Helicobacter pylori coinfection is a confounder, modulating mucosal inflammation in oral submucous fibrosis

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Rajendran R

2009-01-01

Full Text Available The oral cavity has been considered a potential reservoir for Helicobacter pylori (H pylori , from where the organism causes recurrent gastric infections. Aim: With this case-control study we tried to evaluate the role of H pylori in the etiology of mucosal inflammation, a condition that compounds the morbid state associated with oral submucous fibrosis (OSF. Materials and Methods : Subjects ( n = 150 were selected following institutional regulations on sample collection and grouped into test cases and positive and negative controls based on the presence of mucosal fibrosis and inflammation. The negative controls had none of the clinical signs. All patients underwent an oral examination as well as tests to assess oral hygiene/periodontal disease status; a rapid urease test (RUT of plaque samples was also done to estimate the H pylori bacterial load. We used univariate and mutivariate logistic regression for statistical analysis of the data and calculated the odds ratios to assess the risk posed by the different variables. Results : The RUT results differed significantly between the groups, reflecting the variations in the bacterial loads in each category. The test was positive in 52% in the positive controls (where nonspecific inflammation of oral mucosa was seen unassociated with fibrosis, in 46% of the test cases, and in 18% of the negative controls (healthy volunteers (χ2 = 13.887; P < 0.01. A positive correlation was seen between the oral hygiene/periodontal disease indices and RUT reactivity in all the three groups. Conclusions: The contribution of the H pylori in dental plaque to mucosal inflammation and periodontal disease was significant. Logistic regression analysis showed gastrointestinal disease and poor oral hygiene as being the greatest risk factors for bacterial colonization, irrespective of the subject groups. A positive correlation exists between RUT reactivity and the frequency of mucosal inflammation.

Helicobacter pylori infection-induced H3Ser10 phosphorylation in stepwise gastric carcinogenesis and its clinical implications.

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Yang, Tao-Tao; Cao, Na; Zhang, Hai-Hui; Wei, Jian-Bo; Song, Xiao-Xia; Yi, Dong-Min; Chao, Shuai-Heng; Zhang, Li-Da; Kong, Ling-Fei; Han, Shuang-Yin; Yang, Yu-Xiu; Ding, Song-Ze

2018-04-15

Our previous works have demonstrated that Helicobacter pylori (Hp) infection can alter histone H3 serine 10 phosphorylation status in gastric epithelial cells. However, whether Helicobacter pylori-induced histone H3 serine 10 phosphorylation participates in gastric carcinogenesis is unknown. We investigate the expression of histone H3 serine 10 phosphorylation in various stages of gastric disease and explore its clinical implication. Stomach biopsy samples from 129 patients were collected and stained with histone H3 serine 10 phosphorylation, Ki67, and Helicobacter pylori by immunohistochemistry staining, expressed as labeling index. They were categorized into nonatrophic gastritis, chronic atrophic gastritis, intestinal metaplasia, low-grade intraepithelial neoplasia, high-grade intraepithelial neoplasia, and intestinal-type gastric cancer groups. Helicobacter pylori infection was determined by either 13 C-urea breath test or immunohistochemistry staining. In Helicobacter pylori-negative patients, labeling index of histone H3 serine 10 phosphorylation was gradually increased in nonatrophic gastritis, chronic atrophic gastritis, intestinal metaplasia groups, peaked at low-grade intraepithelial neoplasia, and declined in high-grade intraepithelial neoplasia and gastric cancer groups. In Helicobacter pylori-infected patients, labeling index of histone H3 serine 10 phosphorylation followed the similar pattern as above, with increased expression over the corresponding Helicobacter pylori-negative controls except in nonatrophic gastritis patient whose labeling index was decreased when compared with Helicobacter pylori-negative control. Labeling index of Ki67 in Helicobacter pylori-negative groups was higher in gastric cancer than chronic atrophic gastritis and low-grade intraepithelial neoplasia groups, and higher in intestinal metaplasia group compared with chronic atrophic gastritis group. In Helicobacter pylori-positive groups, Ki67 labeling index was increased

Helicobacter pylori-induced IL-33 modulates mast cell responses, benefits bacterial growth, and contributes to gastritis.

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Lv, Yi-Pin; Teng, Yong-Sheng; Mao, Fang-Yuan; Peng, Liu-Sheng; Zhang, Jin-Yu; Cheng, Ping; Liu, Yu-Gang; Kong, Hui; Wang, Ting-Ting; Wu, Xiao-Long; Hao, Chuan-Jie; Chen, Weisan; Yang, Shi-Ming; Zhao, Yong-Liang; Han, Bin; Ma, Qiang; Zou, Quan-Ming; Zhuang, Yuan

2018-04-25

Interleukin (IL)-induced inflammatory responses are critical for the pathogenesis of Helicobacter pylori (H. pylori)-induced gastritis. IL-33 represents a recently discovered proinflammatory cytokine involved in inflammatory diseases, but its relevance to H. pylori-induced gastritis is unknown. Here, we found that gastric IL-33 mRNA and protein expression were elevated in gastric mucosa of both patients and mice infected with H. pylori, which is positively correlated with bacterial load and the degree of gastritis. IL-33 production was promoted via extracellular regulated protein kinases (ERK) signaling pathway activation by gastric epithelial cells in a cagA-dependent manner during H. pylori infection, and resulted in increased inflammation and bacteria burden within the gastric mucosa. Gastric epithelial cell-derived IL-33 promoted TNF-α production from mast cells in vitro, and IL-33 increased TNF-α production in vivo. Increased TNF-α inhibited gastric epithelial cell proliferation, conducing to the progress of H. pylori-associated gastritis and bacteria colonization. This study defined a patent regulatory networks involving H. pylori, gastric epithelial cell, IL-33, mast cell, and TNF-α, which jointly play a pathological effect within the gastric circumstances. It may be a valuable strategy to restrain this IL-33-dependent pathway in the treatment of H. pylori-associated gastritis.

Accumulation of 8-nitroguanine in human gastric epithelium induced by Helicobacter pylori infection

International Nuclear Information System (INIS)

Ma, Ning; Adachi, Yukihiko; Hiraku, Yusuke; Horiki, Noriyuki; Horiike, Shinichirou; Imoto, Ichiro; Pinlaor, Somchai; Murata, Mariko; Semba, Reiji; Kawanishi, Shosuke

2004-01-01

Helicobacter pylori infection causes chronic inflammation, which can lead to gastric carcinoma. A double immunofluorescence labeling study demonstrated that the level of 8-nitroguanine and 8-oxo-7,8-dihydro-2 ' -deoxyguanosine (8-oxodG) apparent in gastric gland epithelium was significantly higher in gastritis patients with H. pylori infection than in those without infection. A significant accumulation of proliferating cell nuclear antigen, a prognostic factor for gastric cancer, was observed in gastric gland epithelial cells in patients with H. pylori infection as compared to those without infection, and its accumulation was closely correlated with the formation of 8-nitroguanine and 8-oxodG. These results suggest that nitrosative and oxidative DNA damage in gastric epithelial cells and their proliferation by H. pylori infection may lead to gastric carcinoma. 8-Nitroguanine could be not only a promising biomarker for inflammation but also a useful indicator of the risk of gastric cancer development in response to chronic H. pylori infection

Chronic infection with Helicobacter pylori does not provoke major systemic inflammation in healthy adults

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Brenner, H; Berg, Gabriele; Fröhlich, M

1999-01-01

It has been suggested that chronic infection with Helicobacter pylori (H. pylori), in particular infection with virulent strains producing the cytotoxin-associated protein CagA, may increase the risk of coronary heart disease by generation of a persistent low-grade inflammatory stimulus. We...... assessed the relation between serological markers of H. pylori infection and various markers of systemic inflammation in a population-based sample of 1834 men and women aged 18-88. A total of 39.3% of the sample had a positive IgG response, and among these a slight majority was CagA positive. Infection...... with H. pylori was unrelated to C-reactive protein and the leukocyte count, regardless of CagA status. There was an inverse relation between H. pylori infection and serum albumin. The adjusted OR (95% CI) of an albumin level in the bottom versus the top third were 2.2 (1.5-3.1) and 2.0 (1...

Inflammation, Immunity, and Vaccines for Helicobacter pylori Infection

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Walduck, Anna; Andersen, Leif P; Raghavan, Sukanya

2015-01-01

studies that contribute with new insights in the host response to H. pylori infection. Also, the adaptive immune response to H. pylori and particularly the role of IL-22 have been addressed in some studies. These advances may improve vaccine development where new strategies have been published. Two major...... studies analyzed H. pylori genomes of 39 worldwide strains and looked at the protein profiles. In addition, multi-epitope vaccines for therapeutic use have been investigated. Studies on different adjuvants and delivery systems have also given us new insights. This review presents articles from the last...... year that reveal detailed insight into immunity and regulation of inflammation, the contribution of immune cells to the development of gastric cancer, and understanding mechanisms of vaccine-induced protection....

How host regulation of Helicobacter pylori-induced gastritis protects against peptic ulcer disease and gastric cancer.

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Dhar, Poshmaal; Ng, Garrett Z; Sutton, Philip

2016-09-01

The bacterial pathogen Helicobacter pylori is the etiological agent of a range of gastrointestinal pathologies including peptic ulcer disease and the major killer, gastric adenocarcinoma. Infection with this bacterium induces a chronic inflammatory response in the gastric mucosa (gastritis). It is this gastritis that, over decades, eventually drives the development of H. pylori-associated disease in some individuals. The majority of studies investigating H. pylori pathogenesis have focused on factors that promote disease development in infected individuals. However, an estimated 85% of those infected with H. pylori remain completely asymptomatic, despite the presence of pathogenic bacteria that drive a chronic gastritis that lasts many decades. This indicates the presence of highly effective regulatory processes in the host that, in most cases, keeps a check on inflammation and protect against disease. In this minireview we discuss such known host factors and how they prevent the development of H. pylori-associated pathologies. Copyright © 2016 the American Physiological Society.

Myeloid HIF-1 is protective in Helicobacter pylori-mediated gastritis.

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Matak, Pavle; Heinis, Mylène; Mathieu, Jacques R R; Corriden, Ross; Cuvellier, Sylvain; Delga, Stéphanie; Mounier, Rémi; Rouquette, Alexandre; Raymond, Josette; Lamarque, Dominique; Emile, Jean-François; Nizet, Victor; Touati, Eliette; Peyssonnaux, Carole

2015-04-01

Helicobacter pylori infection triggers chronic inflammation of the gastric mucosa that may progress to gastric cancer. The hypoxia-inducible factors (HIFs) are the central mediators of cellular adaptation to low oxygen levels (hypoxia), but they have emerged recently as major transcriptional regulators of immunity and inflammation. No studies have investigated whether H. pylori affects HIF signaling in immune cells and a potential role for HIF in H. pylori-mediated gastritis. HIF-1 and HIF-2 expression was examined in human H. pylori-positive gastritis biopsies. Subsequent experiments were performed in naive and polarized bone marrow-derived macrophages from wild-type (WT) and myeloid HIF-1α-null mice (HIF-1(Δmyel)). WT and HIF-1(Δmyel) mice were inoculated with H. pylori by oral gavage and sacrificed 6 mo postinfection. HIF-1 was specifically expressed in macrophages of human H. pylori-positive gastritis biopsies. Macrophage HIF-1 strongly contributed to the induction of proinflammatory genes (IL-6, IL-1β) and inducible NO synthase in response to H. pylori. HIF-2 expression and markers of M2 macrophage differentiation were decreased in response to H. pylori. HIF-1(Δmyel) mice inoculated with H. pylori for 6 mo presented with a similar bacterial colonization than WT mice but, surprisingly, a global increase of inflammation, leading to a worsening of the gastritis, measured by an increased epithelial cell proliferation. In conclusion, myeloid HIF-1 is protective in H. pylori-mediated gastritis, pointing to the complex counterbalancing roles of innate immune and inflammatory phenotypes in driving this pathology. Copyright © 2015 by The American Association of Immunologists, Inc.

Effects of EGFR Inhibitor on Helicobacter pylori Induced Gastric Epithelial Pathology in Vivo

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Philip A. Robinson

2013-10-01

Full Text Available Helicobacter pylori transactivates the Epidermal Growth Factor Receptor (EGFR and predisposes to gastric cancer development in humans and animal models. To examine the importance of EGFR signalling to gastric pathology, this study investigated whether treatment of Mongolian gerbils with a selective EGFR tyrosine kinase inhibitor, EKB-569, altered gastric pathology in chronic H. pylori infection. Gerbils were infected with H. pylori and six weeks later received either EKB-569-supplemented, or control diet, for 32 weeks prior to sacrifice. EKB-569-treated H. pylori-infected gerbils had no difference in H. pylori colonisation or inflammation scores compared to infected animals on control diet, but showed significantly less corpus atrophy, mucous metaplasia and submucosal glandular herniations along with markedly reduced antral and corpus epithelial proliferation to apoptosis ratios. EKB-569-treated infected gerbils had significantly decreased abundance of Cox-2, Adam17 and Egfr gastric transcripts relative to infected animals on control diet. EGFR inhibition by EKB-569 therefore reduced the severity of pre-neoplastic gastric pathology in chronically H. pylori-infected gerbils. EKB-569 increased gastric epithelial apoptosis in H. pylori-infected gerbils which counteracted some of the consequences of increased gastric epithelial cell proliferation. Similar chemopreventative strategies may be useful in humans who are at high risk of developing H.pylori-induced gastric adenocarcinoma.

Epithelial cell kinetics of the gastric mucosa during Helicobacter pylori infection

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Holck, Susanne; Holm, I.L.; Holck, P.P.

2007-01-01

Helicobacter pylori is an important pathogen in major gastroduodenal diseases, including inflammation with ulceration and gastric malignancies. Alterations in H. pylori associated cell turnover in gastric epithelial cells are examined in relation to inflammatory activity, bacteria load and cytoki...

Treatment of helicobacter pylori infection; a controlled randomized comparative clinical trial

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Mehmood, A.; Usmanghani, K.; Mohiuddin, E.; Akram, M.

2010-01-01

Helicobacter pylori induces chronic inflammation of the underlying gastric mucosa and is strongly linked to the development of duodenal and gastric carcinoma. A study was conducted to evaluate the efficacy of Pylorex, a herbal formulation, for treatment of H. pylori infection as compared to triple allopathic therapy (Omeprazole, Amoxicillin, Metronidazole). The therapeutic evaluations of these medicines were conducted on 97 clinically and immunologically diagnosed cases of H. pylori infection. H. pylori was eradicated in 16 (32.6%) out of 49 patients by the use of triple allopathic therapy (Control drugs), and in 9 (18.7%) out of 48 patients by the use of Pylorex (Test drug). Pylorex possesses a therapeutic value for the treatment of H. pylori associated symptoms but the eradication rate is superior in triple allopathic therapy. (author)

II Consenso Brasileiro sobre Helicobacter pylori Second Brazilian Consensus Conference on Helicobacter pylori infection

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Luiz Gonzaga Vaz Coelho

2005-06-01

Full Text Available Avanços significativos ocorridos desde o Primeiro Consenso Brasileiro sobre H. pylori realizado em 1995, em Belo Horizonte, MG, justificam este segundo consenso. O evento foi organizado pela Federação Brasileira de Gastroenterologia e pelo Núcleo Brasileiro para Estudo do Helicobacter, sendo realizado em São Paulo nos dias 19 e 20 de junho de 2004. Contou com a participação das principais autoridades nacionais na área, a partir de lista elaborada pelas duas sociedades organizadoras do evento. Assim, participaram 36 delegados provenientes de 15 estados brasileiros, incluindo gastroenterologistas, patologistas, pediatras e microbiologistas. Os participantes foram alocados em um dos cinco sub-temas a serem contemplados no encontro, a saber: Helicobacter pylori e dispepsia funcional; Helicobacter pylori e AINEs; Helicobacter pylori e doença do refluxo gastroesofágico; tratamento Helicobacter pylori e retratamento Helicobacter pylori. Foi adotado como consensual as decisões que atingissem 70% ou mais de concordância entre os participantes. Os resultados foram apresentados em outubro de 2004 durante sessão especial da VI Semana Brasileira do Aparelho Digestivo, realizada em Recife, PE, e esta publicação apresenta o sumário das principais recomendações e conclusões do evento.Significant progress has been obtained since the First Brazilian Consensus Conference on H. pylori Infection held in 1995, in Belo Horizonte, MG, and justify a second meeting to establish updated guidelines on the current management of H. pylori infection. The Second Brazilian Consensus Conference on H. pylori Infection was organized by the Brazilian Federation of Gastroenterology and Brazilian Nucleus for the Study of Helicobacter and took place on June, 19-20, 2004 in São Paulo, SP. Thirty six delegates coming from 15 different Brazilian states including gastroenterologists, pathologists, microbiologists and pediatricians undertook the meeting. The

Apigenin has anti-atrophic gastritis and anti-gastric cancer progression effects in Helicobacter pylori-infected Mongolian gerbils.

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Kuo, Chao-Hung; Weng, Bi-Chuang; Wu, Chun-Chieh; Yang, Sheau-Fang; Wu, Deng-Chang; Wang, Yuan-Chuen

2014-02-12

Apigenin, one of the most common flavonoids, is abundant in celery, parsley, chamomile, passionflower, and other vegetables and fruits. Celery is recognized as a medicinal vegetable in Oriental countries to traditionally treat inflammation, swelling, blood pressure, serum lipid, and toothache. In this study, we investigated apigenin treatment effects on Helicobacter pylori-induced atrophic gastritis and gastric cancer progression in Mongolian gerbils. Five to eight-week-old Mongolian gerbils were inoculated with Helicobacter pylori for four weeks without (atrophic gastritis group) or with N'-methyl-N'-nitro-N-nitroso-guanidine (MNNG) (gastric cancer group) in drinking water, and were then rested for two weeks. During the 7th-32th (atrophic gastritis group) or the 7th-52th (gastric cancer group) weeks, they were given various doses (0-60 mg/kgbw/day) of apigenin. At the end of the 32th (atrophic gastritis group) or the 52th (atrophic gastritis group) week, all Mongolian gerbils were sacrificed using the CO2 asphyxia method. The histological changes of Helicobacter pylori colonization, neutrophil and monocyte infiltrations, and atrophic gastritis in both atrophic gastritis and gastric cancer Mongolian gerbils were examined using immunohistochemistry stain and Sydney System scoring. Apigenin treatments (30-60 mg/kgbw/day) effectively decreased atrophic gastritis (atrophic gastritis group) and dysplasia/gastric cancer (gastric cancer group) rates in Mongolian gerbils. Apigenin treatment (60 mg/kgbw/day) significantly decreased Helicobacter pylori colonization and Helicobacter pylori-induced histological changes of neutrophil and monocyte infiltrations and atrophic gastritis in both atrophic gastritis and gastric cancer Mongolian gerbils. Apigenin has the remarkable ability to inhibit Helicobacter pylori-induced atrophic gastritis and gastric cancer progression as well as possessing potent anti-gastric cancer activity. Copyright © 2013 Elsevier Ireland Ltd. All rights

Relationship between childhood asthma and Helicobacter pylori infection

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Ying Wu

2016-07-01

Full Text Available Objective: To investigate the correlation between childhood asthma and Helicobacter pylori infection. Methods: A total of 80 children with asthma who were treated in our hospital from May 2012 to May 2015 were selected as the research subjects, and 40 cases of healthy children were selected as control group, the Helicobacter pylori infection of the two groups of patients were compared, the double antibody sandwich enzyme-linked immunosorbent assay was used to detect the serum Helicobacter pylori-IgG, Helicobacter pylori-CagAIgG, IL-4, Helicobacter pylori, IFN-γ and IL-1β, etc., and the correlation between Helicobacter pylori infection and asthma was analyzed. Results: The positive rates of Helicobacter pylori infection in asthma group and children in attack stage were significantly higher than those in control group and children in remission stage (P<0.05. The positive rates of serum Helicobacter pylori-IgG and Helicobacter pylori-CagAIgG in asthma group and children in attack stage were significantly lower than those in control group and children in remission stage (P<0.05. The serum levels of IFN-γ in asthma group and children in attack stage were significantly lower than those in control group and children in remission stage, IL-4 and IL-1β levels in the former were significantly higher than those in the latter (P<0.05. Helicobacter pylori infection positive had significant positive correlation with IL-1β concentration (r=0.75, P<0.05. Conclusions: Helicobacter pylori infection in children has significant positive correlation with the incidence of asthma, suggesting that Helicobacter pylori infection has a certain protective effect on childhood asthma, but persistent Helicobacter pylori infection in children with asthma can aggravate the immune disorder, which is the main reason for the difficulty of treatment of asthma.

Helicobacter pylori infection in patients undergoing appendectomy.

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Pavlidis, T E; Atmatzidis, K S; Papaziogas, B T; Souparis, A; Koutelidakis, I M; Papaziogas, T B

2002-01-01

Helicobacter pylori has been found in the upper gastrointestinal tract; it is incriminated as aetiological factor in various pathological conditions. This prospective study assesses the presence of this microorganism in the appendix flora and the possible role of its infection in the pathogenesis of acute appendicitis. H. pylori was investigated in 46 consecutive patients undergoing emergent appendectomy for presumed acute appendicitis. Blood sample for serological test of H. pylori infection was drawn before operation. The removed appendix specimen was stained for H. pylori; confirmation was made by PCR (Polymerase Chain Reaction) analysis. The intensity of inflammation was determined pathologically grading from no inflammation to gangrenous appendicitis. Statistical analysis was made using the chi-square test. Seropositivity for H. pylori infection was found in 18 patients (39%), but the microbe was detected in just two appendix specimens (4%). In all seropositive patients acute appendicitis was confirmed by the pathology study; serous (33%) and purulent or gangrenous (67%). The latter incidence in the seronegative patients was 50%. There were found eight specimens (17%) negative for inflammation dealing all with seronegative patients. It seems that H. pylori colonizes the appendix in small proportion and is unlikely to be associated in direct correlation with acute appendicitis. However, seropositive patients with acute inflammation are likely to suffer from purulent or gangrenous form.

Epithelial cell kinetics of the gastric mucosa during Helicobacter pylori infection

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Norn, Svend

2007-01-01

Helicobacter pylori is an important pathogen in major gastroduodenal diseases, including inflammation with ulceration and gastric malignancies. Alterations in H. pylori associated cell turnover in gastric epithelial cells are examined in relation to inflammatory activity, bacteria load and cytoki......Helicobacter pylori is an important pathogen in major gastroduodenal diseases, including inflammation with ulceration and gastric malignancies. Alterations in H. pylori associated cell turnover in gastric epithelial cells are examined in relation to inflammatory activity, bacteria load...... and the proliferative marker Ki-67. H. pylori infection, bacteria load and inflammatory activity were associated with increased cell turnover as judged by enhanced activities of TUNEL, p53 and Ki-67. Only p53 was significantly correlated to IFN-γ, IL-8 and IL-10. The H. pylori-positive state was furthermore accompanied...... of the gastrointestinal tract, such studies in cell turnover may provide insights valuable in the investigations of potential precursors of gastric malignancies....

Helicobacter pylori dupA is polymorphic, and its active form induces proinflammatory cytokine secretion by mononuclear cells.

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Hussein, Nawfal R; Argent, Richard H; Marx, Christian K; Patel, Sapna R; Robinson, Karen; Atherton, John C

2010-07-15

Infection with Helicobacter pylori possessing a newly described virulence factor--duodenal ulcer-promoting gene A (dupA)--has been associated with duodenal ulceration and increased gastric inflammation. The dupA locus of 34 strains was sequenced. A panel of dupA mutants was generated and cocultured with human gastric epithelial cells and peripheral blood mononuclear cells; proinflammatory cytokine release was measured. IL8 expression was measured in human gastric biopsy specimens and related to the dupA and cagA status of infecting strains. Most H. pylori strains had a dupA allele that was longer (1884 bp; dupA1) than previously described dupA alleles, although some had truncated versions (dupA2). Unlike the best-characterized H. pylori virulence determinant, the cag pathogenicity island (cag PaI), neither dupA type induced release of interleukin (IL)-8 from gastric epithelial cells. However, infections due to dupA-positive strains were associated with higher-level mucosal IL-8 messenger RNA expression in the human stomach than were infections due to dupA-negative strains. To explain this paradox, we found that dupA1 (but not dupA2 or the cag PaI) substantially increased H. pylori-induced IL-12p40 and IL-12p70 production from CD14(+) mononuclear cells. Other T helper 1-associated cytokines were also modestly induced. We suggest that virulent H. pylori strains cause inflammation by stimulating epithelial cells through cag-encoded proteins and mononuclear inflammatory cells through dupA1 products.

Urease from Helicobacter pylori is inactivated by sulforaphane and other isothiocyanates

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Fahey, Jed W.; Stephenson, Katherine K.; Wade, Kristina L.; Talalay, Paul

2013-01-01

Infections by Helicobacter pylori are very common, causing gastroduodenal inflammation including peptic ulcers, and increasing the risk of gastric neoplasia. The isothiocyanate (ITC) sulforaphane [SF; 1-isothiocyanato-4-(methylsulfinyl)butane] derived from edible crucifers such as broccoli is potently bactericidal against Helicobacter, including antibiotic-resistant strains, suggesting a possible dietary therapy. Gastric H. pylori infections express high urease activity which generates ammonia, neutralizes gastric acidity, and promotes inflammation. The finding that SF inhibits (inactivates) urease (jack bean and Helicobacter) raised the issue of whether these properties might be functionally related. The rates of inactivation of urease activity depend on enzyme and SF concentrations and show first order kinetics. Treatment with SF results in time-dependent increases in the ultraviolet absorption of partially purified Helicobacter urease in the 280–340 nm region. This provides direct spectroscopic evidence for the formation of dithiocarbamates between the ITC group of SF and cysteine thiols of urease. The potencies of inactivation of Helicobacter urease by isothiocyanates structurally related to SF were surprisingly variable. Natural isothiocyanates closely related to SF, previously shown to be bactericidal (berteroin, hirsutin, phenethyl isothiocyanate, alyssin, and erucin), did not inactivate urease activity. Furthermore, SF is bactericidal against both urease positive and negative H. pylori strains. In contrast, some isothiocyanates such as benzoyl-ITC, are very potent urease inactivators, but are not bactericidal. The bactericidal effects of SF and other ITC against Helicobacter are therefore not obligatorily linked to urease inactivation, but may reduce the inflammatory component of Helicobacter infections. PMID:23583386

Persistent colonization of Helicobacter pylori in human gut induces gastroduodenal diseases

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Animesh Sarker

2014-12-01

Full Text Available Helicobacter pylori are gut bacteria colonize in the epithelial cell lining of the stomach and persist there for long du­ration. Around two-thirds of the world’s populations are infected with H. pylori and cause more than 90 percent of ulcers. The development of persistent inflammation is the main cause of chronic gastritis that finally results in a severe consequence known as stomach cancer. Two major virulence factors cytotoxin-associated gene product (cagA and the vacuolating toxin (vacA are mostly investigated as their close association with gastric carcinoma. In this review, host im­munity against H. pylori infection and their evasion mechanism are intensely explored. It is the fact, that understanding pin point molecular mechanisms of any infection is critical to develop novel strategies to prevent pertinent diseases. .J Microbiol Infect Dis 2014; 4(4: 170-176

3rd Brazilian consensus on Helicobacter pylori 3º Consenso Brasileiro para Estudo do Helicobacter pylori

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Luiz Gonzaga Coelho

Full Text Available Significant progress has been obtained since the Second Brazilian Consensus Conference on Helicobacter pylori Infection held in 2004, in São Paulo, SP, Brazil, and justify a third meeting to establish updated guidelines on the current management of H. pylori infection. The Third Brazilian Consensus Conference on H pylori Infection was organized by the Brazilian Nucleus for the Study of Helicobacter, a Department of the Brazilian Federation of Gastroenterology and took place on April 12-15, 2011, in Bento Gonçalves, RS, Brazil. Thirty-one delegates coming from the five Brazilian regions and one international guest, including gastroenterologists, pathologists, epidemiologists, and pediatricians undertook the meeting. The participants were allocated in one of the five main topics of the meeting: H pylori, functional dyspepsia and diagnosis; H pylori and gastric cancer; H pylori and other associated disorders; H pylori treatment and retreatment; and, epidemiology of H pylori infection in Brazil. The results of each subgroup were submitted to a final consensus voting to all participants. Relevant data were presented, and the quality of evidence, strength of recommendation, and level of consensus were graded. Seventy per cent and more votes were considered as acceptance for the final statement. This article presents the main recommendations and conclusions to guide Brazilian doctors involved in the management of H pylori infection.Os avanços significativos ocorridos desde o Segundo Consenso Brasileiro sobre H. pylori realizado em 2004, em São Paulo, justificam este terceiro consenso. O evento foi organizado pelo Núcleo Brasileiro para Estudo do Helicobacter, departamento da Federação Brasileira de Gastroenterologia, tendo sido realizado em Bento Gonçalves, RS, nos dias 12 a 15 de abril de 2011. Contou com a participação de 30 delegados provenientes das cinco regiões brasileiras e um convidado internacional, incluindo gastroenterologistas

Defining the Roles of IFN-γ and IL-17A in Inflammation and Protection against Helicobacter pylori Infection.

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Louise Sjökvist Ottsjö

Full Text Available CD4+ T cells have been shown to be essential for vaccine-induced protection against Helicobacter pylori infection. However, the effector mechanisms leading to reductions in the gastric bacterial loads of vaccinated mice remain unclear. We have investigated the function of IFN-γ and IL-17A for vaccine-induced protection and inflammation (gastritis using IFN-γ-gene-knockout (IFN-γ-/- mice, after sublingual or intragastric immunization with H. pylori lysate antigens and cholera toxin. Bacteria were enumerated in the stomachs of mice and related to the gastritis score and cellular immune responses. We report that sublingually and intragastrically immunized IFN-γ-/- mice had significantly reduced bacterial loads similar to immunized wild-type mice compared to respective unimmunized infection controls. The reduction in bacterial loads in sublingually and intragastrically immunized IFN-γ-/- mice was associated with significantly higher levels of IL-17A in stomach extracts and lower gastritis scores compared with immunized wild-type mice. To study the role of IL-17A for vaccine-induced protection in sublingually immunized IFN-γ-/- mice, IL-17A was neutralized in vivo at the time of infection. Remarkably, the neutralization of IL-17A in sublingually immunized IFN-γ-/- mice completely abolished protection against H. pylori infection and the mild gastritis. In summary, our results suggest that IFN-γ responses in the stomach of sublingually immunized mice promote vaccine-induced gastritis, after infection with H. pylori but that IL-17A primarily functions to reduce the bacterial load.

N-acetylcysteine prevents the development of gastritis induced by Helicobacter pylori infection.

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Jang, Sungil; Bak, Eun-Jung; Cha, Jeong-Heon

2017-05-01

Helicobacter pylori (H. pylori) is a human gastric pathogen, causing various gastric diseases ranging from gastritis to gastric adenocarcinoma. It has been reported that combining N-acetylcysteine (NAC) with conventional antibiotic therapy increases the success rate of H. pylori eradication. We evaluated the effect of NAC itself on the growth and colonization of H. pylori, and development of gastritis, using in vitro liquid culture system and in vivo animal models. H. pylori growth was evaluated in broth culture containing NAC. The H. pylori load and histopathological scores of stomachs were measured in Mongolian gerbils infected with H. pylori strain 7.13, and fed with NAC-containing diet. In liquid culture, NAC inhibited H. pylori growth in a concentration-dependent manner. In the animal model, 3-day administration of NAC after 1 week from infection reduced the H. pylori load; 6-week administration of NAC after 1 week from infection prevented the development of gastritis and reduced H. pylori colonization. However, no reduction in the bacterial load or degree of gastritis was observed with a 6-week administration of NAC following 6-week infection period. Our results indicate that NAC may exert a beneficial effect on reduction of bacterial colonization, and prevents the development of severe inflammation, in people with initial asymptomatic or mild H. pylori infection.

