich ELISA method were a‐dopted to detect the content of Fhb value and ICAM‐1 ;ultrasonography system of HIFU therapeutic instrument was used to meas‐ure the abdominal wall thickness of patients before and after operation .Results The content of FHb and ICAM‐1 in serum were significantly increased after operation than before with the anesthesia time (P<0 .05);compared with group C ,group N increased obviously at the same point in time (P<0 .05);preoperative and postoperative abdominal wall thickness value of group N was in‐creased significantly (P< 0 .05) .Conclusion It may be connected with N2 O enhanced ultrasound cavitation effect that the body produces more FHb and ICAM‐1 of group N in HIFU treatment ,and induces abdominal wall skin markedly swollen .%目的:观察氧化亚氮(N2O)对高强度聚焦超声(HIFU)治疗患者血清游离血红蛋白(FHb)及细胞间黏附分子1(ICAM‐1)含量的影响,探讨其组织损伤的作用机制。方法将50

  11. Cytokine-Induced Cell Surface Expression of Adhesion Molecules in Vascular Endothelial Cells In vitro

    Institute of Scientific and Technical Information of China (English)

    陈红辉; 刘昌勤; 孙圣刚; 梅元武; 童萼塘

    2001-01-01

    Regulation of the adhesion molecules expression by cytokine in vascular endothelial cells was investigated. Human umbilical vein endothelial cells (HUVEC) were stimulated with cytokines, TNF-α (1-250 U/ml) or IL-1β (0.1-50 U/ml) for 24 h. HUVEC were also cultured with cytokines, TNF-α (100 U/ml) or IL-1β (10 U/ml), for 4-72 h, cell surface expression of adhesion molecules (ICAM-1 and VCAM-1) were detected and quantitated by immunocytochemical methods and computerized imaging analysis technique. Adhesion molecules expression were up-regulated by TNF-α, IL-1β in a concentration- and time-dependent manner. Some significant differences were observed between the effects of cytokines on the ICAM-1 and on VCAM-1 expression. Cytokines might directly induce the expression of ICAM-1 and VCAM-1 in vascular endothelial cells. Our observations indicate differential functions of the two adhesion molecules during the evolution of inflammatory responses in stroke.

  12. EXPRESSION OF INTERCELLULAR ADHESION MOLECULE IN LUNG TISSUES OF EXPERIMENTAL ACUTE LUNG INJURY AND THE AFFECT OF RHUBARB ON IT

    Institute of Scientific and Technical Information of China (English)

    李春盛; 桂培春; 何新华

    2000-01-01

    Objeaive. To approach the relation and the possible mechanism between the expression of intercellular adhesion molecule (ICAM-1) mRNA and acute lung injury (ALI) and the mechanisms of rhubarb in the prevention and treatment of the lung injury. Methods. Lipopolysaeeharide (LPS) was injected into the sublingual vein of male Wistar rats to perform ALI animal model. The rats were divided into 4 groups: LPS group, control group, rhubarb group and dexamethasoue group.Macroscopic and histopathological e~aminatiom were performed and biological markers were measured for the lung specimem. The markers included lung wet/dry weight, the rate of neutrophils and protein content in the pulmonary alveolar lavage fluid, pulmonary vascular permeability and pulmonary alveolar permeability index. Molecular hybridization method was used to determine the expression of ICAM-1 mRNA. Results. In the lung tissues, the ICAM-1 mRNA expression was increased in the endothelial cells of pulmonary veins and capillaries, rhubarb and dexamethasone had the action of decreasing the expression. The light reflex value in the gray scale scanning showed that in the comparison between the LPS and the control group, the gray scale value of the lung tissues in ALI was significantly increased, thus the light reflex value was markedly decreased (P < 0.01),demonstrating the expression of ICAM-1 mRNA was increased. In comparison with the LPS group, dexamethasoue and rhubarb emfld decrease the gray scale value of the lung tissue significantly, thus the light reflex value was elevated (P< 0.01, P < 0.05) ; the correslxmding pathologic changes of lung tissues and the biological markers of the lung injury were simifieantlv decreased or ameliorated. Conclusions. The increase of the expression d ICAM-1 mRNA in the lung tissues of ALI plays the roles in ALI.The application of rhubarb and dexamethasone can decrease the expression and ameliorate the lung damage; its mechanism is possibly via the inhibition of ICAM-1 m

  13. EXPRESSION OF INTERCELLULAR ADHESION MOLECULE IN LUNG TISSUES OF EXPERIMENTAL ACUTE LUNG INJURY AND THE AFFECT OF RHUBARB ON IT