A comparison of Helicobacter pylori and non-Helicobacter pylori Helicobacter spp. Binding to canine gastric mucosa with defined gastric glycophenotype.

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Amorim, Irina; Freitas, Daniela P; Magalhães, Ana; Faria, Fátima; Lopes, Célia; Faustino, Augusto M; Smet, Annemieke; Haesebrouck, Freddy; Reis, Celso A; Gärtner, Fátima

2014-08-01

The gastric mucosa of dogs is often colonized by non-Helicobacter pylori helicobacters (NHPH), while H. pylori is the predominant gastric Helicobacter species in humans. The colonization of the human gastric mucosa by H. pylori is highly dependent on the recognition of host glycan receptors. Our goal was to define the canine gastric mucosa glycophenotype and to evaluate the capacity of different gastric Helicobacter species to adhere to the canine gastric mucosa. The glycosylation profile in body and antral compartments of the canine gastric mucosa, with focus on the expression of histo-blood group antigens was evaluated. The in vitro binding capacity of FITC-labeled H. pylori and NHPH to the canine gastric mucosa was assessed in cases representative of the canine glycosylation pattern. The canine gastric mucosa lacks expression of type 1 Lewis antigens and presents a broad expression of type 2 structures and A antigen, both in the surface and glandular epithelium. Regarding the canine antral mucosa, H. heilmannii s.s. presented the highest adhesion score whereas in the body region the SabA-positive H. pylori strain was the strain that adhered more. The canine gastric mucosa showed a glycosylation profile different from the human gastric mucosa suggesting that alternative glycan receptors may be involved in Helicobacter spp. binding. Helicobacter pylori and NHPH strains differ in their ability to adhere to canine gastric mucosa. Among the NHPH, H. heilmannii s.s. presented the highest adhesion capacity in agreement with its reported colonization of the canine stomach. © 2014 John Wiley & Sons Ltd.

(Nutmeg) on Helicobacter pylori induced gastritis in albino rats

African Journals Online (AJOL)

The anti-Helicobacter pylori (H. pylori) activities of dichloromethane and methanol extracts of Myristica fragrans Houtt. seed (nutmeg) was studied to authenticate ... Analysis of variance (ANOVA) tested the effect of the groups on the treatment days and revealed a significant difference between the treatments at p< 0.05.

Suppressed Gastric Mucosal TGF-β1 Increases Susceptibility to H. pylori-Induced Gastric Inflammation and Ulceration: A Stupid Host Defense Response

Science.gov (United States)

Jo, Yunjeong; Han, Sang Uk; Kim, Yoon Jae; Kim, Ju Hyeon; Kim, Shin Tae; Kim, Seong-Jin

2010-01-01

Background/Aims Loss of transforming growth factor β1 (TGF-β1) exhibits a similar pathology to that seen in a subset of individuals infected with Helicobacter pylori, including propagated gastric inflammation, oxidative stress, and autoimmune features. We thus hypothesized that gastric mucosal TGF-β1 levels could be used to determine the outcome after H. pylori infection. Methods Northern blot for the TGF-β1 transcript, staining of TGF-β1 expression, luciferase reporter assay, and enzyme-linked immunosorbent assay for TGF-β1 levels were performed at different times after H. pylori infection. Results The TGF-β1 level was markedly lower in patients with H. pylori-induced gastritis than in patients with a similar degree of gastritis induced by nonsteroidal anti-inflammatory drugs. There was a significant negative correlation between the severity of inflammation and gastric mucosal TGF-β1 levels. SNU-16 cells showing intact TGF-β signaling exhibited a marked decrease in TGF-β1 expression, whereas SNU-638 cells defective in TGF-β signaling exhibited no such decrease after H. pylori infection. The decreased expressions of TGF-β1 in SNU-16 cells recovered to normal after 24 hr of H. pylori infection, but lasted very spatial times, suggesting that attenuated expression of TGF-β1 is a host defense mechanism to avoid attachment of H. pylori. Conclusions H. pylori infection was associated with depressed gastric mucosal TGF-β1 for up to 24 hr, but this apparent strategy for rescuing cells from H. pylori attachment exacerbated the gastric inflammation. PMID:20479912

Suppressed Gastric Mucosal TGF-beta1 Increases Susceptibility to H. pylori-Induced Gastric Inflammation and Ulceration: A Stupid Host Defense Response.

Science.gov (United States)

Jo, Yunjeong; Han, Sang Uk; Kim, Yoon Jae; Kim, Ju Hyeon; Kim, Shin Tae; Kim, Seong-Jin; Hahm, Ki-Baik

2010-03-01

Loss of transforming growth factor beta1 (TGF-beta1) exhibits a similar pathology to that seen in a subset of individuals infected with Helicobacter pylori, including propagated gastric inflammation, oxidative stress, and autoimmune features. We thus hypothesized that gastric mucosal TGF-beta1 levels could be used to determine the outcome after H. pylori infection. Northern blot for the TGF-beta1 transcript, staining of TGF-beta1 expression, luciferase reporter assay, and enzyme-linked immunosorbent assay for TGF-beta1 levels were performed at different times after H. pylori infection. The TGF-beta1 level was markedly lower in patients with H. pylori-induced gastritis than in patients with a similar degree of gastritis induced by nonsteroidal anti-inflammatory drugs. There was a significant negative correlation between the severity of inflammation and gastric mucosal TGF-beta1 levels. SNU-16 cells showing intact TGF-beta signaling exhibited a marked decrease in TGF-beta1 expression, whereas SNU-638 cells defective in TGF-beta signaling exhibited no such decrease after H. pylori infection. The decreased expressions of TGF-beta1 in SNU-16 cells recovered to normal after 24 hr of H. pylori infection, but lasted very spatial times, suggesting that attenuated expression of TGF-beta1 is a host defense mechanism to avoid attachment of H. pylori. H. pylori infection was associated with depressed gastric mucosal TGF-beta1 for up to 24 hr, but this apparent strategy for rescuing cells from H. pylori attachment exacerbated the gastric inflammation.

Helicobacter pylori : the causative agent of peptic ulcer ...

African Journals Online (AJOL)

This review examines Helicobacter pylori as an organism and as the causative agent of peptic ulcers. The review also examined the classification of ulcers, ... Elimination of Helicobacter pylori by treatment with antibiotics in peptic ulcer patients resulted in the healing of the ulcer. Prevention of Helicobacter pylori infections is ...

A pro-inflammatory role for Th22 cells in Helicobacter pylori-associated gastritis.

Science.gov (United States)

Zhuang, Yuan; Cheng, Ping; Liu, Xiao-fei; Peng, Liu-sheng; Li, Bo-sheng; Wang, Ting-ting; Chen, Na; Li, Wen-hua; Shi, Yun; Chen, Weisan; Pang, Ken C; Zeng, Ming; Mao, Xu-hu; Yang, Shi-ming; Guo, Hong; Guo, Gang; Liu, Tao; Zuo, Qian-fei; Yang, Hui-jie; Yang, Liu-yang; Mao, Fang-yuan; Lv, Yi-pin; Zou, Quan-ming

2015-09-01

Helper T (Th) cell responses are critical for the pathogenesis of Helicobacter pylori-induced gastritis. Th22 cells represent a newly discovered Th cell subset, but their relevance to H. pylori-induced gastritis is unknown. Flow cytometry, real-time PCR and ELISA analyses were performed to examine cell, protein and transcript levels in gastric samples from patients and mice infected with H. pylori. Gastric tissues from interleukin (IL)-22-deficient and wild-type (control) mice were also examined. Tissue inflammation was determined for pro-inflammatory cell infiltration and pro-inflammatory protein production. Gastric epithelial cells and myeloid-derived suppressor cells (MDSC) were isolated, stimulated and/or cultured for Th22 cell function assays. Th22 cells accumulated in gastric mucosa of both patients and mice infected with H. pylori. Th22 cell polarisation was promoted via the production of IL-23 by dendritic cells (DC) during H. pylori infection, and resulted in increased inflammation within the gastric mucosa. This inflammation was characterised by the CXCR2-dependent influx of MDSCs, whose migration was induced via the IL-22-dependent production of CXCL2 by gastric epithelial cells. Under the influence of IL-22, MDSCs, in turn, produced pro-inflammatory proteins, such as S100A8 and S100A9, and suppressed Th1 cell responses, thereby contributing to the development of H. pylori-associated gastritis. This study, therefore, identifies a novel regulatory network involving H. pylori, DCs, Th22 cells, gastric epithelial cells and MDSCs, which collectively exert a pro-inflammatory effect within the gastric microenvironment. Efforts to inhibit this Th22-dependent pathway may therefore prove a valuable strategy in the therapy of H. pylori-associated gastritis. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

Host pathogen interactions in Helicobacter pylori related gastric cancer

Science.gov (United States)

Chmiela, Magdalena; Karwowska, Zuzanna; Gonciarz, Weronika; Allushi, Bujana; Stączek, Paweł

2017-01-01

Helicobacter pylori (H. pylori), discovered in 1982, is a microaerophilic, spiral-shaped gram-negative bacterium that is able to colonize the human stomach. Nearly half of the world's population is infected by this pathogen. Its ability to induce gastritis, peptic ulcers, gastric cancer and mucosa-associated lymphoid tissue lymphoma has been confirmed. The susceptibility of an individual to these clinical outcomes is multifactorial and depends on H. pylori virulence, environmental factors, the genetic susceptibility of the host and the reactivity of the host immune system. Despite the host immune response, H. pylori infection can be difficult to eradicate. H. pylori is categorized as a group I carcinogen since this bacterium is responsible for the highest rate of cancer-related deaths worldwide. Early detection of cancer can be lifesaving. The 5-year survival rate for gastric cancer patients diagnosed in the early stages is nearly 90%. Gastric cancer is asymptomatic in the early stages but always progresses over time and begins to cause symptoms when untreated. In 97% of stomach cancer cases, cancer cells metastasize to other organs. H. pylori infection is responsible for nearly 60% of the intestinal-type gastric cancer cases but also influences the development of diffuse gastric cancer. The host genetic susceptibility depends on polymorphisms of genes involved in H. pylori-related inflammation and the cytokine response of gastric epithelial and immune cells. H. pylori strains differ in their ability to induce a deleterious inflammatory response. H. pylori-driven cytokines accelerate the inflammatory response and promote malignancy. Chronic H. pylori infection induces genetic instability in gastric epithelial cells and affects the DNA damage repair systems. Therefore, H. pylori infection should always be considered a pro-cancerous factor. PMID:28321154

Relation between Helicobacter pylori infection and chronic urticaria

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Adianez Sugrañes-Montalván

2017-12-01

Conclusions: In the present study, the relationship between chronic urticaria and Helicobacter pylori infection was demonstrated. Apparently, the eradicating treatment for Helicobacter pylori was effective as the patients had no symptoms after treatment. Specific immunoglobulin G and Urease Test together constitute a suitable diagnostic module for the diagnosis of Helicobacter pylori conditions.

Virulence factor genotypes of Helicobacter pylori affect cure rates of eradication therapy.

Science.gov (United States)

Sugimoto, Mitsushige; Yamaoka, Yoshio

2009-01-01

The cure rates of Helicobacter pylori infection by using a combination of a proton pump inhibitor (PPI) and antimicrobial agents are mainly influenced by bacterial susceptibility to antimicrobial agents and the magnitude of acid inhibition during the treatment. Currently used empirical triple therapies do not reliably produce a > or =80% cure rate on an intention-to-treat basis. Therefore, tailored regimens based on relevant microbiological findings and pharmacogenomics are recommended for attaining an acceptable > or =95% cure rate. Recently, virulence factors of H. pylori, such as cagA and vacA, are reported to be major factors determining the cure rates. Individuals infected with strains with cagA-negative and vacA s2 genotypes have significantly increased risk of eradication failure of H. pylori infection. These virulence factors enhance gastric mucosal inflammation and are associated with the development of peptic ulcer and gastric cancer. H. pylori virulence factors induce proinflammatory cytokines, such as interleukin (IL)-1, IL-8, and tumor necrosis factor (TNF)- which influence mucosal inflammation and/or gastric acid secretion. When physicians select an H. pylori eradication regimen with an acceptable cure rate, they might need to consider H. pylori virulence factors, especially cagA and vacA.

Helicobacter pylori infection generates genetic instability in gastric cells

DEFF Research Database (Denmark)

Machado, Ana Manuel; Figueiredo, C.; Seruca, R.

2010-01-01

The discovery that Helicobacter pylori is associated with gastric cancer has led to numerous studies that investigate the mechanisms by which H. pylori induces carcinogenesis. Gastric cancer shows genetic instability both in nuclear and mitochondrial DNA, besides impairment of important DNA repai...

Pediatric Helicobacter pylori gastropathy demonstrates a unique pattern of gastric foveolar hyperplasia.

Science.gov (United States)

Saghier, Sadaf; Schwarz, Steven M; Anderson, Virginia; Gupta, Raavi; Heidarian, Amin; Rabinowitz, Simon S

2018-04-25

Helicobacter pylori (Hp) are the most common agents causing gastric mucosal injury worldwide. Foveolar hyperplasia is a key component of the stomach's reaction to injury. This study examines histopathologic characteristics associated with Helicobacter pylori and with non- Helicobacter pylori-associated gastropathy in children and adolescents, and compares the prevalence of foveolar hyperplasia among these disease subgroups and normal control subjects. Eighty-one gastric antral and corpus biopsies from subjects 2-19 years of age were studied. Twenty-two subjects with Helicobacter pylori gastritis were compared to 23 with non-Helicobacter pylori gastropathy and to 36 controls (normal biopsies). Foveolar length, full mucosal thickness, and the foveolar length: full mucosal thickness ratio were derived by a morphometric technique previously developed to analyze adult gastric tissue. Compared to controls, Helicobacter pylori gastritis demonstrated significant increases in antral foveolar length (P Helicobacter pylori-associated gastropathy also was characterized by increased antral foveolar length (P Helicobacter pylori gastropathy was increased, when compared to Helicobacter pylori gastritis (P Helicobacter pylori gastropathy group demonstrated increased antral foveolar length: full mucosal thickness ratios, compared with Helicobacter pylori gastritis (P Helicobacter pylori gastritis but is limited to the antrum in non-Helicobacter pylori gastropathy. © 2018 John Wiley & Sons Ltd.

Helicobacter pylori virulence and cancer pathogenesis.

Science.gov (United States)

Yamaoka, Yoshio; Graham, David Y

2014-06-01

Helicobacter pylori is human gastric pathogen that causes chronic and progressive gastric mucosal inflammation and is responsible for the gastric inflammation-associated diseases, gastric cancer and peptic ulcer disease. Specific outcomes reflect the interplay between host-, environmental- and bacterial-specific factors. Progress in understanding putative virulence factors in disease pathogenesis has been limited and many false leads have consumed scarce resources. Few in vitro-in vivo correlations or translational applications have proved clinically relevant. Reported virulence factor-related outcomes reflect differences in relative risk of disease rather than specificity for any specific outcome. Studies of individual virulence factor associations have provided conflicting results. Since virulence factors are linked, studies of groups of putative virulence factors are needed to provide clinically useful information. Here, the authors discuss the progress made in understanding the role of H. pylori virulence factors CagA, vacuolating cytotoxin, OipA and DupA in disease pathogenesis and provide suggestions for future studies.

Halitosis and Helicobacter pylori infection

NARCIS (Netherlands)

Tangerman, A.; Winkel, E. G.; de Laat, L.; van Oijen, A. H.; de Boer, W. A.

There is disagreement about a possible relationship between Helicobacter pylori (H. pylori) infection and objective halitosis, as established by volatile sulfur compounds (VSCs) in the breath. Many studies related to H. pylori used self-reported halitosis, a subjective and unreliable method to

Reflux esophagitis triggered after Helicobacter pylori eradication: a noteworthy demerit of eradication therapy among the Japanese?

Directory of Open Access Journals (Sweden)

Katsunori eIijima

2015-06-01

Full Text Available In the February 2013 Revision of Insured Medical Treatment, bacterial eradication for all Helicobacter pylori-positive individuals in Japan was covered under the insurance scheme. However, reflux esophagitis is believed to occur in approximately 10% of Japanese patients who undergo eradication therapy. Hence, the risk of reflux esophagitis among such cases should be carefully considered, particularly in the treatment for H. pylori-positive patients who are otherwise healthy. The eradication of Helicobacter pylori in cases of H. pylori-positive gastritis markedly suppresses gastric inflammation, and inhibits gastric mucosal atrophy and its progression to intestinal metaplasia. In a long-term follow-up study (10-20 years, eradication treatment was found to reduce the risk of subsequent gastric cancer. However, the fact that eradication-induced reflux esophagitis could increase the long-term risk of Barrett’s esophagus and esophageal adenocarcinoma should also be considered in the Japanese population. Appropriate treatment with proton pump inhibitors should be taken into consideration for patients undergoing eradication therapy in clinical practice.

Helicobacter pylori and non-malignant diseases.

Science.gov (United States)

Furuta, Takahisa; Delchier, Jean-Charles

2009-09-01

It is well known that Helicobacter pylori infection is associated with many nonmalignant disorders such as gastritis, peptic ulcer, gastroesophageal reflux disease (GERD), gastric polyp, nonsteroidal anti-inflammatory drug (NSAID)/aspirin-induced gastric injury, and functional dyspepsia. In 2008, interesting articles on the association of H. pylori infection with these disorders were presented, some of which intended to reveal the mechanisms of inter-individual differences in response to H. pylori infection, and have demonstrated that genetic differences in host and bacterial factors as well as environmental factors account for these differences. A decline in the occurrence of peptic ulcer related to H. pylori was confirmed. An inverse relationship between H. pylori infection and GERD was also confirmed but the impact of gastric atrophy on the prevention of GERD remained debatable. For NSAID-induced gastric injury, eradication of H. pylori infection has been recommended. During this year, eradication of H. pylori infection was recommended for patients treated with antiplatelet therapy as well as aspirin and NSAID. It was also reported that for patients with functional dyspepsia, eradication of H. pylori offers a modest but significant benefit.

HELICOBACTER PYLORI

Science.gov (United States)

Helicobacter pylori is a pathogenic bacteria which inhabits the human stomach and upper gastrointestinal tract. This encyclopedic entry summarizes the potential role of this organism as a waterborne pathogen. Information is provided on the physiology and morphology of this bacter...

Helicobacter pylori infection: past, present and future | Jemilohun ...

African Journals Online (AJOL)

Helicobacter pylori infection: past, present and future. ... The discovery of Helicobacter pylori (H. pylori) by Warren and Marshall in 1982 was preceded by nearly a hundred year of inconspicuous publications in ... A major challenge is the absence of a specific antibiotic monotherapy for effective treatment of the infection.

Characteristics of Helicobacter pylori-positive and Helicobacter pylori-negative gastric mucosa-associated lymphoid tissue lymphoma and their influence on clinical outcome.

Science.gov (United States)

Choi, Yoon Jin; Kim, Nayoung; Paik, Jin Ho; Kim, Jung Mogg; Lee, Sang Hyub; Park, Young Soo; Hwang, Jin-Hyeok; Kim, Jin-Wook; Jeong, Sook-Hyang; Lee, Dong Ho; Jung, Hyun Chae

2013-06-01

To compare clinicopathologic and molecular characteristics of low-grade gastric mucosa-associated lymphoid tissue lymphoma depending on Helicobacter pylori positivity and to find out a predictive factor for unresponsiveness to Helicobacter pylori eradication therapy in Korea. A total of 53 Helicobacter pylori-positive and 13 negative mucosa-associated lymphoid tissue lymphoma patients were enrolled, and tissues from 21 patients were investigated to examine the presence of t(11;18)(q21;q21) with fluorescence in situ hybridization. Clinicopathologic features such as the endoscopic appearance, dominant site of lesion, depth of invasion, clinical stage, and the existence of MALT1 gene rearrangement were compared between these two groups. Fifty-six patients who underwent H. pylori eradication therapy were divided into responder and nonresponder groups. The two groups were analyzed to calculate odds ratios for resistance to the eradication. Helicobacter pylori-negative gastric mucosa-associated lymphoid tissue lymphoma patients averaged a more advanced clinical stage than H. pylori-positive (p = .023) patients. The frequency of t(11;18)/API2-MALT1 did not differ between H. pylori-positive (45.5%) and H. pylori-negative cases (55.6%). Thirty-eight of 51 (74.5%) H. pylori-positive patients achieved complete regression after the eradication, while 2 of 5 (40%) H. pylori-negative patients obtained regression. Presence of lesions in both distal and proximal parts of stomach (p = .041) and bearing of t(11;18)(q21;q21) (p = .007) were predictors for nonresponsiveness for H. pylori eradication. Helicobacter pylori eradication could be performed as a primary therapy regardless of H. pylori status, and assessing t(11;18)/API2-MALT1 would be considered after failure to remission by H. pylori eradication. © 2013 John Wiley & Sons Ltd.

Inactivation of Helicobacter pylori by Chloramination

Science.gov (United States)

Three strains of Helicobacter pylori (H. pylori) were studied to determine their resistance to chloramination. H. pylori is an organism listed on the U.S. Environmental Protection Agency’s (USEPA) Contaminant Control List (CCL). H. pylori was exposed to 2ppm of pre-formed monoc...

Helicobacter pylori infection generates genetic instability in gastric cells

DEFF Research Database (Denmark)

Machado, Ana Manuel Dantas; Figueiredo, Céu; Seruca, Raquel

2010-01-01

The discovery that Helicobacter pylori is associated with gastric cancer has led to numerous studies that investigate the mechanisms by which H. pylori induces carcinogenesis. Gastric cancer shows genetic instability both in nuclear and mitochondrial DNA, besides impairment of important DNA repair...... of the host, such as oxidative damage, methylation, chromosomal instability, microsatellite instability, and mutations. Interestingly, H. pylori infection generates genetic instability in nuclear and mitochondrial DNA. Based on the reviewed literature we conclude that H. pylori infection promotes gastric...

Analysis of the microflora in the stomach of Mongolian gerbils infected with Helicobacter pylori.

Science.gov (United States)

Zaman, Cynthia; Osaki, Takako; Hanawa, Tomoko; Yonezawa, Hideo; Kurata, Satoshi; Kamiya, Shigeru

2010-05-01

Mongolian gerbils are frequently used to study Helicobacter pylori-induced gastritis and its consequences. The presence of some gastric flora with a suppressive effect on H. pylori suggests inhibitory microflora against H. pylori infection. The aim of the present study was to analyze the microflora in the stomach of Mongolian gerbils with H. pylori infection. H. pylori ureA was detected by polymerase chain reaction (PCR) in the fecal samples of infected Mongolian gerbils. H. pylori was isolated from the gastric mucosa of the gerbils by microaerophilic cultivation. Gastric microflora were isolated by aerobic and anaerobic culture, and the identification of gastric bacterial species was performed by API20E and API20A. Oral administration of H. pylori TK1402 induced colonization and gastric inflammation of the stomach of the Mongolian gerbils. According to the frequency of detection of H. pylori ureA in fecal samples, the gerbils were divided into three groups (frequently detected, moderately detected and infrequently detected). According to the analysis of the gastric microflora in the frequently and infrequently detected groups, Lactobacillus spp. and Eubacterium limosum were isolated from the former and latter group, respectively. Some gastric flora, such as Lactobacillus spp., may inhibit colonization by H. pylori.

Helicobacter pylori colonization in infants and its relation to childhood morbidity

International Nuclear Information System (INIS)

Nizami, S.Q.; Bhutta, Z.A.; Weaver, L.

2000-01-01

Helicobacter pylori infection is universally reported from all over the world including both developed and developing countries. The prevalence of Helicobacter pylori infection in Pakistan is unknown. Although a few studies have been done in adults, there are no studies looking at the prevalence of Helicobacter pylori colonization especially in children. In addition, a number of symptoms such as nonspecific abdominal pain, diarrhea and malnutrition etc. are attributed to it though most cases of Helicobacter pylori colonization remain asymptomatic. The association between Helicobacter pylori and gastrointestinal symptoms however, remains controversial. Hence in order to determine the prevalence of Helicobacter pylori infection, its time of acquisition and to look at its correlation with diarrhea-associated morbidity, we proposed to do the present study. In this study we will look for the evidence of Helicobacter colonization in infants with the non-invasive techniques using 13 C urea breath test and stool ELISA for Helicobacter pylori every at three month interval in a cohort of infants from a periurban community in Karachi Pakistan. (author)

Association of mast cells with helicobacter pylori infection in the antral mucosa

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SR KC

2011-03-01

Full Text Available Background: Helicobacter pylori infection is associated with mixed inflammatory cell infiltrate consisting of neutrophils, eosinophils, lymphocytes and plasma cells. Helicobacter pylori lead to mast cell degranulation and release of active chemical compounds in in-vitro conditions. The objective of this study was to find out the association of mast cell density and Helicobacter pylori in the antral mucosa of the stomach. Materials and Methods: A total of 150 endoscopic biopsies were included in the study. In addition to routine Hematoxylin and Eosin stained slides, Giemsa stain was done in each case for the evaluation of Helicobacter pylori and mast cell density in the gastric mucosa. Results: Out of 150 gastric biopsies with histopathological diagnosis of chronic gastritis, 36 cases (24% were positive for Helicobacter pylori. In the antral mucosa, mast cell density was significantly higher in the Helicobacter pylori-positive group than in the Helicobacter pylori-negative group (P<0.01. Conclusion: Mast cells may play a role in the development of Helicobacter pylori gastritis. Keywords: Gastritis; Mast Cell; Helicobacter pylori DOI: 10.3126/jpn.v1i1.4448 Journal of Pathology of Nepal (2011 Vol.1, 34-36

DNA-binding activity of TNF-α inducing protein from Helicobacter pylori

International Nuclear Information System (INIS)

Kuzuhara, T.; Suganuma, M.; Oka, K.; Fujiki, H.

2007-01-01

Tumor necrosis factor-α (TNF-α) inducing protein (Tipα) is a carcinogenic factor secreted from Helicobacter pylori (H. pylori), mediated through both enhanced expression of TNF-α and chemokine genes and activation of nuclear factor-κB. Since Tipα enters gastric cancer cells, the Tipα binding molecules in the cells should be investigated. The direct DNA-binding activity of Tipα was observed by pull down assay using single- and double-stranded genomic DNA cellulose. The surface plasmon resonance assay, indicating an association between Tipα and DNA, revealed that the affinity of Tipα for (dGdC)10 is 2400 times stronger than that of del-Tipα, an inactive Tipα. This suggests a strong correlation between DNA-binding activity and carcinogenic activity of Tipα. And the DNA-binding activity of Tipα was first demonstrated with a molecule secreted from H. pylori

VacA and CagA Status as Biomarker of Two Opposite End Outcomes of Helicobacter pylori Infection (Gastric Cancer and Duodenal Ulcer) in a Moroccan Population

OpenAIRE

El Khadir, Mounia; Alaoui Boukhris, Samia; Benajah, Dafr-Allah; El Rhazi, Karima; Ibrahimi, Sidi Adil; El Abkari, Mohamed; Harmouch, Taoufiq; Nejjari, Chakib; Mahmoud, Mustapha; Benlemlih, Mohamed; Bennani, Bahia

2017-01-01

Helicobacter pylori (H. pylori) infection induces inflammation of the gastric mucosa, which may progress to precancerous lesions leading to gastric cancer. Pathological determinism is associated to some virulence genes of the bacterium, notably the vacA and cagA genes. The present study aimed to determine the H. pylori genotypes distribution and their association with sex, age and gastric diseases in a Moroccan population. Gastric biopsy was taken from 1079 consenting patients. The specimens ...

( Asteraceae ) methanol extracts against Helicobacter pylori

African Journals Online (AJOL)

Methanol vehicle did not affect H. pylori growth. Conclusion: The observed antibacterial effect of G. glutinosum extracts may be of benefit as an adjuvant treatment of diseases caused by H. pylori. Key words: Gymnosperma glutinosum, Helicobacter pylori, methanol extract, minimal inhibitory concentration (MIC).

No evidence for Helicobacter pylori in oral lichen planus.

Science.gov (United States)

Hulimavu, Shwetha R; Mohanty, Leeky; Tondikulam, Narayan V; Shenoy, Sadhana; Jamadar, Saleha; Bhadranna, Abhishek

2014-09-01

Oral lichen planus is a T-cell-mediated mucosal disease of unknown etiology. Numerous predisposing factors have been put forward in the etiology of this disease. This includes stress, drugs, genetic susceptibility, certain viruses, and bacterial infections. Recently, there have been studies published on possible role of Helicobacter pylori infection in pathogenesis of mucocutaneous diseases including oral lichen planus (OLP). The aim of this study was to detect immunohistochemically the presence of Helicobacter pylori in oral lichen planus. Paraffin-embedded tissue blocks of 50 cases of OLP and 10 cases of normal buccal mucosal biopsies and 6 endoscopic biopsies of patients with peptic ulcer (control group) were sectioned and stained by hematoxylin and eosin. Serial sections of same were stained immunohistochemically using Anti-Helicobacter pylori antibody and observed under microscope for presence or absence of Helicobacter pylori. Except for the control group, none of the cases of OLP and normal buccal mucosal biopsies showed positivity for Helicobacter pylori. As we did not detect the presence of Helicobacter pylori in any of the OLP cases, we question the role of these organisms in the pathogenesis of OLP planus if any. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Endoscopic transmission of Helicobacter pylori

NARCIS (Netherlands)

Tytgat, G. N.

1995-01-01

The contamination of endoscopes and biopsy forceps with Helicobacter pylori occurs readily after endoscopic examination of H. pylori-positive patients. Unequivocal proof of iatrogenic transmission of the organism has been provided. Estimates for transmission frequency approximate to 4 per 1000

Serum TNF-α, IL-8, VEGF Levels in Helicobacter pylori Infection and Their Association with Degree of Gastritis

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Gontar A Siregar

2015-04-01

Full Text Available Aim: to investigate the serum levels of TNF-α, IL-8, VEGF in Helicobacter pylori infection, and their association with the degrees of gastritis histopathology. Methods: a cross-sectional study was done on 80 consecutive gastritis patients admitted to endoscopy units at Adam Malik General Hospital and Permata Bunda Hospital, Medan, Indonesia from July-December 2014. The Rapid Urease test was used for the diagnosis of H. pylori infection. The severity of chronic inflammation, neutrophil infiltration, atrophy, and intestinal metaplasia were assessed. Serum samples were obtained to determine circulating TNF-α, IL-8, and VEGF. Univariate and bivariate analysis (chi square, fisher’s exact, and mann-whitney test were done using SPSS version-22. Results: there were 41.25% of 80 patients infected with Helicobacter pylori. Serum TNF-α and VEGF levels in the infected group were significantly higher compared to H. pylori negative, but there were no significant differences between serum levels of IL-8 in H. pylori positive and negative. There were significant associations between serum level of TNF-α and IL-8 with degree of chronic inflammation, and also between serum level of IL-8 and degree of neutrophil infiltration. There were significant associations between serum level of VEGF and degree of atrophy, and also between serum level of VEGF and degree of intestinal metaplasia. Conclusion: High levels of TNF-α were associated with severe degree of chronic inflammation, high levels of IL-8 associated with severe degree of chronic inflammation and neutrophil infiltration, and high levels of VEGF associated with severe degree of premalignant gastric lesion. Key words: cytokine, neoangiogenesis, Helicobacter pylori, atrophic gastritis, intestinal metaplasia.

"Targeted disruption of the epithelial-barrier by Helicobacter pylori"

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Wroblewski Lydia E

2011-11-01

Full Text Available Abstract Helicobacter pylori colonizes the human gastric epithelium and induces chronic gastritis, which can lead to gastric cancer. Through cell-cell contacts the gastric epithelium forms a barrier to protect underlying tissue from pathogenic bacteria; however, H. pylori have evolved numerous strategies to perturb the integrity of the gastric barrier. In this review, we summarize recent research into the mechanisms through which H. pylori disrupts intercellular junctions and disrupts the gastric epithelial barrier.