    Institute of Scientific and Technical Information of China (English)

    2000-01-01

    Objective. To approach the relation and the possible mechanism between the expression of intercellular adhesion molecule (ICAM-1) mRNA and acute lung injury (ALI) and the mechanisms of rhubarb in the prevention and treatment of the lung injury.Methods. Lipopolysaccharide (LPS) was injected into the sublingual vein of male Wistar rats to perform ALI animal model. The rats were divided into 4 groups: LPS group, control group, rhubarb group and dexamethasone group. Macroscopic and histopathological examinations were performed and biological markers were measured for the lung specimens. The markers included lung wet/dry weight, the rate of neutrophils and protein content in the pulmonary alveolar lavage fluid, pulmonary vascular permeability and pulmonary alveolar permeability index. Molecular hybridization method was used to determine the expression of ICAM-1 mRNA.Results. In the lung tissues, the ICAM-1 mRNA expression was increased in the endothelial cells of pulmonary veins and capillaries, rhubarb and dexamethasone had the action of decreasing the expression. The light reflex value in the gray scale scanning showed that in the comparison between the LPS and the control group, the gray scale value of the lung tissues in ALI was significantly increased, thus the light reflex value was markedly decreased (P<0.01), demonstrating the expression of ICAM-1 mRNA was increased. In comparison with the LPS group, dexamethasone and rhubarb could decrease the gray scale value of the lung tissue significantly, thus the light reflex value was elevated (P<0.01, P<0.05); the corresponding pathologic changes of lung tissues and the biological markers of the lung injury were significantly decreased or ameliorated.Conclusions. The increase of the expression of ICAM-1 mRNA in the lung tissues of ALI plays the roles in ALI. The application of rhubarb and dexamethasone can decrease the expression and ameliorate the lung damage; its mechanism is possibly via the inhibition of ICAM

  14. 宫颈癌及其淋巴转移灶淋巴归巢受体L-selectin、CD44、ICAM-1表达的对比研究

    Institute of Scientific and Technical Information of China (English)

    陈江平; 张凡; 常永霞; 张九鸿; 赵秀芳; 成日青; 舒丽莎

    2009-01-01

    目的 探讨L-selectin、CD44、ICAM-1对宫颈癌淋巴转移的作用.方法 应用免疫组织化学方法 对比检测35例宫颈鳞状细胞癌原发灶及其淋巴转移灶中L-selectin、CD44、ICAM-1的表达.结果 L-selectin淋巴转移灶中阳性率明显低于原发灶(P<0.05);CD44淋巴转移灶中阳性率与原发灶无明显区别(P>0.05);ICAM-1淋巴转移灶中阳性率明显高于原发灶(P<0.01);L-selectin与CD44、L-selectin与ICAM-1在原发灶中表达水平之间存在明显相关(r=0.873 7,P<0.01;r=0.795,P<0.01),CD44、ICAM-1在原发灶中表达水平呈明显负相关(r=-0.658 3,P<0.01);淋巴转移灶中L-selectin、CD44、ICAM-1表达水平之间均不存在相关;L-selectin原发灶与淋巴转移中表达水平之间存在明显相关(r=0.753 4,P<0.01),CD44原发灶与淋巴转移中表达水平之间无明显相关,ICAM-1原发灶与淋巴转移中表达水平之间存在明显负相关(r=-0.536 1,P<0.01).原发灶中L-selectin表达与肿瘤分化、淋巴结转移存在相关(r=0.842 0,P<0.01;r=0.768 9,P<0.01);CD44表达与肿瘤侵犯深度、淋巴结转移之间存在相关(r=0.678 2,P<0.01;r=0.863 4,P<0.01);ICAM-1表达与淋巴结转移存在相关(r=0.654 8,P<0.01).结论 L-selectin、CD44、ICAM-1都与宫颈癌淋巴转移相关,其中L-selectin、CD44在淋巴转移的始动阶段发挥重要作用.