Helicobacter pylori

DEFF Research Database (Denmark)

Leth, Peter Mygind

1992-01-01

Helicobacter pylori (HP) are Gram-negative spiral bacteria which occur in the human stomach. The bacteria were cultured in vitro for the first time in 1983. It is suspected that the bacteria may cause chronic gastritis of type B and may also be a contributory cause of chronic ulceration and cancer...

Rosacea is associated with Helicobacter pylori

DEFF Research Database (Denmark)

Jørgensen, A-H R; Egeberg, A; Gideonsson, R

2017-01-01

BACKGROUND: Rosacea is a common skin disease characterized by facial erythema, telangiectasia, papules and pustules. Helicobacter pylori infection has been suggested to play a role in the etiopathogenesis of rosacea. OBJECTIVE: To systematically review and meta-analyse the relationship between...... rosacea and infection with Helicobacter pylori. METHODS: A literature search was performed using PubMed, EMBASE and Web of Science. Data extraction and analyses were performed on descriptive data. Study quality was assessed using the Newcastle-Ottawa Scale. Random-effects models with Der...... in the quantitative meta-analysis, comprising a total of 928 rosacea patients and 1527 controls. The overall association between Helicobacter pylori infection and rosacea was non-significant (OR 1.68, 95% CI 1.00-2.84, P = 0.052), but analysis restricted to C-urea breath test showed a significant association (OR 3...

CD44 plays a functional role in Helicobacter pylori-induced epithelial cell proliferation.

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Nina Bertaux-Skeirik

2015-02-01

Full Text Available The cytotoxin-associated gene (Cag pathogenicity island is a strain-specific constituent of Helicobacter pylori (H. pylori that augments cancer risk. CagA translocates into the cytoplasm where it stimulates cell signaling through the interaction with tyrosine kinase c-Met receptor, leading cellular proliferation. Identified as a potential gastric stem cell marker, cluster-of-differentiation (CD CD44 also acts as a co-receptor for c-Met, but whether it plays a functional role in H. pylori-induced epithelial proliferation is unknown. We tested the hypothesis that CD44 plays a functional role in H. pylori-induced epithelial cell proliferation. To assay changes in gastric epithelial cell proliferation in relation to the direct interaction with H. pylori, human- and mouse-derived gastric organoids were infected with the G27 H. pylori strain or a mutant G27 strain bearing cagA deletion (∆CagA::cat. Epithelial proliferation was quantified by EdU immunostaining. Phosphorylation of c-Met was analyzed by immunoprecipitation followed by Western blot analysis for expression of CD44 and CagA. H. pylori infection of both mouse- and human-derived gastric organoids induced epithelial proliferation that correlated with c-Met phosphorylation. CagA and CD44 co-immunoprecipitated with phosphorylated c-Met. The formation of this complex did not occur in organoids infected with ∆CagA::cat. Epithelial proliferation in response to H. pylori infection was lost in infected organoids derived from CD44-deficient mouse stomachs. Human-derived fundic gastric organoids exhibited an induction in proliferation when infected with H. pylori that was not seen in organoids pre-treated with a peptide inhibitor specific to CD44. In the well-established Mongolian gerbil model of gastric cancer, animals treated with CD44 peptide inhibitor Pep1, resulted in the inhibition of H. pylori-induced proliferation and associated atrophic gastritis. The current study reports a unique

Prevalence and risk factors of Helicobacter pylori infection in Chinese maritime workers.

Science.gov (United States)

Hu, Dongmei; Shao, Jing; Wang, Ligang; Zheng, Huichun; Xu, Yan; Song, Guirong; Liu, Qigui

2013-01-01

Helicobacter pylori infection is very common worldwide. To evaluate the prevalence and identify the risk factors for Helicobacter pylori infection in Chinese maritime workers. Between March 2010 and October 2010, 3995 subjects were selected in the Hospital of Dalian Port. The presence of Helicobacter pylori infection was confirmed using laboratory tests (serum IgG anti-Helicobacter pylori antibodies) and background information, family history, lifestyle and eating habits were collected using questionnaires. The prevalence of Helicobacter pylori infection was 44.9% in these Chinese maritime workers. Prevalence of Helicobacter pylori infection was associated with family income, living space, family history of gastrointestinal diseases, smoking, drinking tea, raw vegetables consumption, spicy food, pickle food, dining outside, no regular meal and dish sharing. Further analysis with multivariate logistic regression analysis indicated that raw vegetables consumption, pickle food consumption, family income and family history of gastrointestinal diseases were independent predictors for Helicobacter pylori infection. No association was found between infection and gender, marital status, education, alcohol consumption and tap water consumption. Helicobacter pylori infection is associated with raw vegetables consumption, pickle food consumption, family income and family history of gastrointestinal disease among Chinese maritime workers.

Helicobacter-negative gastritis: a distinct entity unrelated to Helicobacter pylori infection.

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Genta, R M; Sonnenberg, A

2015-01-01

Helicobacter-negative gastritis is diagnosed when no organisms are detected in a gastric mucosa with typical features of Helicobacter gastritis (Hp-gastritis). If Helicobacter-negative gastritis consisted mostly of 'missed' Helicobacter infections, its prevalence should represent a constant percentage of these infections in a population, and their clinico-epidemiological features would overlap. To compare the epidemiologic patterns of Hp-positive and Hp-negative gastritis. From a pathology database, we extracted demographic, clinical and histopathological data from patients with gastric biopsies (1.2008-12.2013). We allocated patients to high (≥12%) and low (≤6%) H. pylori prevalence regions defined by ZIP code-based data. The prevalence of H. pylori-positive and -negative gastritis by sex, age and state were expressed as a per cent of the total study population stratified accordingly. Of 895 323 patients, 10.6% had Hp-gastritis and 1.5% Helicobacter-negative gastritis. Hp-gastritis, but not Helicobacter-negative gastritis, was more common in males than females (OR 1.17, 95% CI: 1.16-1.19). While Hp-gastritis was more prevalent in high than in low-prevalence areas (OR 3.65, 95% CI: 3.57-3.74), Helicobacter-negative gastritis was only minimally affected by the underlying H. pylori prevalence (1.7% vs. 1.5%). The age-specific prevalence of Hp-gastritis peaked in the 4th to 5th decades; Helicobacter-negative gastritis exhibited a low and relatively flat pattern. The geographic distribution of H. pylori-positive and -negative gastritis showed no significant correlation. Intestinal metaplasia was found in 13.0% of patients with Hp-gastritis and in 6.1% of those with Helicobacter-negative gastritis (OR 0.43, 95% CI: 0.40-0.47). These data suggest that Helicobacter-negative gastritis is, in the vast majority of cases, a nosologically and epidemiologically distinct entity that deserves further investigation. © 2014 John Wiley & Sons Ltd.

Antral atrophy, intestinal metaplasia, and preneoplastic markers in Mexican children with Helicobacter pylori-positive and Helicobacter pylori-negative gastritis.

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Villarreal-Calderon, Rodolfo; Luévano-González, Arturo; Aragón-Flores, Mariana; Zhu, Hongtu; Yuan, Ying; Xiang, Qun; Yan, Benjamin; Stoll, Kathryn Anne; Cross, Janet V; Iczkowski, Kenneth A; Mackinnon, Alexander Craig

2014-06-01

Chronic inflammation and infection are major risk factors for gastric carcinogenesis in adults. As chronic gastritis is common in Mexican children, diagnosis of Helicobacter pylori and other causes of gastritis are critical for the identification of children who would benefit from closer surveillance. Antral biopsies from 82 Mexican children (mean age, 8.3 ± 4.8 years) with chronic gastritis (36 H pylori+, 46 H pylori-) were examined for gastritis activity, atrophy, intestinal metaplasia (IM), and immunohistochemical expression of gastric carcinogenesis biomarkers caudal type homeobox 2 (CDX2), ephrin type-B receptor 4 (EphB4), matrix metalloproteinase 3 (MMP3), macrophage migration inhibitory factor (MIF), p53, β-catenin, and E-cadherin. Atrophy was diagnosed in 7 (9%) of 82, and IM, in 5 (6%) of 82 by routine histology, whereas 6 additional children (7%) (3 H pylori+) exhibited aberrant CDX2 expression without IM. Significant positive correlations were seen between EphB4, MMP3, and MIF (Pgastritis. Copyright © 2014 Elsevier Inc. All rights reserved.

Helicobacter pylori: a risk and severity factor of non-steroidal anti-inflammatory drug induced gastropathy.

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Heresbach, D; Raoul, J L; Bretagne, J F; Minet, J; Donnio, P Y; Ramée, M P; Siproudhis, L; Gosselin, M

1992-01-01

This prospective study aimed to determine the prevalence of Helicobacter pylori infection in relation to the occurrence and severity of NSAIDs induced gastropathy. A total of 111 patients were studied-66 were taking NSAIDs and 45 were control patients. All patients underwent endoscopy during which antral biopsy specimens were taken to determine H pylori status (Gram and Giemsa staining, urease test, and cultures). The NSAID group comprised: group I, patients without mucosal damage (n = 28); group II, patients with gastropathy (n = 26); and group III, patients with bleeding associated with NSAID induced gastropathy (n = 12). Control patients had neither dyspeptic symptoms nor endoscopic lesions. There were no differences in age, sex ratio, or presence of H pylori (26% v 24%) between the NSAID and the control groups. Among patients taking NSAIDs, H pylori infection was more frequently (p gastropathy (groups II and III: 37%) than in those without lesions (group I: 11%). The frequency of H pylori infection increased significantly with the severity of gastropathy (group I = 11%; group II = 31%; group III = 50%; p NSAID induced gastropathy. PMID:1487160

Helicobacter pylori y dispepsia, un problema de salud comunitario

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Miguel González-Carbajal Pascual

2002-06-01

Full Text Available Mientras la relación causal entre el Helicobacter pylori y la gastritis crónica, así como la importante conexión entre esta infección, la úlcera gastroduodenal y el cáncer gástrico han sido bien establecidas, la asociación entre la infección por Helicobacter pylori y la dispepsia "no ulcerosa" es un problema que dista mucho de estar esclarecido. Hay autores que no dudan en utilizar tratamiento de erradicación en la dispepsia "no ulcerosa" con Helicobacter pylori, pero existen enfoques alternativos a este problema. La realización de tratamiento de erradicación en los pacientes con dispepsia "no ulcerosa" pudiera beneficiar o no a los enfermos y a la comunidad, pero seguramente no puede dejar de beneficiar a las transnacionales productoras de medicamentos que cosechan cuantiosas ganancias con la comercialización de los bloqueadores de la bomba de protones y los antibióticos que se incluyen en cualquier esquema de terapia erradicadora de la infección por Helicobacter pylori. El alivio de los síntomas dispépticos como consecuencia del tratamiento de erradicación del Helicobacter pylori no ha sido comprobado. El problema de realizar tratamiento de erradicación de la infección a los pacientes con dispepsia "no ulcerosa" continúa siendo un dilema y, por tanto, no debe indicarse sistemáticamente.Although the causative relationship between Helicobacter pylori and chronic gastritis as well as the important connection of this infection with gastric-duodenal ulcer and gastric cancer are well established, the association of Helicobacter pylori infection and non-ulcer dispepsia is a problem that is still unclear. Some authors do not hesitate in using Helicobacter pylori eradication treatment in cases of non-ulcer dispepsia but there are other alternative approaches to this problem. The eradication treatment in patients with non-ulcer dispepsia may or may not benefit patients and the community, but will benefit for sure the big drug

Possible association between Helicobacter pylori infection and vocal fold leukoplakia.

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Chen, Min; Chen, Jian; Yang, Yue; Cheng, Lei; Wu, Hai-Tao

2018-03-06

Several studies have indicated the larynx as possible Helicobacter pylori (H. pylori) reservoirs. This study explored the association between H. pylori and vocal fold leukoplakia. The case-control study involved 51 patients with vocal fold leukoplakia and 35 control patients with vocal polyps. Helicobacter pylori was detected in tissues by the rapid urease test, nested polymerase chain reaction (PCR), and single-step PCR. The H. pylori-specific immunoglobulin antibodies were detected in plasma by enzyme-linked immunosorbent assay (ELISA). Helicobacter pylori-positive rate of vocal fold leukoplakia and vocal polyps was 23.5% versus 11.4% (P = .157), 37.2% versus 14.3% (P = .020), 27.5% versus 8.6% (P = .031), and 70.6% versus 68.6% (P = .841) detected by rapid urease test, nested PCR, single-step PCR, and ELISA, respectively. Regression analysis indicated that H. pylori infection (P = .044) was the independent risk factor for vocal fold leukoplakia. Helicobacter pylori infection exists in the larynx and may be associated with vocal fold leukoplakia. © 2018 Wiley Periodicals, Inc.

Epidemiology of Helicobacter pylori infection in dyspeptic Ghanaian patients.

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Archampong, Timothy Nii Akushe; Asmah, Richard Harry; Wiredu, Edwin Kwame; Gyasi, Richard Kwasi; Nkrumah, Kofi Nyaako; Rajakumar, Kumar

2015-01-01

Helicobacter pylori is a gram-negative urease-producing bacterium causally linked with gastritis, peptic ulcer disease and gastric adenocarcinoma. Infection is more frequent and acquired at an earlier age in developing countries compared to European populations. The incidence of Helicobacter pylori infection in dyspeptic Ghanaian patients was 75.4%. However, epidemiological factors associated with infection vary across populations. This study used a cross-sectional design to consecutively sample dyspeptic patients at the Endoscopy Unit of the Korle-Bu Teaching Hospital, Accra between 2010 and 2012. The study questionnaire elicited their epidemiological clinical characteristics. Helicobacter pylori infection was confirmed by rapid-urease examination of antral biopsies at upper Gastro-intestinal endoscopy. The sample population of dyspeptic patients attending the Endoscopy Unit for upper GI endoscopy yielded 242 patients of which 47.5% were females. The age distribution of H. pylori-infection was even across most age - groups, ranging from 69.2% (61 - 70) years to 80% (21 - 30) years. Helicobacter pylori prevalence decreased across areas mapping to the three residential classes in accordance with increasing affluence with rural areas having the highest prevalence. The unemployed and patients in farming had relatively high Helicobacter pylori infection rates of 92.3% and 91.7% respectively. Helicobacter pylori is endemic in Ghana but the persistently high prevalence across age groups despite significant community anti-microbial use suggests likely recrudescence or re-infection from multiple sources in a developing country. Socio-cultural factors such as residential class and farming may be facilitating factors for its continued prevalence.

Management of Helicobacter Pylori Infection

African Journals Online (AJOL)

Dr Olaleye

90%, the sequential therapy seems to have a potential of becoming the standard first-line treatment for H pylori infection in the interim, while search is being made for the ideal antimicrobial monotherapy. . Keywords: Helicobacter pylori, Dyspepsia, Gastric cancer, Gastric Ulcer, Duodenal ulcer. INTRODUCTION. 1. Since the ...

Pathobiology of Helicobacter pylori-induced Gastric Cancer

Science.gov (United States)

Amieva, Manuel; Peek, Richard M.

2015-01-01

Colonization of the human stomach by Helicobacter pylori and its role in causing gastric cancer is one of the richest examples of complex relationship among human cells, microbes, and their environment. It is also a puzzle of enormous medical importance given the incidence and lethality of gastric cancer worldwide. We review recent findings that have changed how we view these relationships and affected the direction of gastric cancer research. For example, recent data indicate that subtle mismatches between host and microbe genetic traits greatly affect risk of gastric cancer. The ability of H pylori and its oncoprotein CagA to reprogram epithelial cells and activate properties of stemness demonstrates the sophisticated relationship among H pylori and progenitor cells in the gastric mucosa. The observation that cell-associated H pylori can colonize the gastric glands and directly affect precursor and stem cells supports these observations. The ability to mimic these interactions in human gastric organoid cultures as well as animal models will allow investigators to more fully unravel the extent of H pylori control on the renewing gastric epithelium. Finally, our realization that external environmental factors, such as dietary components and essential micronutrients, as well as the gastrointestinal microbiota, can change the balance between H pylori’s activity as a commensal or a pathogen has provided direction to studies aimed at defining the full carcinogenic potential of this organism. PMID:26385073

Correlation between Helicobacter Pylori Infection and Intra Ocular Pressure

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Hatamizadeh

2012-02-01

Full Text Available Introduction: Glaucoma is one of the most common causes of blindness. It is estimated that more than 60 million people suffer from this disease of all over the world. In other hand helicobacter pylori is a gram negative bacillus that is reported in some extra-gastrointestinal system diseases recently. This study is designed to determine the association between helicobacter pylori infection and intra-ocular pressure. Methods: This was an analytical cross-sectional study that was conducted on 74 persons who were randomly selected after referring to endoscopy ward of Shohadaye Kargar hospital of Yazd in 2009. Data was analyzed by Mann-Whitney U and fisher exact tests using SPSS software (ver16. Results: Mean of intra-ocular pressure in positive helicobacter pylori group was more than negative helicobacter pylori group but there was no significant relationship (P value > 0.05, also there was no significant relationship between helicobacter pylori infection and diabetes, hypertension, hypothyroidism and hyperthyroidism (P value > 0.05. Conclusion: According to the results, more detailed studies with larger sample size are required for more reliable decisions also considering the confounder variables can help us to determine the common risk factors of these two outcomes.

Helicobacter pylori-Induced Chronic Gastritis and Assessing Risks for Gastric Cancer

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Gonzalo Carrasco

2013-01-01

Full Text Available Chronic gastritis is an inflammation of the gastric mucosa and has multiple etiologies. Here we discuss the pathological alterations induced by Helicobacter pylori (HP leading to chronic gastritis and the epigenetic bases underlying these changes. We review the histology of the normal gastric mucosa and overview the role of HP in the multistep cascade of GC. We attempt to define the role of the Operative Link for Gastritis Assessment (OLGA staging system in assessing the risk of GC. The epigenetic bases of chronic gastritis, mainly DNA methylation, are presented through examples such as (i the methylation of the promoter region of E-cadherin in HP-induced chronic gastritis and its reversion after HP eradication and (ii the association of methylation of the promoter region of Reprimo, a p53-mediated cell cycle arrest gene, with aggressive HP strains in high risk areas for GC. In addition, we discuss the finding of RPRM as a circulating cell-free DNA, offering the opportunity for noninvasive risk assessment of GC. Finally, the integration of OLGA and tissue biomarkers, by systems pathology approach, suggests that severe atrophy has a greater risk for GC development if, in addition, overexpressed p73. This trial is registered with ClinicalTrials.gov NCT01774266.

Helicobacter pylori Infection and Anemia in Taiwanese Adults

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Hsiang-Yao Shih

2013-01-01

Full Text Available Background. Chronic Helicobacter pylori infection and iron-deficiency anemia (IDA are common in adults. Although the most common causes of IDA usually arise from the gastrointestinal tract, the association between chronic Helicobacter pylori infection and anemia remains unclear. Aim. To evaluate the association of chronic Helicobacter pylori infection and IDA. Materials and Methods. We enrolled 882 patients from January 2010 to April 2013. The status of Helicobacter pylori (H.p infection was confirmed and blood samples from the same participants were taken on the same day to check the level of hemoglobin, serum iron, ferritin, and total iron-binding capacity (TIBC. Results. No significant difference was noted from the demographic data. The average level of hemoglobin (Hb was not different between negative and positive groups, pos 13.57 g/dL versus neg 13.65 g/dL (P=0.699. Although the levels of serum IDA related parameters were expected in positive group (lower serum iron and ferritin and higher TIBC these differences did not reach statistical significance (P=0.824 for iron, P=0.360 for ferritin, and P=0.252 for TIBC. Conclusion. Chronic Helicobacter pylori infection is not attributed to IDA. The levels of hemoglobin, serum iron and ferritin, and TIBC remain unaffected after chronic H.p infection. Large-scale clinical studies are needed to prove the association.

[Latin American contribution to the study of Helicobacter pylori].

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Ramírez Ramos, Alberto; Sánchez Sánchez, Rolando

2009-09-01

We have reviewed Lilacs, PubMed and Google searching for original articles related to Helicobacter pylori published by Latin American investigators from 2003 to 2008. Contributions in the following fields by countries are: Molecular biology: Brasil, Chile, Colombia, Peru y Venezuela. Argentina, Brasil, Colombia, Cuba, Peru y Venezuela. Argentina, Bolivia, Brasil, Chile, Costa Rica, Colombia, Mexico, Peru y Venezuela. Helicobacter pylori and gastroduodenal diseases: Brasil, Cuba, Peru y Venezuela. Helicobacter pylori and extra digestive diseases: Brasil, Colombia and Venezuela. Pediatrics: Brasil, Cuba y Venezuela. Argentina, Brasil, Chile, Colombia, Costa Rica, Mexico, Peru y Venezuela.

Helicobacter pylori and non-malignant diseases.

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Matysiak-Budnik, Tamara; Laszewicz, Wiktor; Lamarque, Dominique; Chaussade, Stanislas

2006-10-01

The prevalence of Helicobacter pylori-associated peptic ulcers, in particular duodenal ulcers, is decreasing following decreasing prevalence of H. pylori infection, while the frequency of non-steroidal anti-inflammatory drugs (NSAIDs)-induced and H. pylori-negative idiopathic ulcers is increasing. The incidence of bleeding ulcers has been stable during the last decades. Several putative H. pylori virulence genes, i.e., cag, vacA, babA, or dupA, as well as host-related genetic factors like IL-1beta and TNFalpha-gene polymorphism, have been proposed as risk factors for duodenal ulcer. H. pylori eradication may prevent NSAID complications, in particular, when it is performed before introduction of NSAIDs. There is a complex association between H. pylori and gastroesophageal reflux disease (GERD), and the impact of H. pylori eradication on the appearance of GERD symptoms depends on various host- and bacteria-related factors. Eradication of H. pylori in GERD is recommended in patients before instauration of a long-term PPI treatment to prevent the development of gastric atrophy. A small proportion (10%) of non-ulcer dyspepsia cases may be attributed to H. pylori and may benefit from eradication treatment. A test-and-treat strategy is more cost-effective than prompt endoscopy in the initial management of dyspepsia.

Prevalence of Helicobacter pylori in Northern Jordan: Endoscopy based study

International Nuclear Information System (INIS)

Bani-Hani, Kamal E.; Hammouri, Shadi M.

2001-01-01

Helicobacter pylori infection is considered the most common infection worldwide and is associated with many other disorders. The aim of this study is to determine the prevalence of this infection among patients undergoing endoscopy in Northern Jordan. Between November 1998 and September 2000, all patients referred from the Gastro-esophageal Clinic to the Endoscopy Unit at Princess Basma Teaching Hospital, Irbid, Northern Jordan were enrolled in this prospective study. For each patient clinical and epidemiological data was collected and endoscopy was performed. At least 3 antral biopsies were obtained from each patient, and these were examined histologically for the presence of gastritis and stained for Helicobacter pylori using modified Giemsa stain. A total of 197 consecutive patients (113 females) with a mean age of 40.2 years (range 15-91 years) were studied. Abdominal pain was the highest presenting symptom. Gastritis 91% and esophagitis 42% were the most frequent endoscopic findings. Gastritis was documented histologically in 183 (93%) of patients. Helicobacter pylori was found in 161 patients (82%), with all of these having histological gastritis. The 11 patients with gastric ulcer, compared to the 51 out of the 59 (86%) patients with duodenal ulcer, showed Helicobacter pylori in their biopsies. The prevalence of Helicobacter pylori infection in patients subjected to an upper gastrointestinal endoscopy in Jordan is high. This study confirms that Helicobacter pylori is significantly associated with gastritis and peptic ulcer. Further studies are needed to determine the types of Helicobacter pylori strains present in Jordan. (author)

A Novel Assay for Easy and Rapid Quantification of Helicobacter pylori Adhesion

DEFF Research Database (Denmark)

Skindersoe, Mette E; Rasmussen, Lone; Andersen, Leif P

2015-01-01

BACKGROUND: Reducing adhesion of Helicobacter pylori to gastric epithelial cells could be a new way to counteract infections with this organism. We here present a novel method for quantification of Helicobacter pylori adhesion to cells. METHODS: Helicobacter pylori is allowed to adhere to AGS...

NikR mediates nickel-responsive transcriptional induction of urease expression in Helicobacter pylori

NARCIS (Netherlands)

A.H.M. van Vliet (Arnoud); S.W. Poppelaars (Sophie); B.J. Davies; J. Stoof (Jeroen); S. Bereswill (Stefan); M. Kist (Manfred); C.W. Penn (Charles); E.J. Kuipers (Ernst); J.G. Kusters (Johannes)

2002-01-01

textabstractThe important human pathogen Helicobacter pylori requires the abundant expression and activity of its urease enzyme for colonization of the gastric mucosa. The transcription, expression, and activity of H. pylori urease were previously demonstrated to be induced by

Inhibition of Helicobacter pylori CagA-Induced Pathogenesis by Methylantcinate B from Antrodia camphorata

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Chun-Jung Lin

2013-01-01

Full Text Available The bacterial pathogen Helicobacter pylori (Hp is the leading risk factor for the development of gastric cancer. Hp virulence factor, cytotoxin-associated gene A (CagA interacted with cholesterol-enriched microdomains and leads to induction of inflammation in gastric epithelial cells (AGS. In this study, we identified a triterpenoid methylantcinate B (MAB from the medicinal mushroom Antrodia camphoratawhich inhibited the translocation and phosphorylation of CagA and caused a reduction in hummingbird phenotype in HP-infected AGS cells. Additionally, MAB suppressed the Hp-induced inflammatory response by attenuation of NF-κB activation, translocation of p65 NF-κB, and phosphorylation of IκB-α, indicating that MAB modulates CagA-mediated signaling pathway. Additionally, MAB also suppressed the IL-8 luciferase activity and its secretion in HP-infected AGS cells. On the other hand, molecular structure simulations revealed that MAB interacts with CagA similarly to that of cholesterol. Moreover, binding of cholesterol to the immobilized CagA was inhibited by increased levels of MAB. Our results demonstrate that MAB is the first natural triterpenoid which competes with cholesterol bound to CagA leading to attenuation of Hp-induced pathogenesis of epithelial cells. Thus, this study indicates that MAB may have a scope to develop as a therapeutic candidate against Hp CagA-induced inflammation.

Compound 13, an α1-selective small molecule activator of AMPK, inhibits Helicobacter pylori-induced oxidative stresses and gastric epithelial cell apoptosis

International Nuclear Information System (INIS)

Zhao, Hangyong; Zhu, Huanghuang; Lin, Zhou; Lin, Gang; Lv, Guoqiang

2015-01-01

Half of the world's population experiences Helicobacter pylori (H. pylori) infection, which is a main cause of gastritis, duodenal and gastric ulcer, and gastric cancers. In the current study, we investigated the potential role of compound 13 (C13), a novel α1-selective small molecule activator of AMP-activated protein kinase (AMPK), against H. pylori-induced cytotoxicity in cultured gastric epithelial cells (GECs). We found that C13 induced significant AMPK activation, evidenced by phosphorylation of AMPKα1 and ACC (acetyl-CoA carboxylase), in both primary and transformed GECs. Treatment of C13 inhibited H. pylori-induced GEC apoptosis. AMPK activation was required for C13-mediated GEC protection. Inhibition of AMPK kinase activity by the AMPK inhibitor Compound C, or silencing AMPKα1 expression by targeted-shRNAs, alleviated C13-induced GEC protective activities against H. pylori. Significantly, C13 inhibited H. pylori-induced reactive oxygen species (ROS) production in GECs. C13 induced AMPK-dependent expression of anti-oxidant gene heme oxygenase (HO-1) in GECs. Zinc protoporphyrin (ZnPP) and tin protoporphyrin (SnPP), two HO-1 inhibitors, not only suppressed C13-mediated ROS scavenging activity, but also alleviated its activity in GECs against H. pylori. Together, these results indicate that C13 inhibits H. pylori-induced ROS production and GEC apoptosis through activating AMPK–HO–1 signaling. - Highlights: • We synthesized compound 13 (C13), a α1-selective small molecule AMPK activator. • C13-induced AMPK activation requires α1 subunit in gastric epithelial cells (GECs). • C13 enhances Helicobacter pylori-induced pro-survival AMPK activation to inhibit GEC apoptosis. • C13 inhibits H. pylori-induced reactive oxygen species (ROS) production in GECs. • AMPK-heme oxygenase (HO-1) activation is required for C13-mediated anti-oxidant activity

Compound 13, an α1-selective small molecule activator of AMPK, inhibits Helicobacter pylori-induced oxidative stresses and gastric epithelial cell apoptosis

Energy Technology Data Exchange (ETDEWEB)

Zhao, Hangyong; Zhu, Huanghuang; Lin, Zhou; Lin, Gang; Lv, Guoqiang, E-mail: lvguoqiangwuxivip@163.com

2015-08-07

Half of the world's population experiences Helicobacter pylori (H. pylori) infection, which is a main cause of gastritis, duodenal and gastric ulcer, and gastric cancers. In the current study, we investigated the potential role of compound 13 (C13), a novel α1-selective small molecule activator of AMP-activated protein kinase (AMPK), against H. pylori-induced cytotoxicity in cultured gastric epithelial cells (GECs). We found that C13 induced significant AMPK activation, evidenced by phosphorylation of AMPKα1 and ACC (acetyl-CoA carboxylase), in both primary and transformed GECs. Treatment of C13 inhibited H. pylori-induced GEC apoptosis. AMPK activation was required for C13-mediated GEC protection. Inhibition of AMPK kinase activity by the AMPK inhibitor Compound C, or silencing AMPKα1 expression by targeted-shRNAs, alleviated C13-induced GEC protective activities against H. pylori. Significantly, C13 inhibited H. pylori-induced reactive oxygen species (ROS) production in GECs. C13 induced AMPK-dependent expression of anti-oxidant gene heme oxygenase (HO-1) in GECs. Zinc protoporphyrin (ZnPP) and tin protoporphyrin (SnPP), two HO-1 inhibitors, not only suppressed C13-mediated ROS scavenging activity, but also alleviated its activity in GECs against H. pylori. Together, these results indicate that C13 inhibits H. pylori-induced ROS production and GEC apoptosis through activating AMPK–HO–1 signaling. - Highlights: • We synthesized compound 13 (C13), a α1-selective small molecule AMPK activator. • C13-induced AMPK activation requires α1 subunit in gastric epithelial cells (GECs). • C13 enhances Helicobacter pylori-induced pro-survival AMPK activation to inhibit GEC apoptosis. • C13 inhibits H. pylori-induced reactive oxygen species (ROS) production in GECs. • AMPK-heme oxygenase (HO-1) activation is required for C13-mediated anti-oxidant activity.

Dietary Composition Influences Incidence of Helicobacter pylori-Induced Iron Deficiency Anemia and Gastric Ulceration

Science.gov (United States)

Beckett, Amber C.; Piazuelo, M. Blanca; Noto, Jennifer M.; Peek, Richard M.; Washington, M. Kay; Algood, Holly M. Scott

2016-01-01

Epidemiologic studies have provided conflicting data regarding an association between Helicobacter pylori infection and iron deficiency anemia (IDA) in humans. Here, a Mongolian gerbil model was used to investigate a potential role of H. pylori infection, as well as a possible role of diet, in H. pylori-associated IDA. Mongolian gerbils (either H. pylori infected or uninfected) received a normal diet or one of three diets associated with increased H. pylori virulence: high-salt, low-iron, or a combination of a high-salt and low-iron diet. In an analysis of all infected animals compared to uninfected animals (independent of diet), H. pylori-infected gerbils had significantly lower hemoglobin values than their uninfected counterparts at 16 weeks postinfection (P Anemia was associated with the presence of gastric ulceration but not gastric cancer. Infected gerbils consuming diets with a high salt content developed gastric ulcers significantly more frequently than gerbils consuming a normal-salt diet, and the lowest hemoglobin levels were in infected gerbils consuming a high-salt/low-iron diet. These data indicate that H. pylori infection can cause IDA and that the composition of the diet influences the incidence and severity of H. pylori-induced IDA. PMID:27620719

The role of helicobacter pylori infection in the pathogenesis of chronic urticaria

International Nuclear Information System (INIS)

Ghazzawi, I.M.; Obidat, N.A.

2004-01-01

Objective: To determine the prevalence of H. pylori infection in patients with idiopathic chronic urticaria (ICU) and to see if eradication of the bacterium affects the course of the urticaria. Patients and Methods: One hundred patients with idiopathic chronic urticaria and 43 healthy subjects (matched for age and sex) underwent serological testing for H. pylori infection. All patients with idiopathic chronic urticaria were examined for Helicobacter pylori infection with the /sup 13/C-urea test as well as the serological testing. Gastric biopsy was obtained from 36 patients. Patients with proven Helicobacter pylori infection were given treatment for 2 weeks. Six weeks afterwards they were tested again for Helicobacter pylori infection, and their urticaria was clinically assessed. Results: There was no significant difference in the seroprevalence of H. pylori infection between : idiopathic chronic urticaria patients and healthy subjects. Helicobacter pylori was detected in 76% of patients and 69.8% of controls. Out of the 76 patients treated, only 24 showed complete remission of their urticaria after successfully eradicating Helicobacter pylori infection, the others only having some improvement in their symptoms. Conclusion: Patients with idiopathic chronic urticaria have similar high rates of H. pylori infection as healthy subjects. Bacterium eradication is associated with improvement of urticaria symptoms, suggesting a possible role of Helicobacter pylori in the pathogenesis of this skin disorder. (author)

Geographic pathology of Helicobacter pylori gastritis

NARCIS (Netherlands)

Liu, Yi; Ponsioen, Cyriel I. J.; Xiao, Shu-Dong; Tytgat, Guido N. J.; ten Kate, Fiebo J. W.

2005-01-01

Background and aim. Helicobacter pylori is etiologically associated with gastritis and gastric cancer. There are significant geographical differences between the clinical manifestation of H. pylori infections. The aim of this study was to compare gastric mucosal histology in relation to age among H.

Helicobacter Pylori : Serological Testing and Treatment in ...

African Journals Online (AJOL)

Purpose: Helicobacter pylori has been strongly associated with dyspepsia and eradication of H. pylori after a non-invasive testing is an integral part of most management guidelines. This study evaluated the benefit of serological testing and treatment of H. pylori in Nigerian patients presenting with uninvestigated dyspepsia.

Helicobacter pylori and nonmalignant diseases.

LENUS (Irish Health Repository)

Alakkari, Alaa

2012-02-01

Research published over the past year has documented the continued decline of Helicobacter pylori-related peptic ulcer disease and increased recognition of non-H. pylori, non-steroidal anti-inflammatory drugs ulcer disease--idiopathic ulcers. Despite reduced prevalence of uncomplicated PUD, rates of ulcer complications and associated mortality remain stubbornly high. The role of H. pylori in functional dyspepsia is unclear, with some authors considering H. pylori-associated nonulcer dyspepsia a distinct organic entity. There is increasing acceptance of an inverse relationship between H. pylori and gastroesophageal reflux disease (GERD), but little understanding of how GERD might be more common\\/severe in H. pylori-negative subjects. Research has focused on factors such as different H. pylori phenotypes, weight gain after H. pylori eradication, and effects on hormones such as ghrelin that control appetite.

Prevalence of Coinfection with Gastric Non-Helicobacter pylori Helicobacter (NHPH) Species in Helicobacter pylori-infected Patients Suffering from Gastric Disease in Beijing, China.

Science.gov (United States)

Liu, Jie; He, Lihua; Haesebrouck, Freddy; Gong, Yanan; Flahou, Bram; Cao, Qizhi; Zhang, Jianzhong

2015-08-01

The Helicobacter heilmannii sensu lato (H. heilmannii s.l.) group consists of long, spiral-shaped bacteria naturally colonizing the stomach of animals. Moreover, bacteria belonging to this group have been observed in 0.2-6% of human gastric biopsy specimens, and associations have been made with the development of chronic gastritis, peptic ulceration, and gastric MALT lymphoma in humans. To gain insight into the prevalence of H. heilmannii s.l. infections in patients suffering from gastric disease in China, H. heilmannii s.l. species-specific PCRs were performed on DNA extracts from rapid urease test (RUT)-positive gastric biopsies from 1517 patients followed by nucleotide sequencing. At the same time, Helicobacter pylori cultivation and specific PCR was performed to assess H. pylori infection in these patients. In total, H. heilmannii s.l. infection was detected in 11.87% (178/1499) of H. pylori-positive patients. The prevalence of H. suis, H. felis, H. bizzozeronii, H. heilmannii sensu stricto (s.s.), and H. salomonis in the patients was 6.94%, 2.20%, 0.13%, 0.07%, and 2.54%, respectively. Results revealed that all patients with H. heilmannii s.l. infection were co-infected with H. pylori, and some patients were co-infected with more than two different Helicobacter species. Helicobacter heilmannii s.l. infections are fairly common in Chinese patients. This should be kept in mind when diagnosing the cause of gastric pathologies in patients. Helicobacter suis was shown to be by far the most prevalent H. heilmannii s.l.species. © 2014 John Wiley & Sons Ltd.

EKSPRESI ANTI-HELICOBACTER PYLORI PADA GASTRITIS KRONIS, LESI PRAKANKER, DAN KARSINOMA GASTER

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Lina Damayanti

2015-08-01

Full Text Available Prevalence of Helicobacter pylori infection in Indonesia was 36-46%. In Jakarta and Surabaya, the prevalence were 85,7%-93,9%. Helicobacter pylori infection play role in pathogenesis of pectic ulcers, chronic gastritis, carcinoma of gaster and gastric lymphoma. Epidemiologic study showed 80% of carcinoma of gaster related with H pylori infection.This study analyzed expression of anti-Helicobacter pylori in chronic gastritis, precancer lesion , and carcinoma of gaster. This study was a observational descriptive study with case control design. Thirty (30 samples from paraffin bloc that were diagnosed with chronic gastritis, precancer lesion, and carcinoma of gaster at Dokter Kariadi hospital in 2013 was stained by hematoxylin eosin, giemsa and immunohistochemistry of anti-helicobacter pylori. Data was analyzed by descriptive analysis. Thirty (30 samples were diagnosed as gastritis chronis 13 (43,3% , pra cancer lesion(36.6%, and carcinoma(20.1%. Chronic gastritis can be occurred at all age and no distinct difference on sex, while gastric carcinoma predominant in male older than 40 years. Expresion of Helicobacter pylori on chronic gastritis was 84.6%, precancer lesion was 54.5%, and gastric carcinoma was 83.3%. The Giemsa stain gave 23.3% false positive and 20% false negative. Helicobacter pylori expression can be showed in chronic gastritis, precancer lesion, and gastric carcinoma. Keywords: Chronic gastritis, gastric carcinoma, Helicobacter pylori

The relationship between helicobacter pylori infection and gastro-esophageal reflux disease.

Science.gov (United States)

Mahdi, Batool M

2011-03-01

Gastro-esophageal reflux disease is a common condition, affecting 25%-40% of the population. Increasing attention has been paid to the relationship between Helicobacter pylori infection and reflux esophagitis. The aim of this study was to investigate the association between CagA+ H. pylori and endoscopically proven gastro-esophageal reflux disease. The study group included 60 hospital patients with gastro-esophageal reflux disease between 2007 and 2009 as compared with 30 healthy patients from a control group that was age and sex matched. Helicobacter pylori CagA+ was identified by an immunological test (Immunochromatography test) (ACON, USA). Helicobacter pyloriCagA+ was present in 42/60 (70%) of the patients with gastro-esophageal reflux disease and in 11/30 (36.6%) patients in the control group (p=0.002). The Odds ratio = 0.8004 with 95% Confidence Interval = from 0.3188 to 2.0094. The relative risk=1.35 that indicates an association between Helicobacter pylori and disease. The presence of Helicobacter pylori is significantly increased in patients with gastro-esophageal reflux disease as compared with the control group.

Changes in gastric microbiota induced by Helicobacter pylori infection and preventive effects of Lactobacillus plantarum ZDY 2013 against such infection.

Science.gov (United States)

Pan, Mingfang; Wan, Cuixiang; Xie, Qiong; Huang, Renhui; Tao, Xueying; Shah, Nagendra P; Wei, Hua

2016-02-01

Helicobacter pylori is a gram-negative pathogen linked to gastric ulcers and stomach cancer. Gastric microbiota might play an essential role in the pathogenesis of these stomach diseases. In this study, we investigated the preventive effect of a probiotic candidate Lactobacillus plantarum ZDY 2013 as a protective agent against the gastric mucosal inflammation and alteration of gastric microbiota induced by H. pylori infection in a mouse model. Prior to infection, mice were pretreated with or without 400 µL of L. plantarum ZDY 2013 at a concentration of 10(9) cfu/mL per mouse. At 6 wk postinfection, gastric mucosal immune response and alteration in gastric microbiota mice were examined by quantitative real-time PCR and high-throughput 16S rRNA gene amplicon sequencing, respectively. The results showed that L. plantarum ZDY 2013 pretreatment prevented increase in inflammatory cytokines (e.g., IL-1β and IFN-γ) and inflammatory cell infiltration in gastric lamina propria induced by H. pylori infection. Weighted UniFrac principal coordinate analysis showed that L. plantarum ZDY 2013 pretreatment prevented the alteration in gastric microbiota post-H. pylori infection. Linear discriminant analysis coupled with effect size identified 22 bacterial taxa (e.g., Pasteurellaceae, Erysipelotrichaceae, Halomonadaceae, Helicobacteraceae, and Spirochaetaceae) that overgrew in the gastric microbiota of H. pylori-infected mice, and most of them belonged to the Proteobacteria phylum. Lactobacillus plantarum ZDY 2013 pretreatment prevented this alteration; only 6 taxa (e.g., Lachnospiraceae, Ruminococcaceae, and Clostridiaceae), mainly from the taxa of Firmicutes and Bacteroidetes, were dominant in the gastric microbiota of the L. plantarum ZDY 2013 pretreated mice. Administration of L. plantarum ZDY 2013 for 3 wk led to increase in several bacterial taxa (e.g., Rikenella, Staphylococcus, Bifidobacterium), although a nonsignificant alteration was found in the gastric microbiota

Immunohistochemical testing for Helicobacter Pylori existence in neoplasms of the colon

Directory of Open Access Journals (Sweden)

Yasar Nurgul

2008-08-01

Full Text Available Abstract Background Helicobacter pylori is a common pathogen, and its prevalence varies with socioeconomic conditions (10–80%. It has recently been recognized as a class I carcinogen in relation to gastric cancer. The aim of this study was to investigate the presence of Helicobacter pylori in neoplasms of the colon by immunohistochemical methods. Methods The polypectomy materials of 51 patients (19 male and 32 female who had undergone colonoscopic polypectomy were retrieved for retrospective examination. The endoscopic size and colonic localization of the polyps were recorded. Hematoxylin and eosin stains were evaluated according to histological type and grade of dysplasia. Biopsy stains were immunohistochemically treated with Helicobacter pylori antibodies by the streptavidine-biotin immunoperoxidase technique. Helicobacter pylori staining in the gastric mucosa was used as the control for the immunohistochemical method. Specimens were classified according to the presence of Helicobacter pylori under an optical microscope, and Helicobacter pylori positive specimens were stratified according to the respective staining pattern. Results Mean age was 61.88 ± 10.62 (40–82 years. Polyp sizes were 1.45 ± 0.92 (1–4 cm; and 25.5% of polyps were localized in the right colon, 68.6% in the left colon and 5.9% in the transverse colon. Presence of Helicobacter pylori was not correlated with localization (p > 0.05 or size of the polyps (p > 0.05. Eleven (21.6% of all specimens included in the study were Helicobacter pylori positive by immunohistochemical methods. Of the Helicobacter pylori positive specimens, the staining pattern was diffuse: Equivocal in 90.9%, nonspecific with a finely granular type concentrated on the luminal surface in 90.9%, dot-like granular in 54.5%, and spiral in 9.1%. Of the tubular polyps, 17.9% were H. pylori positive, and the staining pattern was equivocal in 100%, luminal in 85.7%, and dot-like granular in 57.1%. Of the

Helicobacter pylori: From Bench to Bedside

Directory of Open Access Journals (Sweden)

N Chiba

1997-01-01

Full Text Available With the exponential increase in research in the field of Helicobacter pylori a paradigm shift has occurred. It is now recognized that H pylori is a chronic infection of the stomach causing inflammation. Some patients remain asymptomatic, while others may develop dyspepsia, duodenal or gastric ulcer, gastric cancer or a mucosa-associated lymphoid tissue lymphoma. However, the role of H pylori in contributing to nonulcer dyspepsia or nonsteroidal anti-inflammatory drug gastropathy remains controversial. An effective vaccine against H pylori is years away. Major interest has focused on the questions "who should be investigated and therefore treated" and "what is the latest gold standard for eradication of H pylori"? In Europe, guidelines have been developed to help the practitioner answer these important questions. Canadian guidelines will soon be available. For persons with known peptic ulcer disease there should be unequivocal acceptance that the good clinical practice of eradicating H pylori will result in substantial savings in health care expenses. The original 'classical triple therapy' (bismuth, metronidazole and tetracycline [BMT] has now been surpassed by the combination of a proton pump inhibitor (PPI plus two antibiotics (metronidazole plus clarithromycin; amoxicillin plus clarithromycin; or amoxicillin plus metronidazole, each given twice a day for one week. In Canada, the regimen of omeprazole plus one antibiotic (amoxicillin or clarithromycin was approved recently but gives an eradication rate that is lower than the current target of 90%. According to the European (Mäastricht recommendations, if a single treatment attempt with PPI plus two antibiotics fails, PPI plus BMT is recommended.

PREVALENCE OF HELICOBACTER PYLORI IN PATIENTS WITH DYSPEPSIA UNDERGOING UPPER GASTRO INTESTINAL ENDOSCOPY IN TERTIARY CARE HOSPITAL

Directory of Open Access Journals (Sweden)

Ajay Babu K

2017-12-01

diagnosis. Rapid urease test and Giemsa staining were conducted on endoscopy biopsy specimens and Helicobacter pylori positivity was based on either Rapid urease test and/or histopathological examination was positive. From the present study it is evident that, there was no specific symptom attributable to H. pylori infection. Helicobacter pylori infection is more common in males than females. Helicobacter pylori is consistently associated with peptic ulcer disease than non-ulcer dyspepsia, which is in broad agreement with the studies done earlier. Thus we conclude that, Helicobacter pylori infection may have a role in the aetiopathogenesis of peptic ulcer disease. There appears to be no significant association between Helicobacter pylori infection and dyspeptic cases with normal endoscopy. This finding does not exclude the possibility that a small undefined subset of infected individuals will have symptoms induced by the infection, but only large randomized trials will be able to establish this. Hence, we recommend eradication of the bacteria only in patients positive for the bacterium, who have peptic ulceration. We believe in, Peter C Robin’s dictum: “If a person with peptic ulcer disease is shown to have Helicobacter pylori, then eradication is indicated”.

Caveolin-1 protects B6129 mice against Helicobacter pylori gastritis.

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Ivana Hitkova

Full Text Available Caveolin-1 (Cav1 is a scaffold protein and pathogen receptor in the mucosa of the gastrointestinal tract. Chronic infection of gastric epithelial cells by Helicobacter pylori (H. pylori is a major risk factor for human gastric cancer (GC where Cav1 is frequently down-regulated. However, the function of Cav1 in H. pylori infection and pathogenesis of GC remained unknown. We show here that Cav1-deficient mice, infected for 11 months with the CagA-delivery deficient H. pylori strain SS1, developed more severe gastritis and tissue damage, including loss of parietal cells and foveolar hyperplasia, and displayed lower colonisation of the gastric mucosa than wild-type B6129 littermates. Cav1-null mice showed enhanced infiltration of macrophages and B-cells and secretion of chemokines (RANTES but had reduced levels of CD25+ regulatory T-cells. Cav1-deficient human GC cells (AGS, infected with the CagA-delivery proficient H. pylori strain G27, were more sensitive to CagA-related cytoskeletal stress morphologies ("humming bird" compared to AGS cells stably transfected with Cav1 (AGS/Cav1. Infection of AGS/Cav1 cells triggered the recruitment of p120 RhoGTPase-activating protein/deleted in liver cancer-1 (p120RhoGAP/DLC1 to Cav1 and counteracted CagA-induced cytoskeletal rearrangements. In human GC cell lines (MKN45, N87 and mouse stomach tissue, H. pylori down-regulated endogenous expression of Cav1 independently of CagA. Mechanistically, H. pylori activated sterol-responsive element-binding protein-1 (SREBP1 to repress transcription of the human Cav1 gene from sterol-responsive elements (SREs in the proximal Cav1 promoter. These data suggested a protective role of Cav1 against H. pylori-induced inflammation and tissue damage. We propose that H. pylori exploits down-regulation of Cav1 to subvert the host's immune response and to promote signalling of its virulence factors in host cells.

Enrichment of Probiotic Yogurt with Broccoli Sprout Extract and its Effect on Helicobacter pylori

Directory of Open Access Journals (Sweden)

Ali Reza Sadeghi

2017-01-01

Full Text Available Background and Objective: Antibiotic consumption is the main way to cure infection induced by Helicobacter pylori. On the other hand, antibiotics have side effects on human body. So, finding an efficient way to replace antibiotic consumption seems necessary. The aim of this study was to investigate the effect of broccoli sprout extract on the viability of probiotic bacteria and yogurt’s physicochemical properties, and examine the synergistic effect of this extract with probiotics on Helicobacter pylori growth inhibition.Material and Methods: Four levels of broccoli sprout extract (22.5, 45, 90 and 180 mg ml-1 were prepared and their effect on probiotic yogurt samples was examined. Moreover, their anti- Helicobacter pylori effect was determined.Results and Conclusion: The research results revealed that Broccoli sprout extract did not have any inhibitory effect on Bifidobacterium lactis and Lactobacillus acidophilus. The variations in acidity of the samples were not significant during storage. A positive correlation was observed between broccoli sprout extract concentration and syneresis. The findings showed the synergistic effect of broccoli sprout extract and probiotics on Helicobacter pylori growth inhibition. Therefore, using broccoli sprout extract and probiotic bacteria, we can produce a yogurt that is effective on the growth inhibition of Helicobacter pylori.Conflict of interest: The authors declare that there is no conflict of interest.

Relationship of Halitosis with Gastric Helicobacter Pylori Infection

Directory of Open Access Journals (Sweden)

Farnaz HajiFattahi

2015-10-01

Full Text Available Objectives: Gastric infection with Helicobacter pylori may be one of the main causes of halitosis. This study was performed to evaluate the relationship of Heli- cobacter pylori infection with halitosis.Materials and Methods: This case control study was performed on 44 dyspeptic patients with a mean age of 34.29±13.71 years (range 17 to 76 years. The case group included 22 patients with halitosis and no signs of diabetes mellitus, renal or liver failure, upper respiratory tract infection, malignancies, deep carious teeth, severe  periodontitis,  coated  tongue,  dry  mouth  or poor  oral  hygiene.  Control group included 22 patients without halitosis and the same age, sex, systemic and oral conditions as the case group. Halitosis was evaluated using organoleptic test (OLT and Helicobacter pylori infection was evaluated by Rapid Urease Test (RUT during endoscopy. The data were statistically analyzed using chi square, Mann Whitney and t-tests.Results: Helicobacter pylori infection was detected in 20 (91% out of 22 halitosis patients, and 7 control subjects (32% (P<0.001.Conclusion: Helicobacter pylori gastric infection can be a cause of bad breath. Dentists should pay more attention to this infection and refer these patients to in- ternists to prevent further gastrointestinal (GI complications and probable malig- nancies.

Polymorphisms at Locus 4p14 of Toll-Like Receptors TLR-1 and TLR-10 Confer Susceptibility to Gastric Carcinoma in Helicobacter pylori Infection.

Directory of Open Access Journals (Sweden)

M Ravishankar Ram

Full Text Available Helicobacter pylori (H. pylori -induced gastric inflammation impacts the functions of leptin- and ghrelin-producing cells in the gastroduodenum. Inflammation resulting from H. pylori sensing via Toll-like receptors (TLRs and the associated downstream signaling largely remain ambiguous. Here, we investigated the role of gut hormones, pro-inflammatory cytokines and single nucleotide polymorphisms (SNPs associated with TLR 4p14 in H. pylori disease in 30 subjects with non-ulcer dyspepsia (NUD, 40 with peptic ulcer disease (PUD and 15 with gastric cancer (GC subjects positive and negative for H. pylori infection. The level of pro-inflammatory cytokines was directly proportional to the severity of gastritis, and disease status influenced the levels of gut hormones and pro-inflammatory cytokines. TLR-1 SNPs rs4833095 and TLR-10 SNPs rs10004195 and were directly associated with H. pylori disease, and were up-regulated in the presence of H. pylori in a genotype-independent manner. We concluded that TLR-1 rs4833095 and TLR10 rs10004195 confer susceptibility to development of gastroduodenal disease, especially GC in H.pylori disease.

Incidence of Helicobacter felis and the effect of coinfection with Helicobacter pylori on the gastric mucosa in the African population

NARCIS (Netherlands)

Fritz, E. Lekunze; Slavik, Tomas; Delport, Wayne; Olivier, Brenda; van der Merwe, Schalk W.

2006-01-01

Helicobacter pylori and Helicobacter felis are two of the Helicobacter spp. that infect humans. H. pylori has been linked to significant gastric pathology. Coinfection with Helicobacter spp. may influence infectious burden, pathogenesis, and antibiotic resistance; however, this has not been studied.

Helicobacter pylori infection, serum pepsinogens, and pediatric abdominal pain: a pilot study.

Science.gov (United States)

Kassem, Eias; Naamna, Medhat; Mawassy, Kadri; Beer-Davidson, Gany; Muhsen, Khitam

2017-08-01

The significance of Helicobacter pylori (H. pylori) infection in pediatric abdominal pain remains poorly recognized. We examined associations of H. pylori infection and serum pepsinogens (PGs), as non-invasive markers of gastritis, with pediatric abdominal pain. A case-control study was conducted among 99 children aged 5-17 years admitted to one hospital for abdominal pain (cases) without an apparent organic reason. Using enzyme-linked immunosorbent assays, sera were tested and compared with 179 controls for anti-H. pylori immunoglobulin G (IgG) antibodies and PGI and PGII levels. Multivariable analysis was performed to adjust for potential confounders. H. pylori IgG sero-positivity was 34.3 and 36.3% in cases and controls, respectively, P = 0.7. H. pylori-infected children had higher median PGI and PGII levels and a lower PGI/PGII ratio than uninfected children. Cases infected with H. pylori had a higher median PGII level (P < 0.001) and lower PGI/PGII ratio (P = 0.036) than controls infected with H. pylori. The percentage of cases with PGII ≥7.5 μg/L, as indication for antral inflammation, was higher than in controls: 58.6 versus 44.7%, P = 0.027. Children with PGII levels ≥7.5 μg/L had increased risk for abdominal pain: adjusted prevalence ratio 1.73 [95% confidence intervals 1.02, 2.93], P = 0.039. Children with increased serum PGII levels, as an indication of gastritis, are more likely to have abdominal pain. Serum PGs can be a useful non-invasive marker for gastritis, in evaluating children with severe abdominal pain with no apparent organic reason. What is Known: • The significance of Helicobacter pylori infection in pediatric abdominal pain remains debated. • Serum pepsinogens (PGs), non-invasive markers of gastric inflammation, were rarely utilized in assessing the association between H. pylori in pediatric abdominal pain of unknown origin. What is New: • High serum PGII level, as an indication of gastritis, rather than H. pylori

Enhanced M1 macrophage polarization in human helicobacter pylori-associated atrophic gastritis and in vaccinated mice.

Directory of Open Access Journals (Sweden)

Marianne Quiding-Järbrink

Full Text Available BACKGROUND: Infection with Helicobacter pylori triggers a chronic gastric inflammation that can progress to atrophy and gastric adenocarcinoma. Polarization of macrophages is a characteristic of both cancer and infection, and may promote progression or resolution of disease. However, the role of macrophages and their polarization during H. pylori infection has not been well defined. METHODOLOGY/PRINCIPAL FINDINGS: By using a mouse model of infection and gastric biopsies from 29 individuals, we have analyzed macrophage recruitment and polarization during H. pylori infection by flow cytometry and real-time PCR. We found a sequential recruitment of neutrophils, eosinophils and macrophages to the gastric mucosa of infected mice. Gene expression analysis of stomach tissue and sorted macrophages revealed that gastric macrophages were polarized to M1 after H. pylori infection, and this process was substantially accelerated by prior vaccination. Human H. pylori infection was characterized by a mixed M1/M2 polarization of macrophages. However, in H. pylori-associated atrophic gastritis, the expression of inducible nitric oxide synthase was markedly increased compared to uncomplicated gastritis, indicative of an enhanced M1 macrophage polarization in this pre-malignant lesion. CONCLUSIONS/SIGNIFICANCE: These results show that vaccination of mice against H. pylori amplifies M1 polarization of gastric macrophages, and that a similar enhanced M1 polarization is present in human H. pylori-induced atrophic gastritis.

Association of Helicobacter pylori infection with peptic ulcer disease ...

African Journals Online (AJOL)

Background: Helicobacter pylori infection has been identified as an important risk factor for the development of peptic ulcer disease and is probably the most important cause of relapse in those previously treated for peptic ulcer disease. The aim of this study was to determine the association of Helicobacter pylori infection as ...

Lactobacillus acidophilus ameliorates H. pylori-induced gastric inflammation by inactivating the Smad7 and NFκB pathways

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Yang Yao-Jong

2012-03-01

Full Text Available Abstract Background H. pylori infection may trigger Smad7 and NFκB expression in the stomach, whereas probiotics promote gastrointestinal health and improve intestinal inflammation caused by pathogens. This study examines if probiotics can improve H. pylori-induced gastric inflammation by inactivating the Smad7 and NFκB pathways. Results Challenge with H. pylori increased IL-8 and TNF-α expressions but not TGF-β1 in MKN45 cells. The RNA levels of Smad7 in AGS cells increased after H. pylori infection in a dose-dependent manner. A higher dose (MOI 100 of L. acidophilus pre-treatment attenuated the H. pylori-induced IL-8 expressions, but not TGF-β1. Such anti-inflammatory effect was mediated via increased cytoplasmic IκBα and depletion of nuclear NFκB. L. acidophilus also inhibited H. pylori-induced Smad7 transcription by inactivating the Jak1 and Stat1 pathways, which might activate the TGF-β1/Smad pathway. L. acidophilus pre-treatment ameliorated IFN-γ-induced Smad7 translation level and subsequently reduced nuclear NF-κB production, as detected by western blotting. Conclusions H. pylori infection induces Smad7, NFκB, IL-8, and TNF-α production in vitro. Higher doses of L. acidophilus pre-treatment reduce H. pylori-induced inflammation through the inactivation of the Smad7 and NFκB pathways.

EXTRAGASTRIC AND ORODENTAL MANIFESTATIONS IN PEDIATRIC INFECTION WITH HELICOBACTER PYLORI. A REVIEW

OpenAIRE

Smaranda DIACONESCU; Raluca STANCA; Maria BOLAT

2015-01-01

Helicobacter pylori is a worlwide spread infection mostly manifested in childhood. Many - both invasive and non-invasive diagnostic tests - are now available,. The colonisation effect of gastric mucosa and its consequences are well known and studied. H. pylori can also induce extra-gastric manifestations, like iron-deficiency anemia. The role of oral cavity colonisation is not clearly defined, several studies stating that the oral cavity represents a reservoir for H. pyloris. The presence of ...

Helicobacter pylori-coccoid forms and biofilm formation

DEFF Research Database (Denmark)

Andersen, Leif Percival; Rasmussen, Lone

2009-01-01

be detected by PCR in water supplies. There is no substantial evidence for viable H. pylori persisting in water supplies. Epidemiological studies suggest that environmental water is a risk factor for H. pylori infection when compared with tap water, and formation of H. pylori biofilm cannot be excluded....... Helicobacter pylori does not seem to take part in biofilm formation in the oral cavity even though the bacterium may be detected....

HELICOBACTER PYLORI: THE CAUSATIVE AGENT OF PEPTIC ...

African Journals Online (AJOL)

DR. AMINU

Helicobacter pylori by treatment with antibiotics in peptic ulcer patients resulted in the healing of the ulcer. ... and gastric cancers. .... H. pyloris cause chronic active gastritis in humans and ... of the night when the stomach is empty and is.

Prevalence of Helicobacter Pylori Infection Among Patients ...

African Journals Online (AJOL)

Conclusion: The prevalence of H. pylori infection is significantly high in rural and suburban population of Ernakulam district, Kerala. Early detection and prompt treatment are essential for prevention of serious complications. Keywords: Gastrointestinal complications, Helicobacter pylori infection, Histopathological ...

IL10 single nucleotide polymorphisms are related to upregulation of constitutive IL-10 production and susceptibility to Helicobacter pylori infection.

Science.gov (United States)

Assis, Shirleide; Marques, Cintia Rodrigues; Silva, Thiago Magalhães; Costa, Ryan Santos; Alcantara-Neves, Neuza Maria; Barreto, Mauricio Lima; Barnes, Kathleen Carole; Figueiredo, Camila Alexandrina

2014-06-01

Helicobacter pylori infection is a strong risk factor for gastric cancer, likely due to the extensive inflammation in the stomach mucosa caused by these bacteria. Many studies have reported an association between IL10 polymorphisms, the risk of gastric cancer, and IL-10 production. The aim of the study was to evaluate the association between IL10 genetic variants, Helicobacter pylori infection, and IL-10 production by peripheral blood leukocytes in children. We genotyped a total of 12 single nucleotide polymorphisms in IL10 in 1259 children aged 4-11 years living in a poor urban area in Salvador, Brazil, using TaqMan probe based, 5' nuclease assay minor groove binder chemistry. Association tests were performed by logistic regression for Helicobacter pylori infection and linear regression for IL-10 spontaneous production (whole-blood cultures) including sex, age, and principal components for informative ancestry markers as covariates, using PLINK. Our results shown that IL10 single nucleotide polymorphisms rs1800896 (OR = 1.63; 95% CI = 1.11-2.39), rs3024491 (OR = 1.71; 95% CI = 1.14-2.57), rs1878672 (OR = 1.79; 95% CI = 1.19-2.68), and rs3024496 (OR = 1.48; 95% CI = 1.05-2.08) were positively associated with Helicobacter pylori infection. Eight single nucleotide polymorphisms were associated with spontaneous production of IL-10 in culture, of which three (rs1800896 and rs1878672, p = .04; rs3024491, p = .01) were strongly associated with infection by Helicobacter pylori. Our results indicate that IL10 variants rs1800896, rs3024491, rs1878672, and rs3024496 are more consistently associated with the presence of anti-H. pylori IgG by inducing increased production of IL-10. Further studies are underway to elucidate the role of additional genetic variants and to investigate their impact on the occurrence of gastric cancer. © 2014 John Wiley & Sons Ltd.

Prevalence of Helicobacter Pylori Infection Among Patients ...

African Journals Online (AJOL)

was seen. Conclusion: The prevalence of H. pylori infection is significantly high in rural and suburban population of Ernakulam district, Kerala. Early detection and prompt treatment are essential for prevention of serious complications. Keywords: Gastrointestinal complications, Helicobacter pylori infection, Histopathological ...

Helicobacter pylori induces vascular endothelial growth factor production in gastric epithelial cells through hypoxia-inducible factor-1α-dependent pathway.