  15. 3,4-oxo-isopropylidene-shikimic acid inhibits adhesion of polyrnorphonuclear leukocyte to TNF-α-induced endothelial cells in vitro

    Institute of Scientific and Technical Information of China (English)

    Yi MA; Jian-ning SUN; Qiu-ping XU; Zi-li YOU; Ya-jian GUO

    2004-01-01

    AIM: To examine the effect of 3,4-oxo-isopropylidene-shikimic acid (ISA) on human polymorphonuclear leukocyte (PMN) adhesion to human umbilical vein endothelial cells (HUVEC) and explore its mechanism. METHODS:Adhesion of PMN to HUVEC was measured by rose bengal staining assay. Cell-ELISA and RT-PCR methods were used to examine the expression of adhesion molecules ICAM-1. Cell viability was detected with MTT assay.RESULTS: ISA (1-100 μmol/L) effectively reduced PMN adhesion to TNF-α-induced HUVEC with the inhibitory rate from 17.2 % to 53.5 %, and exerted no effect on PMN adhesion to normal HUVEC. Adhesion molecule ICAM-1 surface protein and mRNA expression induced by TNF-α(400 kU/L) were significantly inhibited by ISA. In addition, the cell viability of HUVEC was unchanged 48 h after treatment with ISA. CONCLUSION: ISA inhibited TNF-α-stimulated PMN-HUVEC adhesion and expression of ICAM- 1.

  16. Peripheral blood mononuclear cells (PBMCs) from patients with systemic lupus erythematosus me-diate the adhesion of T lymphocytes to endothelial ceils%SLE患者外周血单一核细胞介导T淋巴细胞对血管内皮细胞黏附的实验研究

    Institute of Scientific and Technical Information of China (English)

    杨骥; 储以微; 李明

    2009-01-01

    目的 探讨活动期SLE患者外周血单一核细胞(PBMC)是否介导了T淋巴细胞对血管内皮细胞的黏附.方法 体外培养人脐静脉内皮细胞(HUVEC),活动期SLE PBMC培养上清液预刺激48 h,通过RT-PCR检测PBMC培养上清液诱导HUVEC黏附分子的表达;划痕实验检测PBMC培养上清液诱导内皮细胞运动迁移能力的改变;HUVEC与T细胞共培养,研究PBMC培养上清液预刺激是否影响T细胞对HUVEC的黏附.结果 HUVEC经过活动期SLE PBMC培养上清刺激后,内皮细胞黏附分子ICAM-1mRNA,VCAM-1 mRNA和E-钙黏蛋白mRNA表达明显增加,而IL-17抗体能明显抑制黏附分子的表达.黏附分子表达增加介导了内皮细胞运动能力增加,介导T细胞对内皮细胞的黏附,而IL-17中和抗体能抑制T细胞对内皮细胞的黏附和抑制内皮细胞的运动迁移.结论 活动期SLE PBMC培养上清液可以通过诱导血管内皮细胞黏附分子表达,黏附T细胞,介导狼疮血管炎的发生.%Objective To observe whether peripheral blood mononuclear cells (PBMCs) from patients with active systemic lupus erythematosus (SLE) can induce the adhesion of T lymphocytes to endothelial cells. Methods Sera and PBMCs were obtained from patients with active SLE and normal human controls. PBMCs were cultivated and culture supematants were harvested. Human umbilical vein endothelial cells (HUVECs) were cultured in vitro with or without the presence of the sera or culture super-natants of PBMCs. Some cells were pretreated with the antibody to IL-17 before the treatment with the sera or supematants. After another 48-hour culture, RT-PCR and real-time PCR were used to detect the mRNA expressions of adhesion molecules, including intercellular adhesion moleeule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-cadherin in HUVECs, wound healing assay to estimate the motility of HUVECs. Additionally, T lymphocytes were added to HUVECs 48 hours after stimulation with the sera or

  17. Osteopontin selectively regulates p70S6K/mTOR phosphorylation leading to NF-κB dependent AP-1-mediated ICAM-1 expression in breast cancer cells

    Directory of Open Access Journals (Sweden)