Science.gov (United States)

Kang, Min-Jung; Song, Eun-Jung; Kim, Bo-Yeon; Kim, Dong-Jae; Park, Jong-Hwan

2014-12-01

Although Helicobacter pylori have been known to induce vascular endothelial growth factor (VEGF) production in gastric epithelial cells, the precise mechanism for cellular signaling is incompletely understood. In this study, we investigated the role of bacterial virulence factor and host cellular signaling in VEGF production of H. pylori-infected gastric epithelial cells. We evaluated production of VEGF, activation of nuclear factor nuclear factor-kappaB (NF-κB) and mitogen-activated protein kinases (MAPKs) and hypoxia-inducible factor-1α (HIF-1α) stabilization in gastric epithelial cells infected with H. pylori WT or isogenic mutants deficient in type IV secretion system (T4SS). H. pylori induced VEGF production in gastric epithelial cells via both T4SS-dependent and T4SS-independent pathways, although T4SS-independent pathway seems to be the dominant signaling. The inhibitor assay implicated that activation of NF-κB and MAPKs is dispensable for H. pylori-induced VEGF production in gastric epithelial cells. H. pylori led to HIF-1α stabilization in gastric epithelial cells independently of T4SS, NF-κB, and MAPKs, which was essential for VEGF production in these cells. N-acetyl-cysteine (NAC), a reactive oxygen species (ROS) inhibitor, treatment impaired H. pylori-induced HIF-1α stabilization and VEGF production in gastric epithelial cells. We defined the important role of ROS-HIF-1α axis in VEGF production of H. pylori-infected gastric epithelial cells, and bacterial T4SS has a minor role in H. pylori-induced VEGF production of gastric epithelial cells. © 2014 John Wiley & Sons Ltd.

Helicobacter pylori y enfermedad péptica ulcerosa

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Noel Padrón Pérez

1998-12-01

Full Text Available Se realizó una revisión dirigida a los médicos de la familia sobre la relación del Helicobacter pylori y la enfermedad péptica ulcerosa. Se incluyen datos epidemiológicos y métodos diagnósticos de la infección. El papel de Helicobacter pylori en la génesis de las recidivas ulcerosas y la significativa disminución de las recurrencias posterior a la erradicación con la terapia antimicrobiana, son aspectos abordados en el presente trabajo. La inmunización como arma de prevención y tratamiento sería un importante logro que se menciona como una futura alternativa para combatir la úlcera asociada a la infecciónA review on the connection of Helicobacter pylori with peptic ulcer disease was made for the family physicians. Epidemiological data and diagnostic methods were included. The role of Helicobacter pylori in the genesis of ulcer relapses and the significant reduction of recurrences after the erradication with antimicrobial therapy are approached in the present paper. Immunization as an instrument of prevention and treatment would be an important achievement that is mentioned as a future alternative to fight ulcer associated with the infection

Prevention of Gastric Cancer: Eradication of Helicobacter Pylori and Beyond

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Tetsuya Tsukamoto

2017-08-01

Full Text Available Although its prevalence is declining, gastric cancer remains a significant public health issue. The bacterium Helicobacter pylori is known to colonize the human stomach and induce chronic atrophic gastritis, intestinal metaplasia, and gastric cancer. Results using a Mongolian gerbil model revealed that H. pylori infection increased the incidence of carcinogen-induced adenocarcinoma, whereas curative treatment of H. pylori significantly lowered cancer incidence. Furthermore, some epidemiological studies have shown that eradication of H. pylori reduces the development of metachronous cancer in humans. However, other reports have warned that human cases of atrophic metaplastic gastritis are already at risk for gastric cancer development, even after eradication of these bacteria. In this article, we discuss the effectiveness of H. pylori eradication and the morphological changes that occur in gastric dysplasia/cancer lesions. We further assess the control of gastric cancer using various chemopreventive agents.

Probiotics in Helicobacter pylori-induced peptic ulcer disease.

Science.gov (United States)

Boltin, Doron

2016-02-01

The ideal treatment regimen for the eradication Helicobacter pylori infection has yet to be identified. Probiotics, particularly Lactobacillus, Bifidobacterium and Saccharomyces, have been suggested as adjuncts to antibiotics for the treatment of H. pylori. There is in vitro evidence that probiotics dampen the Th1 response triggered by H. pylori, attenuate H. pylori associated hypochlorhydria and secrete bacteriocidal metabolites. Probiotics interact with the innate host immune system through adherence to the gastric epithelium and secretion of bacterial adhesins. In prospective human studies, probiotic monotherapy effectively decrease H. pylori density (expired (13)CO2) by 2.0%-64.0%. Probiotic monotherapy has also been shown to eradicate H. pylori in up to 32.5%, although subsequent recrudescence is likely. Eleven meta-analyses have evaluated the efficacy of probiotics as adjuvants to antibiotics for the eradication of H. pylori. The addition of a probiotic increased treatment efficacy, OR 1.12-2.07. This benefit is probably strain-specific and may only be significant with relatively ineffective antibiotic regimens. The pooled prevalence of adverse effects was 12.9%-31.5% among subjects receiving adjuvant probiotics, compared with 24.3%-45.9% among controls. Diarrhea in particular was significantly reduced in subjects receiving adjuvant probiotics, compared with controls (OR 0.16-0.47). A reduction in adverse events other than diarrhea is variable. Despite the apparent benefit on efficacy and side effects conferred by probiotics, the optimal probiotic species, dose and treatment duration has yet to be determined. Further studies are needed to identify the probiotic, antibiotic and patient factors which might predict benefit from probiotic supplementation. Copyright © 2015 Elsevier Ltd. All rights reserved.

Review: Impact of Helicobacter pylori on Alzheimer's disease: What do we know so far?

Science.gov (United States)

Doulberis, Michael; Kotronis, Georgios; Thomann, Robert; Polyzos, Stergios A; Boziki, Marina; Gialamprinou, Dimitra; Deretzi, Georgia; Katsinelos, Panagiotis; Kountouras, Jannis

2018-02-01

Helicobacter pylori has changed radically gastroenterologic world, offering a new concept in patients' management. Over time, more medical data gave rise to diverse distant, extragastric manifestations and interactions of the "new" discovered bacterium. Special interest appeared within the field of neurodegenerative diseases and particularly Alzheimer's disease, as the latter and Helicobacter pylori infection are associated with a large public health burden and Alzheimer's disease ranks as the leading cause of disability. However, the relationship between Helicobacter pylori infection and Alzheimer's disease remains uncertain. We performed a narrative review regarding a possible connection between Helicobacter pylori and Alzheimer's disease. All accessible relevant (pre)clinical studies written in English were included. Both affected pathologies were briefly analyzed, and relevant studies are discussed, trying to focus on the possible pathogenetic role of this bacterium in Alzheimer's disease. Data stemming from both epidemiologic studies and animal experiments seem to be rather encouraging, tending to confirm the hypothesis that Helicobacter pylori infection might influence the course of Alzheimer's disease pleiotropically. Possible main mechanisms may include the bacterium's access to the brain via the oral-nasal-olfactory pathway or by circulating monocytes (infected with Helicobacter pylori due to defective autophagy) through disrupted blood-brain barrier, thereby possibly triggering neurodegeneration. Current data suggest that Helicobacter pylori infection might influence the pathophysiology of Alzheimer's disease. However, further large-scale randomized controlled trials are mandatory to clarify a possible favorable effect of Helicobacter pylori eradication on Alzheimer's disease pathophysiology, before the recommendation of short-term and cost-effective therapeutic regimens against Helicobacter pylori-related Alzheimer's disease. © 2017 John Wiley & Sons

Comparative Genomics of H. pylori and Non-Pylori Helicobacter Species to Identify New Regions Associated with Its Pathogenicity and Adaptability

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De-Min Cao

2016-01-01

Full Text Available The genus Helicobacter is a group of Gram-negative, helical-shaped pathogens consisting of at least 36 bacterial species. Helicobacter pylori (H. pylori, infecting more than 50% of the human population, is considered as the major cause of gastritis, peptic ulcer, and gastric cancer. However, the genetic underpinnings of H. pylori that are responsible for its large scale epidemic and gastrointestinal environment adaption within human beings remain unclear. Core-pan genome analysis was performed among 75 representative H. pylori and 24 non-pylori Helicobacter genomes. There were 1173 conserved protein families of H. pylori and 673 of all 99 Helicobacter genus strains. We found 79 genome unique regions, a total of 202,359bp, shared by at least 80% of the H. pylori but lacked in non-pylori Helicobacter species. The operons, genes, and sRNAs within the H. pylori unique regions were considered as potential ones associated with its pathogenicity and adaptability, and the relativity among them has been partially confirmed by functional annotation analysis. However, functions of at least 54 genes and 10 sRNAs were still unclear. Our analysis of protein-protein interaction showed that 30 genes within them may have the cooperation relationship.

The number of Foxp3-positive regulatory T cells is increased in Helicobacter pylori gastritis and gastric cancer.

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Jang, Tae Jung

2010-01-15

Helicobacter pylori (H. pylori) colonization induces vigorous innate and specific immune responses; however, the infection is not removed, a state of chronic active gastritis persists for life if untreated. Recent studies have shown that CD4(+) CD25(+) Foxp3-positive regulatory T cells (Tregs) suppress the immune response to H. pylori. Persistent H. pylori-associated gastritis is closely associated with gastric carcinogenesis. We investigated the number of Tregs in the context of H. pylori colonization in chronic gastritis, examined the relationship between it and histopathological findings and compared it with that of gastric dysplasia and adenocarcinoma. This study was based on the analysis of gastric biopsy specimens from 126 cases of H. pylori-associated gastritis, 16 cases of H. pylori-negative gastritis, 17 cases of gastric dysplasia, and 25 cases of gastric adenocarcinoma. The number of Tregs was elevated in H. pylori-associated gastritis, where it was positively correlated with the grade of chronic inflammation and the number of lymphoid follicles. It was significantly elevated in adenocarcinomas compared to chronic gastritis and gastric dysplasia. In summary, the number of Tregs is increased in H. pylori-associated gastritis and gastric cancer. Copyright 2009 Elsevier GmbH. All rights reserved.

3rd BRAZILIAN CONSENSUS ON Helicobacter pylori

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Luiz Gonzaga Coelho

2013-04-01

Full Text Available Significant progress has been obtained since the Second Brazilian Consensus Conference on Helicobacter pylori Infection held in 2004, in São Paulo, SP, Brazil, and justify a third meeting to establish updated guidelines on the current management of H. pylori infection. The Third Brazilian Consensus Conference on H pylori Infection was organized by the Brazilian Nucleus for the Study of Helicobacter, a Department of the Brazilian Federation of Gastroenterology and took place on April 12-15, 2011, in Bento Gonçalves, RS, Brazil. Thirty-one delegates coming from the five Brazilian regions and one international guest, including gastroenterologists, pathologists, epidemiologists, and pediatricians undertook the meeting. The participants were allocated in one of the five main topics of the meeting: H pylori, functional dyspepsia and diagnosis; H pylori and gastric cancer; H pylori and other associated disorders; H pylori treatment and retreatment; and, epidemiology of H pylori infection in Brazil. The results of each subgroup were submitted to a final consensus voting to all participants. Relevant data were presented, and the quality of evidence, strength of recommendation, and level of consensus were graded. Seventy per cent and more votes were considered as acceptance for the final statement. This article presents the main recommendations and conclusions to guide Brazilian doctors involved in the management of H pylori infection.

cagA positive Helicobacter pylori in Brazilian children related to chronic gastritis

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Luciano Lobo Gatti

Full Text Available Helicobacter pylori is a spiral-shaped Gram-negative bacterium. It colonizes the gastric mucosa of humans and persists for decades if not treated. Helicobacter pylori infection affects more than half of the world's population and invariably results in chronic gastritis. The cagA gene is present in about 60 to 70% of H. pylori strains; it encodes a high-molecular-weight protein (120 to 140 kDa and several investigators have noted a correlation between strains that possess cagA and the severity of gastric mucosal inflammation. We examined the relation between cagA status in H. pylori strains and chronic gastritis with inflammatory processes in children from Marília, São Paulo, Brazil. One-hundred-twenty-one children were analyzed histopathologically and by polymerase chain reaction (PCR to detect H. pylori and cagA. We then looked for an association between cagA presence and inflammatory infiltration. Using histology and PCR, we found 47% H. pylori positive infection; 29 children were diagnosed with chronic gastritis, while 28 showed normal mucosa by histopathological analysis. CagA presence was genotyped in both groups, and an inflammatory infiltrate was studied in all infected children with chronic gastritis. We found cagA strains in 20 of 29 (69% children with chronic gastritis and 18 of 28 (64% with normal mucosa, demonstrating a strong relationship between the strains and the inflammatory process. We found a positive association between an inflammatory process associated with H. pylori of cagA+ strains and chronic gastritis development.

Helicobacter pylori and Peptic Ulcers

Centers for Disease Control (CDC) Podcasts

In this podcast, CDC's Dr. David Swerdlow discusses the relationship between Helicobacter pylori and peptic ulcer disease and trends in hospitalization rates for peptic ulcer disease in the United States between 1998 and 2005.

Prospective study on effect of Helicobacter pylori on gastroesophageal reflux disease

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Sabah Jalal Shareef

2017-08-01

Full Text Available Background and objective: The Helicobacter pylori infections role in etiology of peptic ulcer is well known, but its role in gastroesophageal reflux disease is one of the important issues which has to be confirmed. We tried to find out the effect of Helicobacter pylori infection on gastroesophageal reflux disease. Methods: The current study was done on 100 patients with gastroesophageal reflux disease from January 1st to June 30th, 2014 in Rizgary Teaching Hospital, Erbil city. The diagnosis was made by history, clinical examination, and endoscopy. Helicobacter pylori infection was confirmed by gastric biopsy and histopathological examination. We tried to find out the effects of Helicobacter pylori infection in gastroesophageal reflux disease patients and its eradication on their symptoms. The data was analyzed with the statistical package for the social sciences (version 18. Results: The mean age ± SD of participants was 37.13 ± 12.5 (17-75 years. The prevalence of Helicobacter pylori infection was 75%. The endoscopy showed that 50 out of 75 patients had erosive esophagitis and 25 out of 75 patients had normal appearance known as non-erosive esophagitis. The study showed no significance of its eradication on symptoms of gastroesophageal reflux disease. Conclusion: The effect of Helicobacter pylori infection in gastroesophageal reflux disease patients was significant regarding endoscopic finding while inversely related to symptoms severity. The eradication of infection did not cause improvement in symptom severity i.e. triple therapy not advised in the course of treatment.

Systematic review: Helicobacter pylori infection and impaired drug absorption.

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Lahner, E; Annibale, B; Delle Fave, G

2009-02-15

Impaired acid secretion may affect drug absorption and may be consequent to corporal Helicobacter pylori-gastritis, which may affect the absorption of orally administered drugs. To focus on the evidence of impaired drug absorption associated with H. pylori infection. Data sources were the systematic search of MEDLINE/EMBASE/SCOPUS databases (1980-April 2008) for English articles using the keywords: drug malabsorption/absorption, stomach, Helicobacter pylori, gastritis, gastric acid, gastric pH, hypochlorhydria, gastric hypoacidity. Study selection was made from 2099 retrieved articles, five studies were identified. Data were extracted from selected papers, investigated drugs, study type, main features of subjects, study design, intervention type and results were extracted. In all, five studies investigated impaired absorption of l-dopa, thyroxine and delavirdine in H. pylori infection. Eradication treatment led to 21-54% increase in l-dopa in Parkinson's disease. Thyroxine requirement was higher in hypochlorhydric goitre with H. pylori-gastritis and thyrotropin levels decreased by 94% after treatment. In H. pylori- and HIV-positive hypochlorhydric subjects, delavirdine absorption increased by 57% with orange juice administration and by 150% after eradication. A plausible mechanism of impaired drug absorption is decreased acid secretion in H. pylori-gastritis patients. Helicobacter pylori infection and hypochlorhydria should be considered in prescribing drugs the absorption of which is potentially affected by intragastric pH.

Validation of 14 C-urea breath test for diagnosis of Helicobacter pylori

International Nuclear Information System (INIS)

Mattar, Rejane; Silva, Fernando Marcuz; Alexandrino, Ana Maria; Laudanna, Antonio Atilio

1999-01-01

The aim of this study was to validate the 14 C-urea breath test for use in diagnosis of Helicobacter pylori infection. Thirty H. pylori positive patients, based on histologic test and thirty H. pylori negative patients by histology and anti-H pylori IgG entered the study. Fasting patients drank 5 uCi of 14 C-urea in 20 ml of water. Breath samples were collected at O, 5, 10, 15, 20 and 30 min. The difference of cpm values between the two groups was significant at all the time intervals, besides time 0 (p 14 C-urea breath test is highly accurate for Helicobacter pylori diagnosis. It is fast, simple and should be the non-invasive test used after treating Helicobacter pylori infection. (author)

Seroprevalence of Helicobacter pylori in human immunodeficiency ...

African Journals Online (AJOL)

Background: This study assessed the seroprevalence of Helicobacter pylori antibodies among Iranian patients with human immunodeficiency virus (HIV) infection. It also examines whether anti H. pylori seroprevalence was associated with the severity of the HIV infection or the antiretroviral treatment. Material and Methods: ...

Cholesterol-α-glucosyltransferase gene is present in most Helicobacter species including gastric non-Helicobacter pylori helicobacters obtained from Japanese patients.

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Kawakubo, Masatomo; Horiuchi, Kazuki; Matsumoto, Takehisa; Nakayama, Jun; Akamatsu, Taiji; Katsuyama, Tsutomu; Ota, Hiroyoshi; Sagara, Junji

2018-02-01

Non-Helicobacter pylori helicobacters (NHPHs) besides H. pylori infect human stomachs and cause chronic gastritis and mucosa-associated lymphoid tissue lymphoma. Cholesteryl-α-glucosides have been identified as unique glycolipids present in H. pylori and some Helicobacter species. Cholesterol-α-glucosyltransferase (αCgT), a key enzyme for the biosynthesis of cholesteryl-α-glucosides, plays crucial roles in the pathogenicity of H. pylori. Therefore, it is important to examine αCgTs of NHPHs. Six gastric NHPHs were isolated from Japanese patients and maintained in mouse stomachs. The αCgT genes were amplified by PCR and inverse PCR. We retrieved the αCgT genes of other Helicobacter species by BLAST searches in GenBank. αCgT genes were present in most Helicobacter species and in all Japanese isolates examined. However, we could find no candidate gene for αCgT in the whole genome of Helicobacter cinaedi and several enterohepatic species. Phylogenic analysis demonstrated that the αCgT genes of all Japanese isolates show high similarities to that of a zoonotic group of gastric NHPHs including Helicobacter suis, Helicobacter heilmannii, and Helicobacter ailurogastricus. Of 6 Japanese isolates, the αCgT genes of 4 isolates were identical to that of H. suis, and that of another 2 isolates were similar to that of H. heilmannii and H. ailurogastricus. All gastric NHPHs examined showed presence of αCgT genes, indicating that αCgT may be beneficial for these helicobacters to infect human and possibly animal stomachs. Our study indicated that NHPHs could be classified into 2 groups, NHPHs with αCgT genes and NHPHs without αCgT genes. © 2017 John Wiley & Sons Ltd.

Differential effects of multiplicity of infection on Helicobacter pylori-induced signaling pathways and interleukin-8 gene transcription.

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Ritter, Birgit; Kilian, Petra; Reboll, Marc Rene; Resch, Klaus; DiStefano, Johanna Kay; Frank, Ronald; Beil, Winfried; Nourbakhsh, Mahtab

2011-02-01

Interleukin-8 (IL-8) plays a central role in the pathogenesis of Helicobacter pylori infection. We used four different H. pylori strains isolated from patients with gastritis or duodenal ulcer disease to examine their differential effects on signaling pathways and IL-8 gene response in gastric epithelial cells. IL-8 mRNA level is elevated in response to high (100) multiplicity of infection (MOI) independent of cagA, vacA, and dupA gene characteristics. By lower MOIs (1 or 10), only cagA ( + ) strains significantly induce IL-8 gene expression. This is based on differential regulation of IL-8 promoter activity. Analysis of intracellular signaling pathways indicates that H. pylori clinical isolates induce IL-8 gene transcription through NF-κB p65, but by a MOI-dependent differential activation of MAPK pathways. Thus, the major virulence factors of H. pylori CagA, VacA, and DupA might play a minor role in the level of IL-8 gene response to a high bacterial load.

Helicobacter pylori Stool Antigen test: a reliable non-invasive test for the diagnosis of Helicobacter pylori infection in children

NARCIS (Netherlands)

van Doorn, O. J.; Bosman, D. K.; van't Hoff, B. W.; Taminiau, J. A.; ten Kate, F. J.; van der Ende, A.

2001-01-01

OBJECTIVE: To evaluate the Helicobacter pylori Stool Antigen (HpSA) test for the diagnosis of H. pylori infection in children. DESIGN AND SETTING: Prospective cohort study in an academic medical centre. PATIENTS AND METHODS: A total of 106 consecutive children who underwent gastroscopy were

Magnitude of Helicobacter pylori among Dyspeptic patients ...

African Journals Online (AJOL)

Background: Helicobacter pylori (H.pylori) infection is predominantly acquired in childhood from family members. The infection can cause dypepepsia, chronic and acute gastritis and gastric cancer. Dyspepsia is the most common illness in the Ethiopian population visiting outpatient department of health facilities, and it has ...

Serum prolidase activity and oxidative status in Helicobacter pylori infection.

Science.gov (United States)

Aslan, Mehmet; Nazligul, Yasar; Horoz, Mehmet; Bolukbas, Cengiz; Bolukbas, Fusun F; Aksoy, Nurten; Celik, Hakim; Erel, Ozcan

2007-01-01

During the course of Helicobacter pylori infection, increased oxidative stress plays an important role in the pathogenesis of gastroduodenal mucosal inflammation, which can cause gastric mucosal atrophy that characterized by the replacement of the gastric mucosal glands by collagen fibers. In the present study, we aimed to determine serum prolidase activity and oxidative status, and to find out if there is any association between serum prolidase activity and oxidative status in H. pylori infection. Forty H. pylori-positive and 32 H. pylori-negative subjects were enrolled. Serum prolidase activity was measured spectrophotometrically. Oxidative status was determined using total antioxidant capacity and total oxidant status measurement and calculation of oxidative stress index. Total antioxidant capacity level was lower in H. pylori-positive group than H. pylori-negative group (ptotal oxidant status, oxidative stress index and prolidase activity were higher (all ptotal antioxidant capacity, total oxidant status and oxidative stress index (p<0.01, r=-0.367; p<0.05, r=0.283; p<0.01, r=0.379; respectively) in H. pylori-positive subjects. H. pylori infection may be associated with increased oxidative stress and increased serum prolidase activity. Increased oxidative stress seems to be associated with increased serum prolidase activity and this association may help to provide a better understanding about the pathogenesis of H. pylori infection.

Helicobacter pylori infection in patients with dyspeptic symptoms having normal endoscopy

International Nuclear Information System (INIS)

Malik, M.F.; Hussain, T.; Khan, M.N.; Mirza, S.A.

2010-01-01

To find out the frequency of Helicobacter pylori infection in the local population presenting with dyspeptic symptoms but having normal upper gastrointestinal endoscopic findings. Hundred cases of dyspepsia having normal upper gastrointestinal endoscopy were taken as study population. Although the gold standard for presence or absence of Helicobacter pylori infection is culture but in this study the diagnostic method used was histopathology of gastric antrum. The male and female ratio was 2:1. Majority of the patients were either 40 years of age or less, mean age being 40.52 (sd+-13.22). The chief symptoms were pain epigastrium (46%) and upper abdominal discomfort (27%). Helicobacter pylori gastritis was found in 51% of cases. We conclude that Helicobacter pylori infection is quite common in dyspeptic patients apparently having normal endoscopic gastric mucosal findings. Eradication therapy should be instituted in positive cases to avoid its long-term complications. (author)

Helicobacter pylori and upper digestive diseases - diagnosis ...

African Journals Online (AJOL)

Results: The prevalence of Helicobacter pylori in patients with various upper gastrointestinal problems was 84.7%. The use of medication that can reduce the H. pylori density was common among the infected patients, as history of antibiotics use, acid suppressant use and medications for eradication treatment were ...

Meta-analysis: Association of Helicobacter pylori infection with Parkinson's diseases.

Science.gov (United States)

Shen, Xiaoli; Yang, Huazhen; Wu, Yili; Zhang, Dongfeng; Jiang, Hong

2017-10-01

The results from observational studies on the relationship between helicobacter pylori (H. pylori) infection and Parkinson's disease remain controversial. A meta-analysis was conducted to evaluate the association between helicobacter pylori infection and Parkinson's disease. A comprehensive literature search was performed on relevant studies published from January 1983 to January 2017 in PubMed, Web of Science and EMBASE databases. The fixed or random effects model was used to pool the odds ratio with 95% confidence interval from individual studies. Publication bias was estimated by Egger's test and the funnel plot. Eight eligible studies involving 33 125 participants were included in this meta-analysis. Compared with the no helicobacter pylori infected person, the pooled odds ratio of Parkinson's disease in helicobacter pylori infected person was 1.59 (95% confidence interval: 1.37-1.85). In subgroup analyzes, the combined odds ratios were 1.96 (1.23-3.12) in Asia, 1.55 (1.32-1.82) in Europe, 1.59 (1.35-1.88) in case-control studies, 1.56 (1.01-2.39) in cross-sectional studies, 1.56 (1.32-1.85) in studies with confounders adjusted, and 1.71 (1.21-2.43) in studies with no confounder adjusted, respectively. This meta-analysis indicated that H. pylori infection might be associated with the risk of Parkinson's disease. © 2017 John Wiley & Sons Ltd.

Efecto del tratamiento erradicador para Helicobacter pylori en pacientes con dispepsia funcional Effect to Helicobacter pylori eradication on patients with functional dyspepsia

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T. de Artaza Varasa

2008-09-01

Full Text Available Objetivo: este estudio ha tenido un doble objetivo: por un lado, evaluar el efecto del tratamiento erradicador para Helicobacter pylori en la respuesta sintomática de pacientes diagnosticados de dispepsia funcional y, por otro, determinar si los hallazgos histológicos podían servir como predictor de la efectividad de la terapia. En particular, se trató de averiguar si la presencia de gastritis antral (la que se asocia a la enfermedad ulcerosa péptica podría predecir una mayor respuesta sintomática al tratamiento erradicador en los pacientes con dispepsia funcional e infección por Helicobacter pylori. Pacientes y métodos: estudio prospectivo, monocéntrico y aleatorizado, que incluyó a 48 pacientes con dispepsia funcional e infección por Helicobacter pylori (27 mujeres y 21 hombres, con edad media de 37 ± 13,5 años. Veintisiete pacientes recibieron el tratamiento erradicador (rabeprazol, claritromicina y amoxicilina durante 10 días, seguido de 20 mg/día de rabeprazol 3 meses y 21 el tratamiento control (20 mg/día de rabeprazol 3 meses. Los pacientes fueron seguidos durante un año. Todos rellenaron el Cuestionario de calidad de vida asociada a dispepsia, que evalúa cuatro apartados: intensidad de los síntomas habituales, intensidad del dolor de estómago, incapacidad debida al dolor y satisfacción con la salud. Resultados: existió una mejoría significativa (p Objective: this study evaluated Helicobacter pylori eradication therapy in terms of symptomatic response in patients with functional dyspepsia. On the other hand, we analyzed the importance of histologic findings as a predictor of treatment response. In particular, we studied whether antral gastritis (which is associated with peptic ulcer may predict a greater symptomatic response to Helicobacter pylori eradication in functional dyspepsia. Patients and methods: this prospective, randomized, single-center trial included 48 patients with functional dyspepsia and

Helicobacter pylori: Beginning the Second Decade

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Ann Matisko

1995-01-01

Full Text Available ‘Beginning the Second Decade’ - a recent international meeting on Helicobacter pylori - was held in conjunction with the VIIth International Workshop on Gastroduodenal Pathology and H pylori and with the meeting of the European Helicobacter pylori Study Group in Houston, Texas from September 30 to October 1, 1994. A menu of 476 abstracts, published in the American Journal of Gastroenterology (1994;89:8, highlighted the explosion of advances in this area. The Houston meeting was followed by the Tenth World Congresses of Gastroenterology from October 2 to 7, 1994 in Los Angeles, California, again with scores of presentations and posters on topics ranging from the epidemiology of H pylori infection to steps towards the development of a human vaccine. All this was in addition to important new work presented earlier in 1994 in New Orleans during Digestive Diseases Week. In this digest of these important meetings, the authors will not regurgitate what the informed reader already knows, but will instead focus on the recent developments in important areas, providing selected key published references for background, and referring to this new work in abstract form which is at the cutting edge of “yesterday’s tomorrow today”.

Helicobacter pylori infection in pediatrics

DEFF Research Database (Denmark)

Wewer, Anne Vibeke; Kalach, Nicolas

2003-01-01

A high prevalence and early colonization of Helicobacter pylori infection in childhood was described again this year in developing countries in contrast to developed ones. Upper gastrointestinal endoscopy including gastric biopsies remains the diagnostic gold standard method for this infection. A...

Helicobacter pylori-related chronic gastritis as a risk factor for colonic neoplasms.

Science.gov (United States)

Inoue, Izumi; Kato, Jun; Tamai, Hideyuki; Iguchi, Mikitaka; Maekita, Takao; Yoshimura, Noriko; Ichinose, Masao

2014-02-14

To summarize the current views and insights on associations between Helicobacter pylori (H. pylori)-related chronic gastritis and colorectal neoplasm, we reviewed recent studies to clarify whether H. pylori infection/H. pylori-related chronic gastritis is associated with an elevated risk of colorectal neoplasm. Recent studies based on large databases with careful control for confounding variables have clearly demonstrated an increased risk of colorectal neoplasm associated with H. pylori infection. The correlation between H. pylori-related chronic atrophic gastritis (CAG) and colorectal neoplasm has only been examined in a limited number of studies. A recent large study using a national histopathological database, and our study based on the stage of H. pylori-related chronic gastritis as determined by serum levels of H. pylori antibody titer and pepsinogen, indicated that H. pylori-related CAG confers an increased risk of colorectal neoplasm, and more extensive atrophic gastritis will probably be associated with even higher risk of neoplasm. In addition, our study suggested that the activity of H. pylori-related chronic gastritis is correlated with colorectal neoplasm risk. H. pylori-related chronic gastritis could be involved in an increased risk of colorectal neoplasm that appears to be enhanced by the progression of gastric atrophy and the presence of active inflammation.

Molecular Mechanisms of Antibiotic Resistance in Helicobacter pylori

NARCIS (Netherlands)

M.M. Gerrits (Monique)

2004-01-01

textabstractAn estimated 4 to 5 million individuals in the Netherlands are actively infected with Helicobacter pylori. Eradication of this bacterium becomes more difficult as the prevalence of antibiotic resistance is increasing worldwide. Most H. pylori infections are now diagnosed by

A fluid model for Helicobacter pylori

Science.gov (United States)

Reigh, Shang-Yik; Lauga, Eric

2015-11-01

Swimming microorganisms and self-propelled nanomotors are often found in confined environments. The bacterium Helicobacter pylori survives in the acidic environment of the human stomach and is able to penetrate gel-like mucus layers and cause infections by locally changing the rheological properties of the mucus from gel-like to solution-like. In this talk we propose an analytical model for the locomotion of Helicobacter pylori as a confined spherical squirmer which generates its own confinement. We solve analytically the flow field around the swimmer, and derive the swimming speed and energetics. The role of the boundary condition in the outer wall is discussed. An extension of our model is also proposed for other biological and chemical swimmers. Newton Trust.

Activity calibration in breath test for diagnosis of Helicobacter pylori

International Nuclear Information System (INIS)

Wasilewka-Radwanska, M.; Pysklak, S.; Gilewicz-Wolter, J.; Kuc, T.; Jung, A.; Niziol, J.; Kopanski, J.; Micherdzinski, J.; Cienciala, A.