    Kundu Gopal C

    2010-05-01

    Full Text Available Abstract Background Breast cancer is one of the most frequently diagnosed cancer and accounts for over 400,000 deaths each year worldwide. It causes premature death in women, despite progress in early detection, treatment, and advances in understanding the molecular basis of the disease. Therefore, it is important to understand the in depth mechanism of tumor progression and develop new strategies for the treatment of breast cancer. Thus, this study is aimed at gaining an insight into the molecular mechanism by which osteopontin (OPN, a member of SIBLING (Small Integrin Binding LIgand N-linked Glycoprotein family of protein regulates tumor progression through activation of various transcription factors and expression of their downstream effector gene(s in breast cancer. Results In this study, we report that purified native OPN induces ICAM-1 expression in breast cancer cells. The data revealed that OPN induces NF-κB activation and NF-κB dependent ICAM-1 expression. We also observed that OPN-induced NF-κB further controls AP-1 transactivation, suggesting that there is cross talk between NF-κB and AP-1 which is unidirectional towards AP-1 that in turn regulates ICAM-1 expression in these cells. We also delineated the role of mTOR and p70S6 kinase in OPN-induced ICAM-1 expression. The study suggests that inhibition of mTOR by rapamycin augments whereas overexpression of mTOR/p70S6 kinase inhibits OPN-induced ICAM-1 expression. Moreover, overexpression of mTOR inhibits OPN-induced NF-κB and AP-1-DNA binding and transcriptional activity. However, rapamycin further enhanced these OPN-induced effects. We also report that OPN induces p70S6 kinase phosphorylation at Thr-421/Ser-424, but not at Thr-389 or Ser-371 and mTOR phosphorylation at Ser-2448. Overexpression of mTOR has no effect in regulation of OPN-induced phosphorylation of p70S6 kinase at Thr-421/Ser-424. Inhibition of mTOR by rapamycin attenuates Ser-371 phosphorylation but does not have

  18. Effects of Propyl Gallate on Adhesion of Polymorphonuclear Leukocytes to Human Endothelial Cells Induced by Tumor Necrosis Factor Alpha

    Institute of Scientific and Technical Information of China (English)

    JIANG Yue-rong; CHEN Ke-ji; XU Yong-gang; YANG Xiao-hong; YIN Hui-jun

    2009-01-01

    Objective: To investigate the effects of Prowl Gallate (PrG) on cellular adhesion between human umbilical vein endothelial cells (HUVEC) and polymorphonuclear leukocytes (PMN) as well as the expression of intercellular adhesion molecule-1 (ICAM-1, CD54) and E-selectin (CD62E) on the VEC surface. Methods: A human VEC inflammation model was induced by tumor necrosis factor alpha (TNF-α). VECs were pre-incubated with varying concentrations of PrG (0.001-5 mmol/L) or 1‰ DMSO (v:v) or 10 mmol/L acetylsalicylic acid (ASA) for 1 h, and then were stimulated with 10 ng/mL TNF-α for 6 h. Rose bengal vital staining method was used to measure the adherence rate of PMN to VEC, while flow cytometry was used to determine the expression of CD54 and CD62E on the VEC surface. Results: After 6 h of incubation with TNF-α, the adherence of PMN to HUVECs as well as the percentage of fluorescence-positive cells and mean fluorescence intensity (MFI) of surface CD54 and CD62E in HUVECs increased significantly (P0.05). ASA at 10 mmol/L had no obvious effect on the positive rate of CD62E and CD54. Conclusions: High concentrations of PrG (0.1-5 mmol/L) exert its inhibitory effect on cellular adherence of PMN to HUVECs, and its mechanism may be related to inhibiting surface expression of CD54 and CD62E in HUVECs. Its action concentration was lower than that of ASA.

  19. Diagnostic and prognosis assessment values of serum sICAM-1, sVCA-1 and P-selectin detection for the patients with pancreatic carcinoma%sICAM-1、sVCAM-1和P选择素检测对胰腺癌诊断和预后评估的价值

    Institute of Scientific and Technical Information of China (English)

    朱伟; 黄文; 武新颖; 徐纪平; 蔡全才; 李兆申

    2009-01-01

    目的 探讨血清可溶性细胞间黏附分子-1(slCAM-1)、可溶性血管内皮细胞黏附因-1(sVCAM-1)和 P 选择素检测对胰腺癌诊断和预后评估的临床价值.方法 2007年10月-2008年6月收治的胰腺癌患者70例,包括胰头癌45例,胰体、胰尾癌25例;TNM 分期Ⅰ-Ⅱ期34例,Ⅲ-Ⅳ期36例,采用酶联免疫法(ELISA)法测定患者手术前后血清sICAM-1、sVCAM-1和 P 选择素水平,并与30例胰腺良性病变患者进行比较.结果 胰腺癌患者血清sICAM-1、sVCAM-1和 P 选择素水平明显高于胰腺良性病变患者(P0.05).结论 血清sI-CAM-1、sVCAM-1和P选择素水平是胰腺癌诊断和预后判断的敏感性指标,三者联合应用可提高胰腺癌早期诊断的敏感性.