1996-01-01

Some technical and measurement problems of the breath test for diagnosis of Helicobacter pylori are briefly discussed. Calibrated results obtained for population of 108 cases indicate difference between HP+ (infected with Helicobacter pylori) and HP- (non infected with Helicobacter pylori) in exhaled 14 C activity not less than 3.9 kBq while the lower limit for HP+ cases was set at 6.8 kBq at the detection limit: 0.9 Bq/mmol of CO 2 . It was estimated that in exhalation way up to 29% of the taken activity was removed in HP+ cases during first 35 minutes. Radiation hazard for the patient system is negligibly small - dose equipment not exceeds 0.29% of the natural (environmental) yearly exposure. (author)

Role of Probiotics in the Management of Helicobacter Pylori Infection

Directory of Open Access Journals (Sweden)

A Zare Javid

2014-04-01

Full Text Available Helicobacter pylori is a gram-negative, spiral-shaped, microaerophilic organism that colonizes the stomach of humans and causes chronic-active gastritis, peptic ulcer disease, and gastric cancers, including adenocarcinoma of the stomach and MALT (mucosal-associated lymphoid tumor lymphomas. H. pylori colonizes the stomach of over 50 % the world’s human population, primarily those who reside in developing nations. Infection is generally first acquired in children, who may be entirely asymptomatic, and then persists for life, unless specific eradication therapy is initiated. All infected individuals have mucosal inflammation in the stomach in response to the organism, but only a subset will develop disease complications, such as an ulcer in the stomach or proximal duodenum and cancer in either the body or the antrum of the stomach. It is estimated that the lifetime risk of developing peptic ulceration is roughly 15%. However, this is an exceedingly important disease, because it has serious morbidity and mortality. Eradication of H. pylori infection is not successful when using antibiotics as monotherapy or dual therapy using combinations of an acid-suppressing agent and an antibiotic or two antibiotics without acid blockage. Multiple studies show that some probiotic strains can inhibit the growth of H. pylori. To date, probiotics do not appear to have a role as sole therapy for use in the prevention or treatment of H. pylori infection. However, there is increasing evidence that a variety of probiotic agents are useful as adjunctive therapy, which can both enhance the success of eradicating the gastric pathogen while, reduce the frequency and severity of adverse effects arising from the other agents that are employed in current combination treatment regimens. Future studies should assess the role of prebiotics and synbiotics and products derived from probiotics as additional options for use in the prevention and treatment of H. pylori infection

Motility and chemotaxis mediate the preferential colonization of gastric injury sites by Helicobacter pylori.

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Eitaro Aihara

2014-07-01

Full Text Available Helicobacter pylori (H. pylori is a pathogen contributing to peptic inflammation, ulceration, and cancer. A crucial step in the pathogenic sequence is when the bacterium first interacts with gastric tissue, an event that is poorly understood in vivo. We have shown that the luminal space adjacent to gastric epithelial damage is a microenvironment, and we hypothesized that this microenvironment might enhance H. pylori colonization. Inoculation with 106 H. pylori (wild-type Sydney Strain 1, SS1 significantly delayed healing of acetic-acid induced ulcers at Day 1, 7 and 30 post-inoculation, and wild-type SS1 preferentially colonized the ulcerated area compared to uninjured gastric tissue in the same animal at all time points. Gastric resident Lactobacillus spp. did not preferentially colonize ulcerated tissue. To determine whether bacterial motility and chemotaxis are important to ulcer healing and colonization, we analyzed isogenic H. pylori mutants defective in motility (ΔmotB or chemotaxis (ΔcheY. ΔmotB (10(6 failed to colonize ulcerated or healthy stomach tissue. ΔcheY (10(6 colonized both tissues, but without preferential colonization of ulcerated tissue. However, ΔcheY did modestly delay ulcer healing, suggesting that chemotaxis is not required for this process. We used two-photon microscopy to induce microscopic epithelial lesions in vivo, and evaluated accumulation of fluorescently labeled H. pylori at gastric damage sites in the time frame of minutes instead of days. By 5 min after inducing damage, H. pylori SS1 preferentially accumulated at the site of damage and inhibited gastric epithelial restitution. H. pylori ΔcheY modestly accumulated at the gastric surface and inhibited restitution, but did not preferentially accumulate at the injury site. H. pylori ΔmotB neither accumulated at the surface nor inhibited restitution. We conclude that bacterial chemosensing and motility rapidly promote H. pylori colonization of injury sites

Motility and Chemotaxis Mediate the Preferential Colonization of Gastric Injury Sites by Helicobacter pylori

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Aihara, Eitaro; Closson, Chet; Matthis, Andrea L.; Schumacher, Michael A.; Engevik, Amy C.; Zavros, Yana; Ottemann, Karen M.; Montrose, Marshall H.

2014-01-01

Helicobacter pylori (H. pylori) is a pathogen contributing to peptic inflammation, ulceration, and cancer. A crucial step in the pathogenic sequence is when the bacterium first interacts with gastric tissue, an event that is poorly understood in vivo. We have shown that the luminal space adjacent to gastric epithelial damage is a microenvironment, and we hypothesized that this microenvironment might enhance H. pylori colonization. Inoculation with 106 H. pylori (wild-type Sydney Strain 1, SS1) significantly delayed healing of acetic-acid induced ulcers at Day 1, 7 and 30 post-inoculation, and wild-type SS1 preferentially colonized the ulcerated area compared to uninjured gastric tissue in the same animal at all time points. Gastric resident Lactobacillus spp. did not preferentially colonize ulcerated tissue. To determine whether bacterial motility and chemotaxis are important to ulcer healing and colonization, we analyzed isogenic H. pylori mutants defective in motility (ΔmotB) or chemotaxis (ΔcheY). ΔmotB (106) failed to colonize ulcerated or healthy stomach tissue. ΔcheY (106) colonized both tissues, but without preferential colonization of ulcerated tissue. However, ΔcheY did modestly delay ulcer healing, suggesting that chemotaxis is not required for this process. We used two-photon microscopy to induce microscopic epithelial lesions in vivo, and evaluated accumulation of fluorescently labeled H. pylori at gastric damage sites in the time frame of minutes instead of days. By 5 min after inducing damage, H. pylori SS1 preferentially accumulated at the site of damage and inhibited gastric epithelial restitution. H. pylori ΔcheY modestly accumulated at the gastric surface and inhibited restitution, but did not preferentially accumulate at the injury site. H. pylori ΔmotB neither accumulated at the surface nor inhibited restitution. We conclude that bacterial chemosensing and motility rapidly promote H. pylori colonization of injury sites, and thereby biases

Effect of Helicobacter pylori Eradication on Functional Dyspepsia

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Kim, Sung Eun; Park, Young Soo; Kim, Min Soo; Jo, Hyun Jin; Shin, Cheol Min; Lee, Sang Hyub; Hwang, Jin-Hyeok; Kim, Jin-Wook; Jeong, Sook-Hyang; Lee, Dong Ho; Jung, Hyun Chae

2013-01-01

Background/Aims This study evaluated the effect of Helicobacter pylori eradication on functional dyspepsia (FD), and the relationship between the changes of histological gastritis and FD symptom responses. Methods A total of 213 FD patients diagnosed by Rome III criteria were consecutively enrolled. H. pylori tests and gastritis grade by the Sydney system were performed before and 1 year after the proton pump based-eradication therapy for 7 days. Serum levels of pepsinogen, and genetic polymorphisms IL-6, IL-8 and IL-10 were investigated. Results Total of 91 patients completed the 1 year follow-up. When the response rate of dyspepsia was compared at 1 year between the non-eradicated group (n = 24) and eradicated group (n = 67), each group showed complete response of 62.5% and 62.7%; satisfactory response (≥ 50%) of 0.0% and 19.4%; partial response (gastritis at 1 year, suggesting that inflammation mediates FD. PMID:23667755

Medicinal plants in the treatment of Helicobacter pylori infections.

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Safavi, Maliheh; Shams-Ardakani, Mohammadreza; Foroumadi, Alireza

2015-07-01

Helicobacter pylori is a small, spiral, Gram-negative bacillus that plays a role in the pathogenesis of a number of diseases ranging from asymptomatic gastritis to gastric cancer. Schedule compliance, antibiotic drug resistance, and side-effects of triple or quadruple therapy have led to research for novel candidates from plants. The purpose of this paper is to review the most potent medicinal plants of recently published literature with anti-H. pylori activity. For centuries, herbals have been used by traditional healers around the world to treat various gastrointestinal tract disorders such as dyspepsia, gastritis, and peptic ulcer disease. The mechanism of action by which these botanicals exert their therapeutic properties has not been completely and clearly elucidated. Anti-H. pylori properties may be one of the possible mechanisms by which gastroprotective herbs treat gastrointestinal tract disorders. Electronic databases such as PubMed, Google scholar, EBSCO, and local databases were explored for medicinal plants with anti-H. pylori properties between 1984 and 2013 using key words "medicinal plants" and "Helicobacter pylori" or "anti-Helicobacter pylori". A total of 43 medicinal plant species belonging to 27 families including Amaryllidaceae, Anacardiaceae, Apiaceae, Apocynaceae, Asclepiadoideae, Asteraceae, Bignoniaceae, Clusiaceae, Chancapiedra, Combretaceae, Cyperaceae, Euphorbiaceae, Fabaceae, Geraniaceae, Lamiaceae, Lauraceae, Lythraceae, Menispermaceae, Myristicaceae, Myrtaceae, Oleaceae, Papaveraceae, Plumbaginaceae, Poaceae, Ranunculaceae, Rosaceae, and Theaceae were studied as herbs with potent anti-H. pylori effects. Traditional folk medicinal use of some of these plants to treat gastric infections is substantiated by the antibacterial activity of their extracts against H. pylori.

Inhibitory effect of green tea catechins in combination with sucralfate on Helicobacter pylori infection in Mongolian gerbils.

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Takabayashi, Fumiyo; Harada, Noboru; Yamada, Masami; Murohisa, Binzaburo; Oguni, Itaro

2004-01-01

The occurrence of antibiotic-resistant Helicobacter pylori has been reported. It is desirable to develop an effective method to prevent the occurrence of resistant strains of Helicobacter pylori. Green tea catechins (GTCs) have been reported to have an antibacterial effect. Therefore, the possibility of eradicating Helicobacter pylori by the oral administration of GTCs was investigated. Solutions of GTCs and solutions of GTCs adsorbed to sucralfate (GTC-scf), at concentrations of 20 mg GTCs and/or 20 mg sucralfate/ml were prepared. Then 1 ml of the GTC-scf or the GTC solution was administered daily, for 10 days to Mongolian gerbils infected with Helicobacter pylori. Then the stomachs were extirpated and homogenized. The homogenate was spread on selective medium plates. After 5-day culture, colony-forming units (CFU) of Helicobacter pylori were counted. The CFU of Helicobacter pylori was significantly decreased by GTC-scf. GTC-scf may have a bactericidal effect on Helicobacter pylori infection.

Study on Urea Breath Test (UBT) a tool for helicobacter pylori infection

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Kolekar, R.V.; Bhade, S.P.D.; Reddy, Priyanka; Singh, Rajvir; Gadgil, Anita; Bhandarkar, Prashant; Roy, N.; Patil, S.P.

2016-01-01

Helicobacter pylori commonly called as H. pylori resides in the gastric epithelial mucosa and induces an inflammatory response leading to gastritis, peptic nicer disease and gastric malignancies. Detection and eradication of H.pylori infection is thus an important measure to prevent these. H.pylori has a worldwide prevalence rate of about 50%, with a higher prevalence in developing countries. Urea breath test, an outpatient noninvasive technique achieves up to 95% sensitivity and specificity at half the cost compared to histology, in detecting H. Pylori infection. Indian studies on the use of UBT and its standard protocol are sparse. The present paper discusses the application of Carbon-14 Urea breath test for the diagnosis of H pylori bacterial infection in 261 adult patients

Anti-inflammatory effects of rebamipide according to Helicobacter pylori status in patients with chronic erosive gastritis: a randomized sucralfate-controlled multicenter trial in China-STARS study.

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Du, Yiqi; Li, Zhaoshen; Zhan, Xianbao; Chen, Jie; Gao, Jun; Gong, Yanfang; Ren, Jianlin; He, Liping; Zhang, Zhijian; Guo, Xiaozhong; Wu, Jianshen; Tian, Zibin; Shi, Ruihua; Jiang, Bo; Fang, Dianchun; Li, Youming

2008-11-01

The aim of the study was to investigate the effects of rebamipide on symptom, histology, endogenous prostaglandin, and mucosal oxygen free radicals in chronic erosive gastritis (CEG) patients by using sucralfate as a control. The trial also examined whether Helicobacter pylori infection would affect rebamipide-induced protection. A total of 453 endoscopy-confirmed CEG patients from 11 hospitals in China were enrolled in the study. They randomly received either rebamipide (100 mg t.i.d) or sucralfate (1.0 t.i.d) for 8 weeks with a ratio of 3:1. Per-protocol analysis (n = 415) showed the accumulated symptom score in the rebamipide group dropped from 5.54 +/- 0.97 to 0.80 +/- 0.47 after 8 weeks (P < 0.001 versus control). The endoscopic inflammation score in rebamipide group also decreased from 2.65 +/- 0.09 to 0.60 +/- 0.10, which showed better effects than sucralfate. It was shown a significant improvement (P < 0.01) in prostaglandin E2 (PGE(2)) contents in rebamipide-treated subjects mucosa (225.4 +/- 18.3 pg/g versus 266.7 +/- 14.7 pg/g) compared with that in sucralfate group after 8 weeks of treatment. Malondialdehyde (MDA) contents were significantly depressed both in the trial and control group. When Helicobacter pylori infection was considered, no statistically difference was found in the effect of rebamipide on either symptom or inflammation scores. In conclusion, Rebamipide demonstrated a stronger suppressive effect on the mucosal inflammation in chronic erosive gastritis than sucralfate. The gastroprotection induced by rebamipide is not influenced by H. pylori infection, which indicates its usage in the treatment of H. pylori-associated CEG.

Ursodeoxycholic acid does not interfere with in vivo Helicobacter pylori colonization

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Silva José Guilherme Nogueira da

2000-01-01

Full Text Available A low frequency of Helicobacter pylori in the gastric mucosa of patients with alkaline gastritis has been reported. At the same time, it can be noted that the growth of bacteria can be inhibited by bile acids. We studied 40 patients with chronic gastritis related to Helicobacter pylori in order to determine the effect of ursodeoxycholic acid on this infection. Diagnoses of the infection and the inflammatory process were obtained by histologic study of gastric biopsies collected during endoscopy. Two groups were studied: group I received ursodeoxycholic acid - 300 mg/day, and group II received the placebo, twice a day, both for 28 days. The colonization by Helicobacter pylori and the intensity of the mononuclear and polymorphonuclear inflammatory infiltrate were determined before (time 1 and after (time 2 treatment. Ursodeoxycholic acid had no effect on the Helicobacter pylori infection. A significant reduction in the intensity of the mononuclear inflammatory infiltrate of the gastric antrum mucosa was observed in patients from group I, when we compared not only times 1 and 2 but also groups I and II. However, this was not the case with the body mucosa. We concluded that ursodeoxycholic acid had no action on the colonization by Helicobacter pylori or on the polymorphonuclear inflammatory infiltrate, but it caused a significant reduction in the intensity of the mononuclear inflammatory infiltrate of the gastric antrum.

Helicobacter pylori infection affects mitochondrial function and DNA repair, thus, mediating genetic instability in gastric cells

DEFF Research Database (Denmark)

Machado, Ana Manuel Dantas; Desler, Claus; Boggild, Sisse

2013-01-01

Helicobacter pylori infection is an important factor for the development of atrophic gastritis and gastric carcinogenesis. However, the mechanisms explaining the effects of H. pylori infection are not fully elucidated. H. pylori infection is known to induce genetic instability in both nuclear and....... pylori infection, furthermore, the results demonstrate that multiple DNA repair activities are involved in protecting mtDNA during infection. (C) 2013 Elsevier Ireland Ltd. All rights reserved....

Alteration of histological gastritis after cure of Helicobacter pylori infection.

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Hojo, M; Miwa, H; Ohkusa, T; Ohkura, R; Kurosawa, A; Sato, N

2002-11-01

It is still disputed whether gastric atrophy or intestinal metaplasia improves after the cure of Helicobacter pylori infection. To clarify the histological changes after the cure of H. pylori infection through a literature survey. Fifty-one selected reports from 1066 relevant articles were reviewed. The extracted data were pooled according to histological parameters of gastritis based on the (updated) Sydney system. Activity improved more rapidly than inflammation. Eleven of 25 reports described significant improvement of atrophy. Atrophy was not improved in one of four studies with a large sample size (> 100 samples) and in two of five studies with a long follow-up period (> 12 months), suggesting that disagreement between the studies was not totally due to sample size or follow-up period. Methodological flaws, such as patient selection, and statistical analysis based on the assumption that atrophy improves continuously and generally in all patients might be responsible for the inconsistent results. Four of 28 studies described significant improvement of intestinal metaplasia [corrected]. Activity and inflammation were improved after the cure of H. pylori infection. Atrophy did not improve generally among all patients, but improved in certain patients. Improvement of intestinal metaplasia was difficult to analyse due to methodological problems including statistical power.

Molecular Epidemiology of Helicobacter pylori Infection in a Minor Ethnic Group of Vietnam: A Multiethnic, Population-Based Study.

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Binh, Tran Thanh; Tuan, Vo Phuoc; Dung, Ho Dang Quy; Tung, Pham Huu; Tri, Tran Dinh; Thuan, Ngo Phuong Minh; Tam, Le Quang; Nam, Bui Chi; Giang, Do Anh; Hoan, Phan Quoc; Uchida, Tomohisa; Trang, Tran Thi Huyen; Khien, Vu Van; Yamaoka, Yoshio

2018-03-01

The Helicobacter pylori -induced burden of gastric cancer varies based on geographical regions and ethnic grouping. Vietnam is a multiethnic country with the highest incidence of gastric cancer in Southeast Asia, but previous studies focused only on the Kinh ethnic group. A population-based cross-sectional study was conducted using 494 volunteers (18-78 years old), from 13 ethnic groups in Daklak and Lao Cai provinces, Vietnam. H. pylori status was determined by multiple tests (rapid urease test, culture, histology, and serology). cagA and vacA genotypes were determined by PCR-based sequencing. The overall H. pylori infection rate was 38.1%. Multivariate analysis showed that variations in geographical region, age, and ethnicity were independent factors associated with the risk of H. pylori acquisition. Therefore, multicenter, multiethnic, population based study is essential to assess the H. pylori prevalence and its burden in the general population. Only the E De ethnicity carried strains with Western-type CagA (82%) and exhibited significantly lower gastric mucosal inflammation compared to other ethnic groups. However, the histological scores of Western-type CagA and East-Asian-type CagA within the E De group showed no significant differences. Thus, in addition to bacterial virulence factors, host factors are likely to be important determinants for gastric mucosal inflammation and contribute to the Asian enigma.

Impact of Anti-Helicobacter Therapy of H.pylori-Infected Parents on H.pylori Reinfection Rate in Children after Successful Eradication

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O.P. Volosovets

2012-02-01

Full Text Available The article presents the data about the rate of H.pylori reinfection during 12 months after anti-helicobacter therapy among the children after successful eradication. It was shown that H.pylori reinfection rate was lower in children after successful eradication who were living after the treatment with parents non-infectead with H.pylori than among children who were living with H.pylori-infected parents. It was demonstrated that simultaneous anti-helicobacter therapy in H.pylori-infected parents of children with with chronic gastroduodenal diseases associated with H.pylori decreased H.pylori reinfection rate in children with successful eradication.

Treatment of Helicobacter Pylori in Children

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F Famouri

2014-04-01

Full Text Available Childrenwith Helicobacter infection need treatment. The aim of treatment is elimination of H.Pylori. Most patients with this infection are asymptomatic and without peptic disease. Treatment and management of these patients are controversy. Conventional Treatment: The best treatment for H. pylori eradication regimens should have cure rates of at least 80%, be without major side effects, and induce minimal bacterial resistance. Antibiotics alone have not achieved this. Luminal acidity influences both the effectiveness of some antimicrobial agents and the survival of the bacteri; thus antibiotics have been combined with acid suppression such as proton pump inhibitors (PPIs, bismuth, or H2 antagonists. The “classic” regimen is treatment twice daily for 7 days with a PPI and clarithromycin plus either amoxicillin or metronidazole Bismuth has been used in the treatment of peptic ulcer disease and 1 part o quadruple therapy for H.Pylori but compliance of children for it is low.   Sequential Therapy  Sequential therapyinvolves dual therapy with a PPI and amoxicillin for 5 days followed sequentially by clarithromycin, Tinidazole and omeperazole for 5 days or other triple therapy for 7 days. This treatment has had 97% efficacy.   Adjunctive Therapies A number of studies have showed the potential benefits of probiotic therapy in H. pylori treatment regimens.Consumption of these drugs accompanied with other medications increase H.Pylori eradication.    

A comparative study of clinicopathological features between chronic cholecystitis patients with and without Helicobacter pylori infection in gallbladder mucosa.

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Di Zhou

Full Text Available BACKGROUND: Helicobacter pylori has been isolated from 10%-20% of human chronic cholecystitis specimens but the characteristics of "Helicobacter pylori positive cholecystitis" remains unclear. This study aims to compare the clinicopathological features between chronic cholecystitis patients with and without Helicobacter pylori infection in gallbladder mucosa. METHODS: Three hundred and twenty-six chronic cholecystitis patients were divided into two groups according to whether Helicobacter pylori could be detected by culture, staining or PCR for Helicobacter 16s rRNA gene in gallbladder mucosa. Positive samples were sequenced for Helicobacter pylori-specific identification. Clinical parameters as well as pathological characteristics including some premalignant lesions and the expression levels of iNOS and ROS in gallbladder were compared between the two groups. RESULTS: Helicobacter pylori infection in gallbladder mucosa was detected in 20.55% of cholecystitis patients. These patients had a higher prevalence of acid regurgitation symptoms (p = 0.001, more histories of chronic gastritis (p = 0.005, gastric ulcer (p = 0.042, duodenal ulcer (p = 0.026 and higher presence of Helicobacter pylori in the stomach as compared to patients without Helicobacter pylori infection in the gallbladder mucosa. Helicobacter pylori 16s rRNA in gallbladder and gastric-duodenal mucosa from the same individual patient had identical sequences. Also, higher incidences of adenomyomatosis (p = 0.012, metaplasia (p = 0.022 and higher enhanced expressions of iNOS and ROS were detected in Helicobacter pylori infected gallbladder mucosa (p<0.05. CONCLUSIONS: Helicobacter pylori infection in gallbladder mucosa is strongly associated with Helicobacter pylori existed in stomach. Helicobacter pylori is also correlated with gallbladder premalignant lesions including metaplasia and adenomyomatosis. The potential mechanism might be related with higher ROS

Pathogenesis of Helicobacter pylori-Related Gastroduodenal Diseases from Molecular Epidemiological Studies.

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Yamaoka, Yoshio

2012-01-01

Helicobacter pylori is a major human pathogen that infects the stomach and produces inflammation that is responsible for various gastroduodenal diseases. Despite the high prevalence of H. pylori infections in Africa and South Asia, the incidence of gastric cancer in these areas is much lower than in other countries. The incidence of gastric cancer also tends to decrease from north to south in East Asia. Data from molecular epidemiological studies show that this variation in different geographic areas could be explained in part by different types of H. pylori virulence factors, especially CagA, VacA, and OipA. H. pylori infection is thought to be involved in both gastric cancer and duodenal ulcer, which are at opposite ends of the disease spectrum. This discrepancy can also be explained in part by another H. pylori factor, DupA, as well as by CagA typing (East Asian type versus Western type). H. pylori has a genome of approximately 1,600 genes; therefore, there might be other novel virulence factors. Because genome wide analyses using whole-genome sequencing technology give a broad view of the genome of H. pylori, we hope that next-generation sequencers will enable us to efficiently investigate novel virulence factors.

Pathogenesis of Helicobacter pylori-Related Gastroduodenal Diseases from Molecular Epidemiological Studies

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Yoshio Yamaoka

2012-01-01

Full Text Available Helicobacter pylori is a major human pathogen that infects the stomach and produces inflammation that is responsible for various gastroduodenal diseases. Despite the high prevalence of H. pylori infections in Africa and South Asia, the incidence of gastric cancer in these areas is much lower than in other countries. The incidence of gastric cancer also tends to decrease from north to south in East Asia. Data from molecular epidemiological studies show that this variation in different geographic areas could be explained in part by different types of H. pylori virulence factors, especially CagA, VacA, and OipA. H. pylori infection is thought to be involved in both gastric cancer and duodenal ulcer, which are at opposite ends of the disease spectrum. This discrepancy can also be explained in part by another H. pylori factor, DupA, as well as by CagA typing (East Asian type versus Western type. H. pylori has a genome of approximately 1,600 genes; therefore, there might be other novel virulence factors. Because genome wide analyses using whole-genome sequencing technology give a broad view of the genome of H. pylori, we hope that next-generation sequencers will enable us to efficiently investigate novel virulence factors.

Helicobacter pylori infection in apparently healthy South Indian children

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Kurpad, A.V.; Caszo, B.; Raj, T.; Vaz, M.

2000-01-01

Helicobacter pylori infection has been established as a major cause of chronic gastritis in adults, and it has been implicated in the genesis of gastric carcinomas and the development of gastric and duodenal ulcers. It is now postulated that neatly 90% of the adult population in developing countries may be affected with the infection since childhood. Earlier studies on Indians using serology and endoscopic biopsy have shown a high incidence of H. pylori infection in small numbers of patients. The 13 C-urea breath test, which is simple, specific and non-invasive, is also increasingly being used to determine the presence of Helicobacter pylori infection. Preliminary data from India has shown a high prevalence in the urban Indian environment, and there is an urgent need to quantify the prevalence of H. pylori infections on an epidemiological basis in both urban and rural settings. It is also important to study the possible impact of this infection on growth in children, particularly in environments with low sanitation and high crowding. In this paper, we outline a proposal to study the prevalence of Helicobacter pylori infections in children from the following different environments: urban middle socio-economic class, urban slum, rural middle socio-economic class and rural village. (author)

Helicobacter Pylori – A Moving Target | Lambiotte | South African ...

African Journals Online (AJOL)

Pylori) continues to grow. Testing is also now advised for patients with immune thrombocytopenia purpura, unexplained vitamin B12 or iron deficiency anemia. Despite the indications for treatment of Helicobacter pylori infection widening, definitive ...

Gastric angiogenesis and Helicobacter pylori infection

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I. D. Pousa

Full Text Available The formation of new blood vessels seen in conditions commonly associated with Helicobacter pylori (H. pylori infection, including gastritis, peptic ulcer, and gastric carcinoma, prompts consideration of a potential relationship between mucosal colonization by this organism and the angiogenic process. H. pylori directly or indirectly damages endothelial cells, which induces a number of changes in the microvasculature of the gastric mucosa. In H. pylori-associated conditions, that is, in gastritis, peptic ulcer and gastric carcinoma, there is an increased concentration of angiogenic factors, and subsequently a formation of new blood vessels. However, this early angiogenesis -which is activated to repair the gastric mucosa- is subsequently inhibited in patients with peptic ulcer, and ulcer healing is thus delayed. This may be due to the antiproliferative action of this organism on endothelial cells. While the angiogenic process becomes inhibited in infected patients with peptic ulcer, it remains seemingly active in those with gastritis or gastric cancer. This fact is in support of the notion suggested by various studies that peptic ulcer and gastric cancer are mutually excluding conditions. In the case of gastric cancer, neoangiogenesis would enhance nutrient and oxygen supply to cancer cells, and thus tumor growth and metastatic spread.

Overview of the phytomedicine approaches against Helicobacter pylori

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Vale, Filipa F; Oleastro, Mónica

2014-01-01

Helicobacter pylori (H. pylori) successfully colonizes the human stomach of the majority of the human population. This infection always causes chronic gastritis, but may evolve to serious outcomes, such as peptic ulcer, gastric carcinoma or mucosa-associated lymphoid tissue lymphoma. H. pylori first line therapy recommended by the Maastricht-4 Consensus Report comprises the use of two antibiotics and a proton-pomp inhibitor, but in some regions failure associated with this treatment is already undesirable high. Indeed, treatment failure is one of the major problems associated with H. pylori infection and is mainly associated with bacterial antibiotic resistance. In order to counteract this situation, some effort has been allocated during the last years in the investigation of therapeutic alternatives beyond antibiotics. These include vaccines, probiotics, photodynamic inactivation and phage therapy, which are briefly revisited in this review. A particular focus on phytomedicine, also described as herbal therapy and botanical therapy, which consists in the use of plant extracts for medicinal purposes, is specifically addressed, namely considering its history, category of performed studies, tested compounds, active principle and mode of action. The herbs already experienced are highly diverse and usually selected from products with a long history of employment against diseases associated with H. pylori infection from each country own folk medicine. The studies demonstrated that many phytomedicine products have an anti-H. pylori activity and gastroprotective action. Although the mechanism of action is far from being completely understood, current knowledge correlates the beneficial action of herbs with inhibition of essential H. pylori enzymes, modulation of the host immune system and with attenuation of inflammation. PMID:24914319

Prevalence of Helicobacter pylori and risk factors among dyspepsia ...

African Journals Online (AJOL)

Helicobacter pylori antibody conjugated with colloid gold nitrocellulose membrane strip and a structured face-to-face interview was also administered to assess risk factors for H. pylori infection. Data were analyzed using SPSS version 20. Logistic ...

Autophagy-related genes in Helicobacter pylori infection.

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Tanaka, Shingo; Nagashima, Hiroyuki; Uotani, Takahiro; Graham, David Y; Yamaoka, Yoshio

2017-06-01

In vitro studies have shown that Helicobacter pylori (H. pylori) infection induces autophagy in gastric epithelial cells. However, prolonged exposure to H. pylori reduces autophagy by preventing maturation of the autolysosome. The alterations of the autophagy-related genes in H. pylori infection are not yet fully understood. We analyzed autophagy-related gene expression in H. pylori-infected gastric mucosa compared with uninfected gastric mucosa obtained from 136 Bhutanese volunteers with mild dyspeptic symptoms. We also studied single nucleotide polymorphisms (SNPs) of autophagy-related gene in 283 Bhutanese participants to identify the influence on susceptibility to H. pylori infection. Microarray analysis of 226 autophagy-related genes showed that 16 genes were upregulated (7%) and nine were downregulated (4%). We used quantitative reverse transcriptase polymerase chain reaction to measure mRNA levels of the downregulated genes (ATG16L1, ATG5, ATG4D, and ATG9A) that were core molecules of autophagy. ATG16L1 and ATG5 mRNA levels in H. pylori-positive specimens (n=86) were significantly less than those in H. pylori-negative specimens (n=50). ATG16L1 mRNA levels were inversely related to H. pylori density. We also compared SNPs of ATG16L1 (rs2241880) among 206 H. pylori-positive and 77 H. pylori-negative subjects. The odds ratio for the presence of H. pylori in the GG genotype was 0.40 (95% CI: 0.18-0.91) relative to the AA/AG genotypes. Autophagy-related gene expression profiling using high-throughput microarray analysis indicated that downregulation of core autophagy machinery genes may depress autophagy functions and possibly provide a better intracellular habit for H. pylori in gastric epithelial cells. © 2017 John Wiley & Sons Ltd.

Medicinal plant activity on Helicobacter pylori related diseases

OpenAIRE

Wang, Yuan-Chuen

2014-01-01

More than 50% of the world population is infected with Helicobacter pylori (H. pylori). The bacterium highly links to peptic ulcer diseases and duodenal ulcer, which was classified as a group I carcinogen in 1994 by the WHO. The pathogenesis of H. pylori is contributed by its virulence factors including urease, flagella, vacuolating cytotoxin A (VacA), cytotoxin-associated gene antigen (Cag A), and others. Of those virulence factors, VacA and CagA play the key roles. Infection with H. pylori ...

Helicobacter pylori and histopathological changes of gastric mucosa ...