  20. Correlation between the levels of circulating adhesion molecules and atherosclerosis in type-2 diabetic normotensive patients

    Science.gov (United States)

    Vargas-Robles, Hilda; Serrano, Alberto Maceda; Lozano-Nuevo, Jose Juan; Escalante-Acosta, Bruno Alfonso

    2009-01-01

    Endothelial dysfunction is a common feature in type-2 diabetic patients and is associated with inflammation, increased levels of circulating soluble adhesion molecules and atherosclerosis. The aim of this study was to evaluate the relationship between the levels of circulating soluble adhesion molecules and the degree of atherosclerosis in normotensive type-2 diabetic patients. Results: We found significant correlations between ICAM-1 (r = 0.69, p < 0.001 95% IC 0.65 to 0.82) and VCAM-1 (r = 0.4, p < 0.03, 95% IC 0.65 to 0.82) levels and maximal carotid artery intimal-medial thickness, whereas no correlation was observed with E-selectin. Methods: We studied 30 normotensive type-2 diabetic patients in whom VCAM-1, ICAM-1 and E-selectin were measured by ELISA. Additionally, the intimal-medial thickness of both the common and internal carotid arteries was measured (B-mode ultrasound). The levels of circulating adhesion molecules and maximal carotid artery intimal-medial thicknesses were correlated using the Spearman correlation coefficient test. Statistical analysis was performed with ANOVA. Conclusion: Our results suggest that ICAM-1 and VCAM-1 are markers associated, and correlated with the degree of atherosclerosis in normotensive type-2 diabetic patients. PMID:19717975

  1. Evaluation of the association between the common E469K polymorphism in the ICAM-1 gene and diabetic nephropathy among type 1 diabetic patients in GoKinD population

    Directory of Open Access Journals (Sweden)

    Efendic Suad

    2008-05-01

    Full Text Available Abstract Background The ICAM-1 gene is a strong positional and biological candidate for susceptibility to the development of T1D and DN. We have recently demonstrated that SNP rs5498(E469K confers susceptibility to the development of T1D and might be associated with DN in Swedish Caucasians. The present study aimed to further evaluate the association between the ICAM-1 genetic polymorphisms and DN. Methods Two common non-synonymous SNPs, including rs5498(E469K and rs1799969(R241G, in the ICAM-1 gene were genotyped in 662 (312 female/350 male T1D patients with DN and 620 (369/251 without DN. All patients were selected from the GoKinD study. Results Genotype distributions of both SNPs were in Hardy-Weinberg equilibrium but SNP rs5498(E469K had high heterozygous index. In this SNP, the heterozygosity and positivity for the allele G were found to be significantly associated with DN in female T1D patients (P = 0.010, OR = 0.633, CI 95% 0.447–0.895 and P = 0.026, OR = 0.692, CI 95% 0.500–0.958. Furthermore, the female patients without DN carrying three genotypes A/A, A/G and G/G had different cystatin levels (0.79 ± 0.17, 0.81 ± 0.14 and 0.75 ± 0.12 mg/L, P = 0.021. No significant association of SNP rs1799969 (R241G with DN was found. Conclusion The present study provides further evidence that SNP rs5498(E469K in the ICAM-1 gene presents a high heterozygous index and the allele G of this polymorphism may confers the decreased risk susceptibility to the development of DN in female T1D patients among the GoKinD population.

  2. 可溶性细胞间粘附分子-1放免法在三种甲状腺疾病中的初步临床应用%A preliminary clinical application of sICAM-1 RIA in three kinds of thyroid disease

    Institute of Scientific and Technical Information of China (English)

    吕枚; 方佩华; 张志友; 何红鹏; 高硕; 侯秉璋; 郑荣秀; 肖茜; 杨立平

    2002-01-01

    目的目前,国内外尚未见有关可溶性细胞间粘附分子-1(sICAM-1)放免法 (RIA)的报道,为此用本室研制的125Ⅰ-sICAM-1 RIA,检测正常人和三种甲状腺疾病(单纯性甲肿,Graves'病或Hashimoto'病)患者血清sICAM-1水平.方法用125Ⅰ-sICAM-1 RIA,检测400例正常人以及1020例患有单纯性甲状腺肿、Graves'病或者Hashimoto'病患者血清sICAM-1水平.结果正常组sICAM-1水平(±s)为:168.43±36.23 μg/L.正常组与单纯性甲肿组间无显著性差别(P>0.05),而自身免疫性甲状腺疾病(Graves'病和Hashimoto' 病)均分别明显高于正常组或单纯性甲肿组(P<0.05).三种治疗均可降低Graves' 病患者血清sICAM-1水平(P<0.05).药物治疗后甲状腺功能恢复正常的Graves'病组 sICAM-1水平明显低于Graves'病停药复发组(P<0.05).结论 125Ⅰ-sICAM-1 RIA可用于检测自身免疫性甲状腺疾病;血清sICAM-1水平可作为自身免疫性甲状腺疾病诊断的一个指标,及在评价Graves'病的疗效、停药或者复发等方面的一个指标.%Objective To examine serum levels of sICAM-1 from normal controls and patients with thyroid diseases (simple goitre, Graves' disease or Hashimoto'sthyroiditis) with 125Ⅰ-sICAM-1 RIA established in our lab.Methods Using 125Ⅰ-sICAM-1 RIA, serum sICAM-1 levels of 400 healthy in dividuals as the normal group and 1020 patients with simple goitre (SG), Graves' disease (GD) or Hashimoto's thyroiditis (HT) were examined for a comporative chinical study.Conclusions sICAM-1 RIA can be used to examine autoimmune thyroid diseases. Serum levels of sICAM-1 can be used as a parameter in diagnosing autoimmune thyroid disease and in evaluating the effects of therapy, drug administration or relapse in GD.