African Journals Online (AJOL)

Helicobacter pylori and histopathological changes of gastric mucosa in Uganda population with varying prevalence of stomach cancer. ... Results: The severity of gastritis correlated with the presence of H. pylori in Ganda and Nyarwanda but not in Nkole. Intestinal metaplasia (IM) was observed in Nyarwanda and Nkole and ...

EXTRAGASTRIC AND ORODENTAL MANIFESTATIONS IN PEDIATRIC INFECTION WITH HELICOBACTER PYLORI. A REVIEW

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Smaranda DIACONESCU

2015-12-01

Full Text Available Helicobacter pylori is a worlwide spread infection mostly manifested in childhood. Many - both invasive and non-invasive diagnostic tests - are now available,. The colonisation effect of gastric mucosa and its consequences are well known and studied. H. pylori can also induce extra-gastric manifestations, like iron-deficiency anemia. The role of oral cavity colonisation is not clearly defined, several studies stating that the oral cavity represents a reservoir for H. pyloris. The presence of this rod in the dental plaque may lead to periodontitis, dental caries, dental calculus and tooth loos. Dental treatment associated with eradication therapy decreases the prevalence of oral H. pylori and improves the eradication rate of gastric H. pylori. Dental treatment in H. pylori infection management should be taken into consideration, especially in children and teens.

Frequency of helicobacter pylori antibodies in porto-systemic encephalopathy,

International Nuclear Information System (INIS)

Sethar, G.H.; Ahmed, R.; Afsar, S.; Zuberi, B.F.

2004-01-01

Objective: To study the frequency of Helicobacter pylori antibodies in patients presenting with porto-systemic encephalopathy due to liver disease. Patients and Methods: During the study period, seventy-six patients of porto-systemic encephalopathy due to liver diseases was selected. These subjects were evaluated for hepatic encephalopathy grade, modified Child-Pugh classification and were managed according to the standard practices. These patients were evaluated for Helicobacter (H. pylori) antibody status by ELlSA (Abbott Laboratories) method. Results: Out of 76 patients studied and tested for H. pylori antibodies, 48(63.2%) were males and 28(36.8%) were females with age ranging between 17 and 85 years. Out of 76 patients who presented with porto-systemic encephalopathy, 59(77.6%) had a positive H. pylori antibody test. Thirty-five of these were males and 24 were females. A significant number of patients who presented with higher grade of encephalopathy were H. pylori antibody positive (p<0.001). Conclusion: In this study, frequency of H. pylori antibodies was significantly high in patients of porto-systematic encephalopathy. (author)

Helicobacter pylori infection and serum ferritin

DEFF Research Database (Denmark)

Berg, Gabriele; Bode, G; Blettner, M

2001-01-01

OBJECTIVE: Helicobacter pylori may possibly affect the iron metabolism by occult bleeding, impaired absorption of non-hem iron, and by scavenging hem iron or ferritin, as some studies have suggested. The aim of this study was to analyze the association between H. pylori infection and serum ferritin...... in 1987/1988. The examination included a detailed questionnaire on medical history and lifestyle factors, a 7-day food record, and blood samples. Infection with H. pylori was measured serologically by ELISA and Westernblot. RESULTS: In total, 39.2% of 1806 persons aged 18 to 89 yr included in the study...... were H. pylori positive, of whom 57.6% had an infection with a CagA-positive H. pylori strain. Age- and sex-adjusted geometric mean of ferritin was 54.5 microg/dl among H. pylori-infected compared with 63.8 microg/dl among uninfected persons. A multiple linear regression model with log...

Alcohol consumption and Helicobacter pylori infection

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Brenner, H; Berg, Gabriele; Lappus, N

1999-01-01

Alcohol has strong antimicrobial activity and stimulates gastric acid secretion. Alcohol consumption may therefore compromise the living conditions of Helicobacter pylori in the stomach. We assessed the relation of alcohol consumption with H. pylori infection among 1,785 participants ages 18...... prevalence of H. pylori infection was 39.2%. There was a clear inverse dose-response-relation between reported alcohol consumption and H. pylori infection. The relation persisted after control for potential confounding factors. The adjusted prevalence ratios (95% confidence intervals) for H. pylori infection...... among persons who consumed up to 10, 10 to 20, and more than 20 gm of alcohol per day compared with non-drinkers were 0.93 (0.77-1.13), 0.82 (0.65-1.04), and 0.71 (0.55-0.92). The inverse relation between alcohol consumption and H. pylori infection was even stronger when individuals with an indication...

Helicobacter pylori

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Leth, Peter Mygind

1992-01-01

Helicobacter pylori (HP) are Gram-negative spiral bacteria which occur in the human stomach. The bacteria were cultured in vitro for the first time in 1983. It is suspected that the bacteria may cause chronic gastritis of type B and may also be a contributory cause of chronic ulceration and cancer...... of the stomach. The bacteria are accompanied by characteristic inflammatory changes in the gastric mucosa. The significance for gastritis, chronic ulceration, non-ulcer dyspepsia and carcinoma of the stomach is discussed. HP occurs in a great proportion of the population of the world and the frequency increases...

Helicobacter pylori vaccine: from past to future.

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Agarwal, Kanishtha; Agarwal, Shvetank

2008-02-01

Helicobacter pylori infection is highly prevalent worldwide and is an important cause of gastritis, peptic ulcer disease, gastric mucosa-associated lymphoid tissue lymphoma (MALToma), and gastric adenocarcinoma. Infection is usually acquired during childhood and tends to persist unless treated. Because eradication requires treatment with multidrug regimens, prevention of initial infection by a suitable vaccine is attractive. Although immunization with H pylori protein subunits has been encouraging in animals, similar vaccine trials in humans have shown adjuvant-related adverse effects and only moderate effectiveness. Newer immunization approaches (use of DNA, live vectors, bacterial ghosts, and microspheres) are being developed. Several questions about when and whom to vaccinate will need to be appropriately answered, and a cost-effective vaccine production and delivery strategy will have to be useful for developing countries. For this review, we searched MEDLINE using the Medical Subject Heading (MeSH) terms Helicobacter pylori and vaccines for articles in English from 1990 to 2007.

Early or late antibiotic intervention prevents Helicobacter pylori-induced gastric cancer in a mouse model.

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Zhang, Songhua; Lee, Dong Soo; Morrissey, Rhiannon; Aponte-Pieras, Jose R; Rogers, Arlin B; Moss, Steven F

2014-12-01

H. pylori infection causes gastritis, peptic ulcers and gastric cancer. Eradicating H. pylori prevents ulcers, but to what extent this prevents cancer remains unknown, especially if given after intestinal metaplasia has developed. H. pylori infected wild-type (WT) mice do not develop cancer, but mice lacking the tumor suppressor p27 do so, thus providing an experimental model of H. pylori-induced cancer. We infected p27-deficient mice with H. pylori strain SS1 at 6-8 weeks of age. Persistently H. pylori-infected WT C57BL/6 mice served as controls. Mice in the eradication arms received antimicrobial therapy (omeprazole, metronidazole and clarithromycin) either "early" (at 15 weeks post infection, WPI) or "late" at 45 WPI. At 70 WPI, mice were euthanized for H. pylori determination, histopathology and cytokine/chemokine expression. Persistently infected mice developed premalignant lesions including high-grade dysplasia, whereas those given antibiotics did not. Histologic activity scores in the eradication groups were similar to each other, and were significantly decreased compared with controls for inflammation, epithelial defects, hyperplasia, metaplasia, atrophy and dysplasia. IP-10 and MIG levels in groups that received antibiotics were significantly lower than controls. There were no significant differences in expression of IFN-γ, TNF-α, IL-1β, RANTES, MCP-1, MIP-1α or MIP-1β among the three groups. Thus, H. pylori eradication given either early or late after infection significantly attenuated gastric inflammation, gastric atrophy, hyperplasia, and dysplasia in the p27-deficient mice model of H. pylori-induced gastric cancer, irrespective of the timing of antibiotic administration. This was associated with reduced expression of IP-10 and MIG. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

Helicobacter pylori eradication in patients on long-term treatment with NSAIDs reduces the severity of gastritis: a rondomized controlled trial

NARCIS (Netherlands)

de Leest, Helena T.J.I.; Steen, Kirsti S.; Bloemena, Elisabeth; Lems, Willem F.; Kuipers, Ernst J.; van de Laar, Mart A F J; Bijlsma, J.W.J.; Janssen, Matthijs; Houben, Harry H.M.L.; Kostense, Piet J.; Boers, Maarten; Dijkmans, Ben A.C.

2009-01-01

Background: Maintenance use of nonsteroidal anti-inflammatory drugs (NSAIDs) is often complicated by gastropathy. In non-NSAID users, eradication of Helicobacter pylori is associated with decreased mucosal inflammation, and may halt the progression to atrophy and intestinal metaplasia, but the

Helicobacter pylori Eradication in Patients on Long-term Treatment With NSAIDs Reduces the Severity of Gastritis A Randomized Controlled Trial

NARCIS (Netherlands)

Leest, de H.T.J.I.; Steen, K.S.S.; Bloemena, E.; Lems, W.F.; Kuipers, E.; Laar, van der M.C.; Bijlsma, J.J.E.; Janssen, M.M.J.; Houben, H.H.; Kostense, P.J.; Boers, M.; Dijkmans, B.A.C.

2009-01-01

Background: Maintenance use of nonsteroidal anti-inflammatory drugs (NSAIDs) is often complicated by gastropathy. In non-NSAID users, eradication of Helicobacter pylori is associated with decreased mucosal inflammation, and may halt the progression to atrophy and intestinal metaplasia, but the

Helicobacter pylori Eradication in Patients on Long-term Treatment With NSAIDs Reduces the Severity of Gastritis A Randomized Controlled Trial

NARCIS (Netherlands)

de Leest, H.T.J.I.; Steen, K.S.S.; Bloemena, E.; Lems, W.F.; Kuipers, E.; van der Laar, M.C.; Bijlsma, J.J.E.; Janssen, M.M.J.; Houben, H.H.; Kostense, P.J.; Boers, M.; Dijkmans, B.A.C.

2009-01-01

BACKGROUND: Maintenance use of nonsteroidal anti-inflammatory drugs (NSAIDs) is often complicated by gastropathy. In non-NSAID users, eradication of Helicobacter pylori is associated with decreased mucosal inflammation, and may halt the progression to atrophy and intestinal metaplasia, but the

Helicobacter heilmannii-associated Gastritis: Clinicopathologic Findings and Comparison with Helicobacter pylori-associated Gastritis

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Kwak, Ji Eun; Chang, Sun Hee; Kim, Hanseong; Chi, Je G.; Kim, Kyung-Ah; Yang, Jeon Ho; Lee, June Sung; Moon, Young-Soo; Kim, Kyoung-Mee

2007-01-01

The aims of this study were to evaluate the clinicopathologic features of Helicobacter heilmannii-associated gastritis and to compare H. heilmannii-associated gastritis with H. pylori-associated gastritis. We reviewed 5,985 consecutive gastric biopsy specimens. All cases of chronic gastritis with Helicobacter infection were evaluated with the Updated Sydney System, and the grades of all gastritis variables were compared between H. heilmannii-associated gastritis and H. pylori-associated gastritis groups. There were 10 cases of H. heilmannii-associated gastritis (0.17%) and 3,285 cases of H. pylori-associated gastritis (54.9%). The organisms were superficially located within the mucous layer without adhesion to epithelial cells. Interestingly, in one case many intracytoplasmic H. heilmannii organisms were observed in parietal cells with cell damage. A case of low-grade mucosa-associated lymphoid tissue (MALT) lymphoma concomitant with H. heilmannii infection was detected. Compared to H. pylori-associated gastritis, H. heilmannii-associated gastritis showed less severe neutrophilic activity (pgastritis devoid of erosion or ulcer (p=0.0309). In conclusion, we present the detailed clinicopathologic findings of H. heilmannii-associated gastritis compared to H. pylori-associated gastritis. H. heilmannii-associated gastritis is uncommon and milder than H. pylori-associated gastritis, however it may be noteworthy with respect to the development of MALT lymphoma. PMID:17297253

High Serum Pepsinogen I and beta Helicobacter pylori Infection Are Risk Factors for Aspirin-Induced Gastroduodenal Injury.

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Shan, Jing; Lei, Hongjun; Shi, Wei; Sun, Xiaobin; Tang, Yu; Ren, Chunrong

2018-01-01

Whether gastric hyperchlorhydria and Helicobacter pylori infection contribute to aspirin-induced gastroduodenal injury still lacks evidence. Because serum pepsinogens (PGs) and gastrin-17 (G17) can reflect gastric acid secretion, this study intended to elucidate whether serum PGs, serum G17, and H. pylori infection are associated with aspirin-induced gastrointestinal injury. A total of 60 patients taking low-dose aspirin for more than 1 month were enrolled in this study. Serum PG I, PG II, and G17 were determined using ELISA. A 14C-urea breath test was used for the detection of an H. pylori infection. The modified Lanza score was used to evaluate the degree of gastroduodenal injury under endoscopy. The median serum PG I level was significantly higher in the intensive gastroduodenal injury (IGI) group compared to that in the mild gastroduodenal injury group (155.0 vs. 116.6 ng/mL, p = 0.006). The H. pylori infection rate was significantly higher in the IGI group (73 vs. 40%, p = 0.037). Receiver operator characteristic curves analysis revealed that the cutoff value of PG I was 123 ng/mL, with 80% sensitivity and 61.4% specificity. H. pylori infection combined with PG I at >123 ng/mL had an OR (95% CI) of 15.8 (2.4 ± 104.5) for the prediction of aspirin-induced gastroduodenal injury. Key Messages: Serum PG I and H. pylori infection could be used to identify potential high-risk aspirin-induced gastroduodenal injury patients. © 2017 S. Karger AG, Basel.

Receptores tipo Toll, patogénesis y respuesta inmune a Helicobacter pylori Toll-like receptors, pathogenesis and immune response to Helicobacter pylori

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Norma Angélica Sánchez-Zauco

2010-10-01

Full Text Available Helicobacter pylori coloniza el epitelio gástrico y la mayoría de las personas infectadas es asintomática, de 10 al 20% desarrolla gastritis atrófica, úlcera péptica, y menos de 3% genera cáncer gástrico. Estas patologías están determinadas por la relación entre los factores de virulencia de la bacteria y los factores del hospedero como predisposición genética y respuesta inmune. La inmunidad innata, representada principalmente por los receptores tipo Toll y tipo Nod, reconocen a sus ligandos específicos y activan factores de transcripción como NF-kB, AP-1, CREB-1, induciendo la producción de citocinas inflamatorias como IL-8, IL-12, IL-6, IL-1β, IL-18 y TNF-α, e IL-10. La inflamación crónica favorece los cambios de morfología gástrica, evita la apoptosis y favorece la angiogénesis, ocasionando lesiones neoplásicas y cáncer. El objetivo de esta revisión es analizar los mecanismos propuestos a la fecha de la respuesta inmune innata y adaptativa, involucrados en la infección por H. pylori, y se puntualiza en los mecanismos de eliminación o persistencia de la infección.Helicobacter pylori colonize the gastric epithelial, most infected people are asymptomatic, 10 to 20% develop atrophic gastritis, peptic ulcer and less than 3% gastric cancer. These diseases are determined by the relationship between virulence factors of bacteria, host factors such as, genetic predisposition, and immune response. The innate immune response mainly represented by Toll-like receptors and Nod-like receptors that recognize their specific ligands, activate transcription factors as NF-kB, AP-1, CREB-1, inducing production of inflammatory cytokines such as IL -8, IL-12, IL-6, IL-1β, IL-18, TNF-α and IL-10. Chronic inflammation promotes gastric morphological changes, prevents apoptosis and allows angiogenesis generating neoplasic lesions and cancer. The aim of this review is to analyze the mechanisms proposed to date of the innate and adaptative

SURVIVAL OF HELICOBACTER PYLORI IN A NATURAL FRESHWATER ENVIRONMENT

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The mode by which Helicobacter pylori, the causative agent of most gastric ulcers, is transmitted remains undetermined. Epidemiological evidence suggests these organisms are waterborne; however, H. pylori has rarely been grown from potential water sources. This may be due to th...

[Unpleasant Journey from Helicobacter pylori-associated Gastritis to Gastric Cancer: Cancer Prevention by Taking a Detour].

Science.gov (United States)

Lee, Sang Hwan; Park, Jong Min; Han, Young Min; Ko, Weon Jin; Hahm, Ki Baik

2015-12-01

As a commensal or a pathogen, Helicobacter pylori can change the balance of a complex interaction that exists among gastric epithelial cells, microbes, and their environment. Therefore, unraveling this complex relationship of these mixtures can be expected to help prevent cancer as well as troublesome unmet medical needs of H. pylori infection. Though gastric carcinogenesis is a multi-step process, precancerous lesion can be reversible in the early phase of mucosal damage before reaching the stage of no return. However, biomarkers to predict rejuvenation of precancerous atrophic gastritis have not been identified yet and gastric cancer prevention is still regarded as an impregnable fortress. However, when we take the journey from H. pylori-associated gastritis to gastric cancer, it provides us with the clue for prevention since there are two main preventive strategies: eradication and anti-inflammation. The evidence supporting the former strategy is now ongoing in Japan through a nation-wide effort to eradicate H. pylori in patients with chronic gastritis, but suboptimal apprehension to increasing H. pylori resistance to antibiotics and patient non-compliance still exists. The latter strategy has been continued in the author'sresearch center under siTRP (short-term intervention to revert premalignant lesion) strategy. By focusing on the role of inflammation in the development of H. pylori-associated gastric carcinogenesis, this review is intended to explain the connection between inflammation and gastric cancer. Strategies on H. pylori eradication, removal of inflammation, and reverting preneoplastic lesion will also be introduced. In the end, we expect to be able to prevent gastric cancer by take a detour from the unpleasant journey, i.e. from H. pylori-associated gastritis to gastric cancer.

Detection of Helicobacter pylori in gastric cancer Detecção do Helicobacter pylori no câncer gástrico

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Luana Paredes Leite de Barros PEREIRA

2001-10-01

Full Text Available Background and Objectives — Considering the high prevalence of stomach cancer in the northern region of Brazil and the recognized relationship between chronic gastric inflammation caused by Helicobacter pylori, and its carcinogenic potential, the objective we had with this study was to investigate the presence of the microorganism in macro and microscopic presentations of neoplasm in different regions of the stomach, and in non-malignant lesions concomitant to the adenocarcinoma in patients originating from the metropolitan area of Belém (State of Pará, Brazil. Methods - Examinations were made on 172 patients divided into two groups: group I, formed by 75 patients with gastric carcinoma, and group II, formed by 97 patients with mild enanthematic gastritis, considered control group. The diagnosis was obtained during endoscopic examination and the respective biopsy. Gastric neoplasms were classified macroscopically in accordance with Borrmann's classification, and microscopically in accordance with Laurén's classification. In group I, 54 patients were male and 21 female while in group II, 22 patients were male and 75 female. The average age in group I was 61.2 years (range 27 to 86 years, while in group II it was 37.5 years (range 16 to 69 years. Thin sections were prepared and stained using the hematoxylin-eosin method. In the Helicobacter pylori research, the modified Gram stain was utilized. Statistical analysis was done by utilizing the chi-squared (chi ² test, Mann-Whitney test (U, and Fisher's exact test. Results - The results showed the detection of Helicobacter pylori were significantly greater in patients with mild enanthematic gastritis than in patients with gastric carcinoma. The presence of Helicobacter pylori in patients with gastric carcinoma and mild enanthematic gastritis was significantly greater in the antral region than in other gastric regions. Helicobacter pylori detection in patients with gastric carcinoma did not

Critical pathogenic steps to high risk Helicobacter pylori gastritis and gastric carcinogenesis.

Science.gov (United States)

Lee, Inchul

2014-06-07

Helicobacter pylori (H. pylori) gastritis may progress to high risk gastropathy and cancer. However, the pathological progression has not been characterized in detail. H. pylori induce persistent inflammatory infiltration. Neutrophils are unique in that they directly infiltrate into foveolar epithelium aiming the proliferative zone specifically. Neutrophilic proliferative zone foveolitis is a critical pathogenic step in H. pylori gastritis inducing intensive epithelial damage. Epithelial cells carrying accumulated genomic damage and mutations show the Malgun (clear) cell change, characterized by large clear nucleus and prominent nucleolus. Malgun cells further undergo atypical changes, showing nuclear folding, coarse chromatin, and multiple nucleoli. The atypical Malgun cell (AMC) change is a novel premalignant condition in high risk gastropathy, which may progress and undergo malignant transformation directly. The pathobiological significance of AMC in gastric carcinogenesis is reviewed. A new diagnosis system of gastritis is proposed based on the critical pathologic steps classifying low and high risk gastritis for separate treatment modality. It is suggested that the regulation of H. pylori-induced neutrophilic foveolitis might be a future therapeutic goal replacing bactericidal antibiotics approach.

Helicobacter pylori infection and typhoid fever in Jakarta, Indonesia.

NARCIS (Netherlands)

Vollaard, A.M.; Verspaget, H.W.; Ali, S.; Visser, L.G.; Veenendaal, R.A.; Asten, H.A.G.H. van; Widjaja, S.; Surjadi, C.; Dissel, J.T. van

2006-01-01

We evaluated the association between typhoid fever and Helicobacter pylori infection, as the latter microorganism may influence gastric acid secretion and consequently increase susceptibility to Salmonella typhi infection. Anti-H. pylori IgG and IgA antibody titres (ELISA) and gastrin concentration

Helicobacter pylori induces cell migration and invasion through casein kinase 2 in gastric epithelial cells.

Science.gov (United States)

Lee, Yeo Song; Lee, Do Yeon; Yu, Da Yeon; Kim, Shin; Lee, Yong Chan

2014-12-01

Chronic infection with Helicobacter pylori (H. pylori) is causally linked with gastric carcinogenesis. Virulent H. pylori strains deliver bacterial CagA into gastric epithelial cells. Induction of high motility and an elongated phenotype is considered to be CagA-dependent process. Casein kinase 2 plays a critical role in carcinogenesis through signaling pathways related to the epithelial mesenchymal transition. This study was aimed to investigate the effect of H. pylori infection on the casein kinase 2-mediated migration and invasion in gastric epithelial cells. AGS or MKN28 cells as human gastric epithelial cells and H. pylori strains Hp60190 (ATCC 49503, CagA(+)) and Hp8822 (CagA(-)) were used. Cells were infected with H. pylori at multiplicity of infection of 100 : 1 for various times. We measured in vitro kinase assay to examine casein kinase 2 activity and performed immunofluorescent staining to observe E-cadherin complex. We also examined β-catenin transactivation through promoter assay and MMP7 expression by real-time PCR and ELISA. H. pylori upregulates casein kinase 2 activity and inhibition of casein kinase 2 in H. pylori-infected cells profoundly suppressed cell invasiveness and motility. We confirmed that casein kinase 2 mediates membranous α-catenin depletion through dissociation of the α-/β-catenin complex in H. pylori-infected cells. We also found that H. pylori induces β-catenin nuclear translocation and increases MMP7 expressions mediated through casein kinase 2. We show for the first time that CagA(+) H. pylori upregulates cellular invasiveness and motility through casein kinase 2. The demonstration of a mechanistic interplay between H. pylori and casein kinase 2 provides important insights into the role of CagA(+) H. pylori in the gastric cancer invasion and metastasis. © 2014 John Wiley & Sons Ltd.

The Efficacy of Eradication of Helicobacter pylori Infection in Primary Prevention of NSAID-induced Gastropathy

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S.M. Tkach

2015-09-01

Full Text Available With the aim of clarifying the efficacy of eradication therapy for Helicobacter pylori (Hp infection in primary prevention of NSAID-induced gastropathy, we have examined 39 Hp-positive patients, in whom we planned to administer non-steroidal anti-inflammatory drugs (NSAIDs for various arthritis. In group I, non-steroidal anti-inflammatory drugs were prescribed after anti-helicobacter therapy, in group II eradication was not carried out, and the patients immediately received diclofenac. In both groups the incidence of peptic ulcers has been compared in 1 month after receiving diclofenac. In group I, peptic ulcers occurred in 2 patients (10.5 %, in group II — in 5 patients (26.3 %, ie in the group of eradication therapy they occurred significantly less frequently (χ2 = 0.5221. It is concluded that eradication of Hp-infection can be considered as an effective strategy for primary prevention of NSAID-induced gastropathy.

[The relationship of halitosis and Helicobacter pylori].

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Chen, Xi; Tao, Dan-ying; Li, Qing; Feng, Xi-ping

2007-06-01

The aim of the study was to investigate the relationship between halitosis and Helicobacter pylori infection in stomach. Fifty subjects without periodontal diseases and systematic disease (exclude gastrointestinal diseases) were included. Infection of H.pylori was diagnosed by biopsy and (14)C-urea breath test. SPSS11.5 software package was used to analyze the data. All the subjects were periodontal healthy according to the periodontal index. The prevalence of H.pylori infection in halitosis subjects was significantly higher than that in the normal subjects (57.1% VS 18.2%, Pperiodontal healthy subjects.

"Helicobacter Pylori" Infection in Five Inpatient Units for People with Intellectual Disability and Psychiatric Disorder

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Clarke, David; Vemuri, Murali; Gunatilake, Deepthi; Tewari, Sidhartha

2008-01-01

Background: A high prevalence of "Helicobacter pylori" infection has been reported among people with intellectual disability, especially those residing in hospital and similar settings. Surveys of inpatients have found unusually high rates of gastrointestinal malignancy, to which "H. pylori" infection predisposes. Methods: "Helicobacter pylori"…

Comparison of Salivary Anti Helicobacter pylori IgG with Serum IgG and Bacteriological Tests in Detecting Helicobacter pylori Infections

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H Ghasemian safaei

2005-01-01

Full Text Available Background: This study was conducted to compare the efficacy of enzyme-linked immunosorbent assay (ELISA for detecting anti-Helicobacter pylori (H. pylori specific IgG antibodies in specimens of oral fluid and serum with bacteriological tests. Methods: Antral biopsy specimens, as well as serum and oral fluid samples were collected from 97 patients who underwent upper gastrointestinal endoscopy. The presence or absence of current H. pylori infection was determined by culture, histology and urease detection. Anti-H. pylori specific IgG was detected in serum and oral fluid, using an established lab-made, and a commercial ELISA kit. The obtained data were compared with results of bacteriological tests. Results: In all, 62 (64% of 97 patients were positive for H. pylori by one or more of the gold standard tests (culture, histology and urease detection. Lab-made enzyme-linked immunoassay of oral fluid had a sensitivity and specificity of 92% and 83% respectively. A sensitivity and specificity of 87% and 83%, respectively, was obtained with the commercial kit. Lab-made enzyme-linked immunoassay of serum samples had a sensitivity and specificity of 90% and 88%, respectively. A sensitivity of 86% and specificity of 86% was obtained with the commercial kit. Conclusion: Detection of anti-H. pylori specific IgG in oral fluid by ELISA is comparable in sensitivity and specificity with serum based methods. Oral fluid based ELISA could provide a reliable, non-invasive method for the diagnosis of H. pylori infection. Saliva testing may have a role in epidemiological studies. Keywords: Helicobacter pylori, ELISA, Oral fluid

Outer membrane vesicles enhance the carcinogenic potential of Helicobacter pylori.

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Chitcholtan, Kenny; Hampton, Mark B; Keenan, Jacqueline I

2008-12-01

Chronic Helicobacter pylori infection is associated with an increased risk of gastric carcinogenesis. These non-invasive bacteria colonize the gastric mucosa and constitutively shed small outer membrane vesicles (OMV). In this study, we investigated the direct effect of H.pylori OMV on cellular events associated with carcinogenesis. We observed increased micronuclei formation in AGS human gastric epithelial cells treated with OMV isolated from a toxigenic H.pylori strain (60190). This effect was absent in OMV from strain 60190v:1 that has a mutant vacA, indicating VacA-dependent micronuclei formation. VacA induces intracellular vacuolation, and reduced acridine orange staining indicated disruption in the integrity of these vacuoles. This was accompanied by an alteration in iron metabolism and glutathione (GSH) loss, suggesting a role for oxidative stress in genomic damage. Increasing intracellular GSH levels with a GSH ester abrogated the VacA-mediated increase in micronuclei formation. In conclusion, OMV-mediated delivery of VacA to the gastric epithelium may constitute a new mechanism for H.pylori-induced gastric carcinogenesis.

Validation of {sup 14} C-urea breath test for diagnosis of Helicobacter pylori

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Mattar, Rejane; Silva, Fernando Marcuz; Alexandrino, Ana Maria; Laudanna, Antonio Atilio [Sao Paulo Univ., SP (Brazil). Hospital das Clinicas. Dept. de Gastroenterologia]. E-mail: shiroineko@uol.com.br

1999-02-01

The aim of this study was to validate the {sup 14} C-urea breath test for use in diagnosis of Helicobacter pylori infection. Thirty H. pylori positive patients, based on histologic test and thirty H. pylori negative patients by histology and anti-H pylori IgG entered the study. Fasting patients drank 5 uCi of {sup 14} C-urea in 20 ml of water. Breath samples were collected at O, 5, 10, 15, 20 and 30 min. The difference of cpm values between the two groups was significant at all the time intervals, besides time 0 (p < 0.0001). At 20 min, the test gave 100% sensitivity and specificity with a cut-off value of 562 cpm. Females were higher expirers than males (p=0.005). {sup 14} C-urea breath test is highly accurate for Helicobacter pylori diagnosis. It is fast, simple and should be the non-invasive test used after treating Helicobacter pylori infection. (author)

Helicobacter pylori HP1034 (ylxH) is required for motility

NARCIS (Netherlands)

van Amsterdam, Karin; van der Ende, Arie

2004-01-01

Background. Helicobacter pylori motility is essential for the colonization and persistence in the human gastric mucosa. So far, more than 50 genes have been described to play a role in flagellar biosynthesis. H. pylori YlxH (HP1034) is annotated as an ATP-binding protein. However, H. pylori YlxH

Helicobacter pylori and early gastric cancer

NARCIS (Netherlands)

Craanen, M. E.; Blok, P.; Dekker, W.; Tytgat, G. N.

1994-01-01

The relation between Helicobacter pylori, intestinal metaplasia, and early gastric cancer was studied by examining gastrectomy specimens from 31 intestinal type and 22 diffuse type carcinomas. A total of 298 patients with antral gastritis were used as controls. Atrophic changes and intestinal

Adherence of Helicobacter pylori to the Gastric Mucosa

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Marguerite Clyne

1997-01-01

Full Text Available Bacterial adhesion to the intestinal epithelium is a critical initial step in the pathogenesis of many enteric diseases. Helicobacter pylori is a duodenal pathogen that adheres to the gastric epithelium and causes gastritis and peptic ulceration. The mechanism by which H pylori causes disease has not yet been elucidated but adherence to the gastric mucosa is thought to be an important virulence determinant of the organism. What is known about adherence of H pylori to the gastric mucosa is summarized. Topics discussed are the mechanism of H pylori adherence; in vitro and in vivo models of H pylori infection; and adherence and potential adhesins and receptors for H pylori.

Altered mucosal DNA methylation in parallel with highly active Helicobacter pylori-related gastritis.