  3. Air Pollution, Obesity, Genes, and Cellular Adhesion Molecules

    Science.gov (United States)

    Madrigano, Jaime; Baccarelli, Andrea; Wright, Robert O.; Suh, Helen; Sparrow, David; Vokonas, Pantel S.; Schwartz, Joel

    2011-01-01

    Objectives Particulate matter (PM) has been associated with acute cardiovascular outcomes, but our understanding of the mechanism is incomplete. We examined the association between PM and cell adhesion molecules. We also investigated the modifying effect of genotype and phenotype variation to gain insight into the relevant biological pathways for this association. Methods We used mixed regression models to examine the association of PM2.5 and black carbon (BC) with serum concentrations of soluble Intercellular Adhesion Molecule (sICAM-1) and soluble Vascular Cell Adhesion Molecule (sVCAM-1), markers of endothelial function and inflammation, in a longitudinal study of 809 participants in the Normative Aging Study (1819 total observations). We also examined whether this association was modified by genotype, obesity, or diabetes status. Genes selected for analyses were either related to oxidative stress, endothelial function, lipid metabolism or metal processing. Results BC during the 2 days prior to blood draw was significantly associated with increased sVCAM-1 (4.5% increase per 1μg/m3 95% CI 1.1, 8.0). Neither pollutant was associated with sICAM-1. Larger effects of BCon sVCAM were seen in subjects with obesity (p=0.007) and who were GSTM1 null (p=0.02). Conclusions BC is associated with markers of endothelial function and inflammation. Genes related to oxidative defense may modify this association. PMID:19884647

  4. Biophysically inspired model for functionalized nanocarrier adhesion to cell surface: roles of protein expression and mechanical factors

    Science.gov (United States)

    Ramakrishnan, N.; Tourdot, Richard W.; Eckmann, David M.; Ayyaswamy, Portonovo S.; Muzykantov, Vladimir R.; Radhakrishnan, Ravi

    2016-06-01

    In order to achieve selective targeting of affinity-ligand coated nanoparticles to the target tissue, it is essential to understand the key mechanisms that govern their capture by the target cell. Next-generation pharmacokinetic (PK) models that systematically account for proteomic and mechanical factors can accelerate the design, validation and translation of targeted nanocarriers (NCs) in the clinic. Towards this objective, we have developed a computational model to delineate the roles played by target protein expression and mechanical factors of the target cell membrane in determining the avidity of functionalized NCs to live cells. Model results show quantitative agreement with in vivo experiments when specific and non-specific contributions to NC binding are taken into account. The specific contributions are accounted for through extensive simulations of multivalent receptor-ligand interactions, membrane mechanics and entropic factors such as membrane undulations and receptor translation. The computed NC avidity is strongly dependent on ligand density, receptor expression, bending mechanics of the target cell membrane, as well as entropic factors associated with the membrane and the receptor motion. Our computational model can predict the in vivo targeting levels of the intracellular adhesion molecule-1 (ICAM1)-coated NCs targeted to the lung, heart, kidney, liver and spleen of mouse, when the contributions due to endothelial capture are accounted for. The effect of other cells (such as monocytes, etc.) do not improve the model predictions at steady state. We demonstrate the predictive utility of our model by predicting partitioning coefficients of functionalized NCs in mice and human tissues and report the statistical accuracy of our model predictions under different scenarios.

  5. The Duffy-Binding-Like β domain (DBLβ) of the Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) variant, PFD1235w, binds ICAM1

    DEFF Research Database (Denmark)

    Andersen, M. A.; Bengtsson, A.; Rask, Thomas Salhøj

    2012-01-01

    Plasmodium falciparum is by far the most virulent human malaria parasite. P. falciparum variant erythrocyte surface antigens, known as PfEMP1, play a crucial role in malaria pathogenesis as they mediate adhesion to host endothelial receptors. The PfEMP1 variant, PFD1235w, encoded by the 3D7 group...

  6. The study of changes and correlation betwee sICAM-1,U-ALB in pregnancy induced hypertension with early renal injury%sICAM-1、U-ALB在妊娠期高血压疾病早期肾损伤中的变化及相关性研究

    Institute of Scientific and Technical Information of China (English)

    张燕; 刘爱敏; 蒋玉红; 山洁; 于春波

    2011-01-01

    目的 探讨妊娠期高血压疾病早期肾损伤中尿微量白蛋白(U-ALB)与可溶性细胞间粘附因子-1水平变化及相关性分析.方法 测定正常妊娠组、妊娠期高血压组U-ALB含量;测定正常未孕组、正常妊娠组、妊娠期高血压组、子痫前期组4组(孕32-35周)sIACM-1值;所测值进行组间比较并对sIACM-1、U-ALB进行相关性分析.结果 妊娠期高血压患者U-ALB阳性率(60.00%)明显高于正常妊娠组(10.00%),P<0.01;sIACM-1正常妊娠组高于未孕组,P<0.05;与正常妊娠组比较,妊娠期高血压组高于正常妊娠组,P<0.05;子痫前期组明显高于正常妊娠组,P<0.01:与妊娠高血压组比较P<0.05.妊娠期高血压组sIACM-1与U-ALB相关性分析,相关系数(r)为0.723;P值<0.01.结论 U-ALB、sIACM-1在妊娠期高血压疾病早期肾损伤中含量明显增高,两者之间呈正相关.%Objective: To investigate the early renal injury in hypertensive disorders in pregnancy in the urine albumin (U -ALB) and soluble intercellular adhesion molecule - 1 levels and correlation analysis. Methods: Determined the normal pregnancy group,gestational hypertension group U - ALB levels; determination of the normal nonpregnant group, normal pregnancy, gestational hypertension, preeclampsia group 4 (32 - 35 weeks gestation) sIACM - 1 value; The measured value of the comparison between groups and sIACM - 1, U - ALB correlation analysis. Results: Gestational hypertension U - ALB - positive rate (60. 00% ) was significantly higher than the normal pregnancy group ( 10. 00% ), P < 0. 01; sIACM - 1 higher than those of normal pregnancy and pregnancy group, P <0. 05; with normal pregnancy compared with gestational hypertension group was higher than the normal pregnancy group, P <0. 05; preeclampsia group were significantly higher than the normal pregnancy group, P <0. 01; and pregnancy induced hypertension group P <0. 05. Gestational hypertension group slACM - 1 and U - ALB correlation

  7. Association of ICAM-1 gene polymorphism with sudden sensorineural hearing loss%细胞粘附分子-1469K/E基因多态性与突发性聋的相关性研究

    Institute of Scientific and Technical Information of China (English)

    张芳; 田广永; 段永畅; 杨静雅; 唐玲

    2015-01-01

    Objective To determine the relationship between the 469K/E polymorphism (rs5498) of the ICAM-1 gene and sudden sensorineural hearing loss. Methods Subjects used in this study were derived from the Third Affiliated Hospital of Southern Medical University. Two milliliters of venous blood were obtained from each participant for genomic DNA extraction. Detection of SNPs rs5498 was performed by polymerase chain reaction (PCR), followed by restriction fragment length polymorphism (RFLP) analysis. The restriction enzyme-digested PCR products were analyzed by 2% agarose gel electrophoresis. The Chi-square test was used to compare the frequency of alleles and genotypes between case and control groups. Results Seven-ty-five SSNHL patients (39 male and 36 female patients) were compared with 165 controls (86 male and 79 female subjects) enrolled in this study from June 2014 to July 2015. No significant differences in ICAM-1 469K/E genotype and allele frequencies were found between the SSNHL group and controls. However, there were significant differences in ICAM-1 469K/E polymorphism between patients with different types of hear-ing loss. Conclusion Our study results do not show significant association between 469K/E polymorphism of the ICAM-1 gene and sudden sensorineural hearing loss. The E allele may influence the susceptibility to the development of flat type of hearing loss.%目的:探讨细胞粘附分子-1(ICAM-1)469K/E基因多态性是否与突发性聋存在相关性。方法按照入选标准共选取了240例研究对象,包括突发性聋患者75例(男39例,女36例),对照者165例(男86,女79例),分别抽取2ml外周静脉血,提取DNA,PCR扩增目的片段,扩增产物经限制性酶切后行琼脂凝胶电泳,以此确定所有研究对象ICAM-1469K/E的基因分型。通过统计分析明确ICAM-1469K/E与突发性聋是否相关。结果两组之间ICAM-1469K/E基因分型及等位基因分布频率差异无统计学意义,

  8. Expression of vascular cell adhesion molecule-1 facilitates angiogenesis in gastric carcinoma

    Institute of Scientific and Technical Information of China (English)

    Yongbin Ding; Tianson Xia; Guoyu Chen; Jianguo Xia

    2006-01-01

    Objective: To investigate the relationship between the expression of VCAM-1 and oncogenesis, tumor angiogenesis and metastasis in gastric carcinoma. Methods: Using RT-PCR and immunohistochemistry technique, the expression of VCAM-1 were detected in specimens from 44 patients with gastric cancer, 8 with ulcer. Microvessel density (MVD) was also counted by endothelial cells immunostained with monoclonal antibodies CD34. In addition, Circulating sVCAM-1 concentrations were measured by an enzyme linked immunosorbent assay. Results:Of 44 gastric cancer tumor tissues, 36were detected the ex pressions of VCAM-1 mRNA. The rates of VCAM-1 mRNA in the primary gastric cancer tissues were significantly higher than those in the para-cancerous tissues and benign ulcer tissues (P < 0.05). The VCAM-1 posithoseive isolates had more lymph node metastases than that of VCAM-l-negative ones (P < 0.05). MVD of positive VCAM-1 expression tissues were higher than those of negative VCAM-1 (P < 0.05). Circulating sVCAM-1 levels decreased significantly after operation (P < 0.05). Furthermore, the levels of sVCAM-1 were positively correlated with the expressions of VCAM-1 in the tumor tissues (r = 0.64, P <0.05). Conclusion: Expressions of VCAM-1 mRNA was closely related to oncogenesis, tumor angiogenesis and metastasis in gastric carcinoma. The concentration of sVCAM-1 may be considered as an effective mark of tumor burden of gastric cancer.

  9. Decrease of breast cancer cell invasiveness by sodium phenylacetate (NaPa) is associated with an increased expression of adhesive molecules.

    Science.gov (United States)

    Vasse, M; Thibout, D; Paysant, J; Legrand, E; Soria, C; Crépin, M

    2001-03-23

    Sodium phenylacetate (NaPa), a non-toxic phenylalanine metabolite, has been shown to induce in vivo and in vitro cytostatic and antiproliferative effects on various cell types. In this work, we analysed the effect of NaPa on the invasiveness of breast cancer cell (MDA-MB-231, MCF-7 and MCF-7 ras). Using the highly invasive breast cancer cell line MDA-MB-231, we demonstrated that an 18-hour incubation with NaPa strongly inhibits the cell invasiveness through Matrigel (86% inhibition at 20 mM of NaPa). As cell invasiveness is greatly influenced by the expression of urokinase (u-PA) and its cell surface receptor (u-PAR) as well as the secretion of matrix metalloproteinases (MMP), we tested the effect of NaPa on these parameters. An 18-hour incubation with NaPa did not modify u-PA expression, either on MDA-MB-231 or on MCF-7 and MCF-7 ras cell lines, and induced a small u-PA decrease after 3 days of treatment of MDA-MB-321 with NaPa. In contrast, an 18 h incubation of MDA-MB-231 increased the expression of u-PAR and the secretion of MMP-9. As u-PAR is a ligand for vitronectin, a composant of the extracellular matrix, these data could explain the increased adhesion of MDA-MB-231 to vitronectin, while cell adhesivity of MCF-7 and MCF-7 ras was unmodified by NaPa treatment. NaPa induced also an increased expression of both Lymphocyte Function-Associated-1 (LFA-1) and Intercellular Adhesion Molecule-1 (ICAM-1), which was obvious from 18 hour incubation with NaPa for the MDA-MB-231 cells, but was delayed (3 days) for MCF-7 and MCF-7 ras. Only neutralizing antibodies against LFA-1 reversed the decreased invasiveness of NaPa-treated cells. Therefore we can conclude that the strong inhibition of MDA-MB-231 invasiveness is not due to a decrease in proteases involved in