Science.gov (United States)

Yoshida, Takeichi; Kato, Jun; Maekita, Takao; Yamashita, Satoshi; Enomoto, Shotaro; Ando, Takayuki; Niwa, Tohru; Deguchi, Hisanobu; Ueda, Kazuki; Inoue, Izumi; Iguchi, Mikitaka; Tamai, Hideyuki; Ushijima, Toshikazu; Ichinose, Masao

2013-10-01

Chronic inflammation triggered by Helicobacter pylori causes altered DNA methylation in stomach mucosae, which is deeply involved in gastric carcinogenesis. This study aimed to elucidate the correlation between altered mucosal DNA methylation levels and activity of H. pylori-related gastritis, because inflammatory activity shows particular correlations with the development of diffuse-type cancer. Methylation levels in stomach mucosae of 78 healthy volunteers were determined by real-time methylation-specific PCR or bisulfite pyrosequencing. Examined loci were the promoter CpG islands of six genes (FLNc, HAND1, THBD, p41ARC, HRASLS, and LOX) and the CpG sites of non-coding repetitive elements (Alu and Satα) that are reportedly altered by H. pylori infection. Activity of H. pylori-related gastritis was evaluated using two serum markers: H. pylori antibody titer and pepsinogen II. Methylation levels of the six CpG islands were consistently increased, and those of the two repetitive elements were consistently decreased in a stepwise manner with the activity of gastric inflammation as represented by serum marker levels. Each serum marker level was well correlated with the overall DNA methylation status of stomach mucosa, and these two serologic markers were additive in the detection of the mucosa with severely altered DNA methylation. Alteration in mucosal DNA methylation level was closely correlated with activity of H. pylori-related gastritis as evaluated by serum markers. The observed correlation between altered DNA methylation levels and activity of H. pylori-related gastritis appears to be one of the relevant molecular mechanisms underlying the development of diffuse-type cancer.

Indigenous Greenlanders have a higher sero-prevalence of IgG antibodies to Helicobacter pylori than Danes

DEFF Research Database (Denmark)

Milman, Nils; Byg, Keld-Erik; Andersen, Leif P

2003-01-01

To assess the sero-prevalence of IgG antibodies to Helicobacter pylori (H. pylori) in Greenlanders and compare with the sero-prevalence in Caucasian Danes.......To assess the sero-prevalence of IgG antibodies to Helicobacter pylori (H. pylori) in Greenlanders and compare with the sero-prevalence in Caucasian Danes....

Interleukin 10 in Helicobacter pylori associated gastritis: immunohistochemical localisation and in vitro effects on cytokine secretion

Science.gov (United States)

Bodger, K; Bromelow, K; Wyatt, J; Heatley, R

2001-01-01

Background/Aims—Interleukin 10 (IL-10) is a counterinflammatory peptide implicated in the downregulation of human intestinal immune responses. Enhanced secretion of IL-10 has been documented in gastric biopsy organ culture in Helicobacter pylori infection. This study aimed to define the cellular origins of IL-10 in H pylori associated gastritis, and to determine the effects of endogenous IL-10 on proinflammatory cytokine secretion in vitro. Methods—Endoscopic biopsies were obtained from the gastric antrum at endoscopy from patients with dyspepsia. Two pairs of antral biopsies were cultured in vitro for 24 hours, one pair in the presence of neutralising anti-IL-10 monoclonal antibody, the other pair as controls. The cytokine content of culture supernatants (tumour necrosis factor α (TNF-α), IL-6, and IL-8) was determined by enzyme linked immunosorbent assay and corrected for biopsy weight. Helicobacter pylori status was established by histology and biopsy urease test, and histopathology graded by the Sydney system. In a subgroup of patients, western blotting was used to establish CagA serological status. Immunohistochemistry for IL-10 was performed on formalin fixed tissues using a combination of microwave antigen retrieval and the indirect avidin–biotin technique. Immunoreactivity was scored semiquantitatively. Results—In vitro culture was performed in 41 patients: 31 with H pylori positive chronic gastritis and 10 H pylori negative. In vitro secretion of TNF-α, IL-6, and IL-8 for "control" biopsies was significantly higher in H pylori positive versus negative samples, with values of TNF-α and IL-6 correlating with the degree of active and chronic inflammation and being higher in CagA seropositive cases. No evidence for enhanced cytokine secretion was seen in biopsies cocultured in the presence of anti-IL-10 monoclonal antibody. Immunohistochemistry was performed in 29 patients, of whom 13 were H pylori positive. IL-10 immunoreactivity was observed in

Treatment for Helicobacter pylori infection and risk of Parkinson's disease in Denmark

DEFF Research Database (Denmark)

Nielsen, H H; Qiu, J; Friis, S

2012-01-01

It has been speculated that gastrointestinal infection with Helicobacter pylori (HP) contributes to the development of Parkinson's disease (PD). We used nationwide Danish registers to investigate this hypothesis.......It has been speculated that gastrointestinal infection with Helicobacter pylori (HP) contributes to the development of Parkinson's disease (PD). We used nationwide Danish registers to investigate this hypothesis....

Endoscopic gastritis, serum pepsinogen assay, and Helicobacter pylori infection.

Science.gov (United States)

Lee, Sun-Young

2016-09-01

Endoscopic findings of the background gastric mucosa are important in the Helicobacter pylori-seroprevalent population. It is strongly correlated not only with the risk of gastric cancer, but also with the excretion ability of gastric mucosa cells. In noninfected subjects, common endoscopic findings are regular arrangement of collecting venules, chronic superficial gastritis, and erosive gastritis. In cases of active H. pylori infection, nodularity on the antrum, hemorrhagic spots on the fundus, and thickened gastric folds are common endoscopic findings. The secreting ability of the gastric mucosa cells is usually intact in both noninfected and actively infected stomachs, and the intragastric condition becomes hyperacidic upon inflammation. Increased serum pepsinogen II concentration correlates well with active H. pylori infection, and also indicates an increased risk of diffuse-type gastric cancer. In chronic inactive H. pylori infection, metaplastic gastritis and atrophic gastritis extending from the antrum (closed-type chronic atrophic gastritis) toward the corpus (open-type chronic atrophic gastritis) are common endoscopic findings. The intragastric environment is hypoacidic and the risk of intestinal-type gastric cancer is increased in such conditions. Furthermore, there is a decrease in serum pepsinogen I concentration when the secreting ability of the gastric mucosa cells is damaged. Serologic and endoscopic changes that occur upon H. pylori infection are important findings for estimating the secreting ability of the gastric mucosa cells, and could be applied for the secondary prevention of gastric cancer.

Frequency of virulence factors in Helicobacter pylori-infected patients with gastritis.

Science.gov (United States)

Salimzadeh, Loghman; Bagheri, Nader; Zamanzad, Behnam; Azadegan-Dehkordi, Fatemeh; Rahimian, Ghorbanali; Hashemzadeh-Chaleshtori, Morteza; Rafieian-Kopaei, Mahmoud; Sanei, Mohammad Hossein; Shirzad, Hedayatollah

2015-03-01

The outcome of Helicobacter pylori infection has been related to specific virulence-associated bacterial genotypes. The vacuolating cytotoxin (vacA), cagA gene, oipA and babA2 gene are important virulence factor involving gastric diseases. The objective of this study was to assess the relationship between virulence factors of H. pylori and histopathological findings. Gastroduodenoscopy was performed in 436 dyspeptic patients. Antrum biopsy was obtained for detection of H. pylori, virulence factors and for histopathological assessment. The polymerase chain reaction was used to detect virulence factors of H. pylori using specific primers. vacA genotypes in patients infected with H. pylori were associated with cagA, iceA1 and iceA2. In the patients with H. pylori infection there was a significant relationship between cagA positivity and neutrophil activity (P = 0.004) and chronic inflammation (P = 0.013) and with H. pylori density (P = 0.034). Neutrophil infiltration was found to be more severe in the s1 group than in the s2 group (P = 0.042). Also was a significant relationship between oipA positivity and neutrophil activity (P = 0.004) and with H. pylori density (P = 0.018). No significant relationships were observed between other vacA genotypes and histopathological parameters. H. pylori strains showing cagA, vacA s1 and oipA positivity are associated with more severe gastritis in some histological features but virulence factors of H. pylori do not appear to determine the overall pattern of gastritis. Copyright © 2015 Elsevier Ltd. All rights reserved.

Helicobacter pylori prevalence in dyspeptic patients in the Eastern ...

African Journals Online (AJOL)

Helicobacter pylori prevalence in dyspeptic patients in the Eastern Cape province – race and disease status. ... Fisher's exact test was used to assess the univariate association between H. pylori infection and the possible risk factors. ... Gender, antibiotic treatment and alcohol consumption may be risk factors for infection.

Helicobacter pylori eradication therapy: A review of current trends ...

African Journals Online (AJOL)

Helicobacter pylori has been implicated in the formation of chronic gastritis, peptic ulcer disease, mucosa‑associated lymphoid tissue lymphoma and gastric cancer. Eradication of H. Pylori has been recommended as treatment and prevention for these complications. This review is based on a search of Medline, the ...

49 Marked susceptibility of South African Helicobacter pylori strains ...

African Journals Online (AJOL)

Objectives. Helicobacter pylori-associated infection is common in South Africa, as in other developing countries. Antibiotic resistance is recognised as a major cause of treatment failure. We studied the susceptibility and resistance patterns of H. pylori to guide empiric treatment and prevent the emergence of resistance.

Assessment of Helicobacter pylori eradication by virgin olive oil.

Science.gov (United States)

Castro, Manuel; Romero, Concepción; de Castro, Antonio; Vargas, Julio; Medina, Eduardo; Millán, Raquel; Brenes, Manuel

2012-08-01

 A recent study conducted by Medina et al. disclosed that virgin olive oil has a bactericidal effect in vitro against Helicobacter pylori because of its contents of certain phenolic compounds with dialdehydic structures. We carried out two clinical trials to evaluate the effect of virgin olive oil on H. pylori-infected individuals.  Two different pilot studies were performed with 60 H. pylori-infected adults. In the first study, thirty subjects who tested positive for H. pylori received 30 g of washed virgin olive oil for 14 days, and after 1 month, the patients took 30 g of unwashed virgin olive oil for another 14 days. In a second study, a group of 30 subjects received 30 g of a different virgin olive oil for 14 days. Helicobacter pylori-infection status was checked by the urea breath test.  Helicobacter pylori was eradicated in 8 of 30 individuals when microorganism status was checked after 4-6 weeks from the first clinical intervention although 12 of 30 individuals did not show H. pylori infection at 24-72 hour of the last oil dose. Eradication rates were 27 and 40% by intention to treat and per protocol, respectively. Moreover, only 3 of 30 individuals were H. pylori negative after 4-6 weeks from the second clinical intervention but 5 of 30 were negative at 24-72 hour of the last oil dose. Eradication rates were 10 and 11% by intention to treat and per protocol, respectively. It must also be noted that 13 subjects withdrew from the studies because of taste and nausea drawbacks.  The administration of virgin olive oil showed moderate effectiveness in eradicating H. pylori. Further studies are needed to confirm these findings, especially with longer periods, different administration conditions, and several types of olive oils. © 2012 Blackwell Publishing Ltd.

Induction of premalignant host responses by cathepsin x/z-deficiency in Helicobacter pylori-infected mice.

Directory of Open Access Journals (Sweden)

Sabine Krueger

Full Text Available Helicobacter pylori are responsible for the induction of chronic gastric inflammation progressing to atrophy, metaplasia, and gastric cancer. The overexpression of Cathepsin X/Z (Ctsz in H. pylori-infected mucosa and gastric cancer is mediated predominantly by an augmented migration of ctsz(-/-positive macrophages and the up-regulation of Ctsz in tumor epithelium. To explore the Ctsz-function in the context of chronic inflammation and the development of preneoplastic lesions, we used Ctsz-deficient mice in a H. pylori gastritis model. Ctsz (-/- and wild-type (wt mice were infected with H. pylori strain SS1. The mice were sacrificed at 24, 36, and 50 weeks post infection (wpi. The stomach was removed, and gastric strips were snap-frozen or embedded and stained with H&E. Tissue sections were scored for epithelial lesions and inflammation. Ki-67 and F4/80 immunostaining were used to measure epithelial cell proliferation and macrophage infiltration, respectively. The upregulation of compensating cathepsins and cytokines were confirmed by Western blotting and quantitative RT-PCR. SS1-infected wt and ctsz (-/- mice showed strong inflammation, foveolar hyperplasia, atrophy, and cystically-dilated glands. However, at 50 wpi, ctsz (-/- mice developed significantly more severe spasmolytic polypeptide-expressing metaplasia (SPEM, showed enhanced epithelial proliferation, and higher levels of infiltrating macrophages. Induction of cytokines was higher and significantly prolonged in ctsz (-/- mice compared to wt. Ctsz deficiency supports H. pylori-dependent development of chronic gastritis up to metaplasia, indicating a protective, but not proteolytic, function of Ctsz in inflammatory gastric disease.

Helicobacter pylori and Peptic Ulcers

Centers for Disease Control (CDC) Podcasts

2010-08-17

In this podcast, CDC's Dr. David Swerdlow discusses the relationship between Helicobacter pylori and peptic ulcer disease and trends in hospitalization rates for peptic ulcer disease in the United States between 1998 and 2005.  Created: 8/17/2010 by National Center for Emerging and Zoonotic Infectious Diseases.   Date Released: 8/17/2010.

Induction of CD69 expression by cagPAI-positive Helicobacter pylori infection

Institute of Scientific and Technical Information of China (English)

Naoki Mori; Chie Ishikawa; Masachika Senba

2011-01-01

AIM: To investigate and elucidate the molecular mech-anism that regulates inducible expression of CD69 by Helicobacter pylori (H. pylori ) infection.METHODS: The expression levels of CD69 in a T-cell line, Jurkat, primary human peripheral blood mononu-clear cells (PBMCs), and CD4+T cells, were assessed by immunohistochemistry, reverse transcription polymerase chain reaction, and flow cytometry. Activation of CD69 promoter was detected by reporter gene. Nuclear factor (NF)-κB activation in Jurkat cells infected with H. pylori was evaluated by electrophoretic mobility shift assay. The role of NF-κB signaling in H. pylori -induced CD69 expression was analyzed using inhibitors of NF-κB and dominant-negative mutants. The isogenic mutants with disrupted cag pathogenicity island ( cagPAI) and virD4 were used to elucidate the role of cagPAI-encoding type Ⅳ secretion system and CagA in CD69 expression.RESULTS: CD69 staining was detected in mucosal lymphocytes and macrophages in specimens of pa-tients with H. pylori -positive gastritis. Although cagPAI-positive H. pylori and an isogenic mutant of virD4 induced CD69 expression, an isogenic mutant of cag-PAI failed to induce this in Jurkat cells. H. pylori also induced CD69 expression in PBMCs and CD4+T cells. The activation of the CD69 promoter by H. pylori was mediated through NF-κB. Transfection of dominant-negative mutants of IκBs, IκB kinases, and NF-κB-inducing kinase inhibited H. pylori -induced CD69 activation. Inhibitors of NF-κB suppressed H. pylori -induced CD69 mRNA expression.CONCLUSION: The results suggest that H. pylori in-duces CD69 expression through the activation of NF-κB. cagPAI might be relevant in the induction of CD69 expression in T cells. CD69 in T cells may play a role in H. pylori -induced gastritis.

Nitric oxide synthetase and Helicobacter pylori in patients undergoing appendicectomy.

LENUS (Irish Health Repository)

Kell, M R

2012-02-03

BACKGROUND: This study was designed to determine whether Helicobacter pylori forms part of the normal microenvironment of the appendix, whether it plays a role in the pathogenesis of acute appendicitis, and whether it is associated with increased expression of inducible nitric oxide synthetase (iNOS) in appendicular macrophages. METHODS: Serology for H. pylori was performed on 51 consecutive patients undergoing emergency appendicectomy. Appendix samples were tested for urease activity, cultured and stained for H. pylori, graded according to the degree of inflammatory infiltrate, and probed immunohistochemically for iNOS expression. RESULTS: The mean age of the patients was 21 (range 7-51) years. Seventeen patients (33 per cent) were seropositive for H. pylori but no evidence of H. pylori was found in any appendix specimen. However, an enhanced inflammatory cell infiltration was observed in seropositive patients (P < 0.04) and the expression of macrophage iNOS in the mucosa of normal and inflamed appendix specimens was increased (P < 0.01). CONCLUSION: H. pylori does not colonize the appendix and is unlikely to be a pathogenic stimulus for appendicitis. Priming effects on mucosal immunology downstream from the foregut may occur after infection with H. pylori.

Oral and gastric helicobacter pylori : Effects and associations

OpenAIRE

Veiga, Nélio; Pereira, Carlos; Resende, Carlos; Amaral, Odete; Ferreira, Manuela; Nelas, Paula; Chaves, Claudia; Duarte, João; Cirnes, Luis; Machado, José Carlos; Ferreira, Paula; Correia, Ilídio J.

2015-01-01

Introduction This study consisted in the comparison of the prevalence of Helicobacter pylori (H. pylori) present in the stomach and in saliva of a sample of Portuguese adolescents and the assessment of the association between H. pylori infection with socio-demographic variables and prevalence of dental caries. Materials and Methods A cross-sectional study was designed including a sample of 447 adolescents aged 12 to 19 years old, attending a public school in S?t?o, Portugal. A questionnaire a...

A Novel Assay for Easy and Rapid Quantification of Helicobacter pylori Adhesion.

Science.gov (United States)

Skindersoe, Mette E; Rasmussen, Lone; Andersen, Leif P; Krogfelt, Karen A

2015-06-01

Reducing adhesion of Helicobacter pylori to gastric epithelial cells could be a new way to counteract infections with this organism. We here present a novel method for quantification of Helicobacter pylori adhesion to cells. Helicobacter pylori is allowed to adhere to AGS or MKN45g cells in a 96-well microtiter plate. Then wells are added saponin, which lyses the cells without affecting the bacteria. After addition of alamarBlue(®) (resazurin) and 1- to 2-hour incubation, fluorescence measurements can be used to quantify the number of adherent bacteria. By use of the method, we demonstrate that adhesion of both a sabA and babA deletion mutant of H. pylori is significantly reduced compared to the wild type. The method offers a number of applications and may be used to compare the adherence potential of different strains of H. pylori to either cells or different materials or to screen for potential anti-adhesive compounds. The results presented here suggest that this easy and reproducible assay is well suited for quantitative investigation of H. pylori adhesion. © 2015 John Wiley & Sons Ltd.

Helicobacter pylori genetic diversification in the Mongolian gerbil model.

Science.gov (United States)

Beckett, Amber C; Loh, John T; Chopra, Abha; Leary, Shay; Lin, Aung Soe; McDonnell, Wyatt J; Dixon, Beverly R E A; Noto, Jennifer M; Israel, Dawn A; Peek, Richard M; Mallal, Simon; Algood, Holly M Scott; Cover, Timothy L

2018-01-01

Helicobacter pylori requires genetic agility to infect new hosts and establish long-term colonization of changing gastric environments. In this study, we analyzed H. pylori genetic adaptation in the Mongolian gerbil model. This model is of particular interest because H. pylori -infected gerbils develop a high level of gastric inflammation and often develop gastric adenocarcinoma or gastric ulceration. We analyzed the whole genome sequences of H. pylori strains cultured from experimentally infected gerbils, in comparison to the genome sequence of the input strain. The mean annualized single nucleotide polymorphism (SNP) rate per site was 1.5e -5 , which is similar to the rates detected previously in H. pylori- infected humans. Many of the mutations occurred within or upstream of genes associated with iron-related functions ( fur , tonB1 , fecA2 , fecA3 , and frpB3 ) or encoding outer membrane proteins ( alpA, oipA, fecA2, fecA3, frpB3 and cagY ). Most of the SNPs within coding regions (86%) were non-synonymous mutations. Several deletion or insertion mutations led to disruption of open reading frames, suggesting that the corresponding gene products are not required or are deleterious during chronic H. pylori colonization of the gerbil stomach. Five variants (three SNPs and two deletions) were detected in isolates from multiple animals, which suggests that these mutations conferred a selective advantage. One of the mutations (FurR88H) detected in isolates from multiple animals was previously shown to confer increased resistance to oxidative stress, and we now show that this SNP also confers a survival advantage when H. pylori is co-cultured with neutrophils. Collectively, these analyses allow the identification of mutations that are positively selected during H. pylori colonization of the gerbil model.

Biological evaluation and molecular docking of baicalin and scutellarin as Helicobacter pylori urease inhibitors.

Science.gov (United States)

Yu, Xiao-Dan; Zheng, Rong-Bo; Xie, Jian-Hui; Su, Ji-Yan; Huang, Xiao-Qi; Wang, Yong-Hong; Zheng, Yi-Feng; Mo, Zhi-Zhun; Wu, Xiao-Li; Wu, Dian-Wei; Liang, Ye-er; Zeng, Hui-Fang; Su, Zi-Ren; Huang, Ping

2015-03-13

Baicalin and scutellarin are the principal bioactive components of Scutellaria baicalensis Georgi which has extensively been incorporated into heat-clearing and detoxification formulas for the treatment of Helicobacter pylori-related gastrointestinal disorders in traditional Chinese medicine. However, the mechanism of action remained to be defined. To explore the inhibitory effect, kinetics and mechanism of Helicobacter pylori urease (the vital pathogenetic factor for Helicobacter pylori infection) inhibition by baicalin and scutellarin, for their therapeutic potential. The ammonia formations, indicator of urease activity, were examined using modified spectrophotometric Berthelot (phenol-hypochlorite) method. The inhibitory effect of baicalin and scutellarin was characterized with IC50 values, compared to acetohydroxamic acid (AHA), a well known Helicobacter pylori urease inhibitor. Lineweaver-Burk and Dixon plots for the Helicobacter pylori urease inhibition of baicalin and scutellarin was constructed from the kinetic data. SH-blocking reagents and competitive active site Ni(2+) binding inhibitors were employed for mechanism study. Molecular docking technique was used to provide some information on binding conformations as well as confirm the inhibition mode. Moreover, cytotoxicity experiment using Gastric Epithelial Cells (GES-1) was evaluated. Baicalin and scutellarin effectively suppressed Helicobacter pylori urease in dose-dependent and time-independent manner with IC50 of 0.82±0.07 mM and 0.47±0.04 mM, respectively, compared to AHA (IC50=0.14±0.05 mM). Structure-activity relationship disclosed 4'-hydroxyl gave flavones an advantage to binding with Helicobacter pylori urease. Kinetic analysis revealed that the types of inhibition were non-competitive and reversible with inhibition constant Ki of 0.14±0.01 mM and 0.18±0.02 mM for baicalin and scutellarin, respectively. The mechanism of urease inhibition was considered to be blockage of the SH groups of

Nobeli auhinna tõi Helicobacter pylori / Juhan Kaldre

Index Scriptorium Estoniae

Kaldre, Juhan

2005-01-01

Nobeli meditsiiniauhind määrati sel aastal Austraalia teadlastele Robin Warrenile ja Barry Marshallile, kes avastasid, et gastriit ning peptiline haavand tekib Helicobacter pylori infektsiooni tulemusena

DRUG RESISTANCE IN HELICOBACTER PYLORI

Directory of Open Access Journals (Sweden)

Júlia Silveira VIANNA

Full Text Available ABSTRACT Background Helicobacter pylori has a worldwide distribution and is associated with the pathogenesis of various diseases of the digestive system. Treatment to eradicate this microorganism involves the use of a combination of antimicrobials, such as amoxicillin, metronidazole, clarithromycin, and levofloxacin, combined with proton pump inhibitors. Although the current therapy is effective, a high rate of treatment failure has been observed, mainly because of the acquisition of point mutations, one of the major resistance mechanisms developed by H. pylori. This phenomenon is related to frequent and/or inappropriate use of antibiotics. Conclusion This review reported an overview of the resistance to the main drugs used in the treatment of H. pylori, confirming the hypothesis that antibacterial resistance is a highly local phenomenon and genetic characteristics of a given population can influence which therapy is the most appropriate.

Evidence of mother-child transmission of Helicobacter pylori infection

OpenAIRE

Escobar,Mario Luis; Kawakami,Elisabete

2004-01-01

BACKGROUND: Low socioeconomical status is a major risk factor for natural acquisition of Helicobacter pylori (H. pylori) infection in developing countries. Its transmission route is unknown but studies suggest person-to-person transmission. AIM: To evaluate seropositivity of anti-H. pylori antibodies in family members of infected symptomatic index patients as compared to family members of symptomatic uninfected index patients. PATIENTS AND METHODS: One hundred and twelve family members of 38 ...

Gastric angiogenesis and Helicobacter pylori infection Angiogénesis gástrica e infección por Helicobacter pylori

Directory of Open Access Journals (Sweden)

I. D. Pousa

2006-06-01

Full Text Available The formation of new blood vessels seen in conditions commonly associated with Helicobacter pylori (H. pylori infection, including gastritis, peptic ulcer, and gastric carcinoma, prompts consideration of a potential relationship between mucosal colonization by this organism and the angiogenic process. H. pylori directly or indirectly damages endothelial cells, which induces a number of changes in the microvasculature of the gastric mucosa. In H. pylori-associated conditions, that is, in gastritis, peptic ulcer and gastric carcinoma, there is an increased concentration of angiogenic factors, and subsequently a formation of new blood vessels. However, this early angiogenesis -which is activated to repair the gastric mucosa- is subsequently inhibited in patients with peptic ulcer, and ulcer healing is thus delayed. This may be due to the antiproliferative action of this organism on endothelial cells. While the angiogenic process becomes inhibited in infected patients with peptic ulcer, it remains seemingly active in those with gastritis or gastric cancer. This fact is in support of the notion suggested by various studies that peptic ulcer and gastric cancer are mutually excluding conditions. In the case of gastric cancer, neoangiogenesis would enhance nutrient and oxygen supply to cancer cells, and thus tumor growth and metastatic spread.

Transcriptional Regulation of the Nickel and Iron Metabolism in Helicobacter pylori

NARCIS (Netherlands)

F.D.J. Ernst (Florian)

2005-01-01

textabstractUp to 50 % of the world's population is infected with Helicobacter pylori. Colonization of the mucus layer of the human stomach by H. pylori, is lifelong unless treated with antibiotics (26). H. pylori, which is a neutralophilic bacterium, survives in the mucus layer of the human

Helicobacter pylori-derived Heat shock protein 60 enhances angiogenesis via a CXCR2-mediated signaling pathway

Energy Technology Data Exchange (ETDEWEB)

Lin, Chen-Si [Department of Biological Science and Technology, National Chiao-Tung University, Hsin-Chu, Taiwan (China); School of Veterinary Medicine, National Taiwan University, Taipei, Taiwan (China); He, Pei-Juin; Hsu, Wei-Tung [Department of Biological Science and Technology, National Chiao-Tung University, Hsin-Chu, Taiwan (China); Wu, Ming-Shiang [Department of Internal Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan (China); Wu, Chang-Jer [Department of Food Science, National Taiwan Ocean University, Keelung, Taiwan (China); Shen, Hsiao-Wei [Institute of Molecular Medicine and Bioengineering, National Chiao-Tung University, Hsin-Chu, Taiwan (China); Hwang, Chia-Hsiang [Yung-Shin Pharmaceutical Industry Co., Ltd., Tachia, Taichung, Taiwan (China); Lai, Yiu-Kay [Department of Life Science, Institute of Biotechnology, National Tsing Hua University, Hsin-Chu, Taiwan (China); Tsai, Nu-Man [School of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan (China); Liao, Kuang-Wen, E-mail: kitchhen@yahoo.com.tw [Institute of Molecular Medicine and Bioengineering, National Chiao-Tung University, Hsin-Chu, Taiwan (China)

2010-06-25

Helicobacter pylori is a potent carcinogen associated with gastric cancer malignancy. Recently, H. pylori Heat shock protein 60 (HpHSP60) has been reported to promote cancer development by inducing chronic inflammation and promoting tumor cell migration. This study demonstrates a role for HpHSP60 in angiogenesis, a necessary precursor to tumor growth. We showed that HpHSP60 enhanced cell migration and tube formation, but not cell proliferation, in human umbilical vein endothelial cells (HUVECs). HpHSP60 also indirectly promoted HUVEC proliferation when HUVECs were co-cultured with supernatants collected from HpHSP60-treated AGS or THP-1 cells. The angiogenic array showed that HpHSP60 dramatically induced THP-1 cells and HUVECs to produce the chemotactic factors IL-8 and GRO. Inhibition of CXCR2, the receptor for IL-8 and GRO, or downstream PLC{beta}2/Ca2+-mediated signaling, significantly abolished HpHSP60-induced tube formation. In contrast, suppression of MAP K or PI3 K signaling did not affect HpHSP60-mediated tubulogenesis. These data suggest that HpHSP60 enhances angiogenesis via CXCR2/PLC{beta}2/Ca2+ signal transduction in endothelial cells.

Helicobacter pylori-derived Heat shock protein 60 enhances angiogenesis via a CXCR2-mediated signaling pathway

International Nuclear Information System (INIS)

Lin, Chen-Si; He, Pei-Juin; Hsu, Wei-Tung; Wu, Ming-Shiang; Wu, Chang-Jer; Shen, Hsiao-Wei; Hwang, Chia-Hsiang; Lai, Yiu-Kay; Tsai, Nu-Man; Liao, Kuang-Wen

2010-01-01

Helicobacter pylori is a potent carcinogen associated with gastric cancer malignancy. Recently, H. pylori Heat shock protein 60 (HpHSP60) has been reported to promote cancer development by inducing chronic inflammation and promoting tumor cell migration. This study demonstrates a role for HpHSP60 in angiogenesis, a necessary precursor to tumor growth. We showed that HpHSP60 enhanced cell migration and tube formation, but not cell proliferation, in human umbilical vein endothelial cells (HUVECs). HpHSP60 also indirectly promoted HUVEC proliferation when HUVECs were co-cultured with supernatants collected from HpHSP60-treated AGS or THP-1 cells. The angiogenic array showed that HpHSP60 dramatically induced THP-1 cells and HUVECs to produce the chemotactic factors IL-8 and GRO. Inhibition of CXCR2, the receptor for IL-8 and GRO, or downstream PLCβ2/Ca2+-mediated signaling, significantly abolished HpHSP60-induced tube formation. In contrast, suppression of MAP K or PI3 K signaling did not affect HpHSP60-mediated tubulogenesis. These data suggest that HpHSP60 enhances angiogenesis via CXCR2/PLCβ2/Ca2+ signal transduction in endothelial cells.

Correlation of Serum Anti- Helicobacter pylori Immunoglobulin A (IGA)

African Journals Online (AJOL)

Background: The seroprevalence of anti-H. pylori IgA antibodies has been reported to vary among populations and in relation to strains of Helicobacter pylori bacterium. However, there has been conflicting reports on the association between IgA serological status and the histological variables of chronic gastritis. This study ...

Helicobacter Pylori –Infected Patients | Eltayeb | Sudan Journal of ...

African Journals Online (AJOL)

Background: The role of Helicobacter pylori on gastric carcinogenesis is still unclear but it is considered to predispose carriers to gastric cancer. Objective: The aim of this study is to investigate the relationship between the extent of DNA damage of normal gastric epithelial cells and H. Pylori positive & negative gastritis ...

Development of gastric cancer in nonatrophic stomach with highly active inflammation identified by serum levels of pepsinogen and Helicobacter pylori antibody together with endoscopic rugal hyperplastic gastritis.

Science.gov (United States)

Watanabe, Mika; Kato, Jun; Inoue, Izumi; Yoshimura, Noriko; Yoshida, Takeichi; Mukoubayashi, Chizu; Deguchi, Hisanobu; Enomoto, Shotaro; Ueda, Kazuki; Maekita, Takao; Iguchi, Mikitaka; Tamai, Hideyuki; Utsunomiya, Hirotoshi; Yamamichi, Nobutake; Fujishiro, Mitsuhiro; Iwane, Masataka; Tekeshita, Tatsuya; Mohara, Osamu; Ushijima, Toshikazu; Ichinose, Masao

2012-12-01

This study aimed to elucidate groups at high risk of developing cancer among patients with serologically identified Helicobacter pylori infection and nonatrophic stomach. Annual endoscopy was performed for a mean of 5.4 years in 496 asymptomatic middle-aged men who were H. pylori antibody-positive and pepsinogen (PG) test-negative. Subjects were stratified according to the activity of H. pylori-associated gastritis measured by serum levels of PG and H. pylori antibody, and/or by endoscopic findings of rugal hyperplastic gastritis (RHG), and cancer development was investigated. During the study period, seven cases of cancer developed in the cohort (incidence rate, 261/100,000 person-years), with 85.7% developing in the group showing a PGI/II ratio ≤ 3.0, reflecting active inflammation-based high PGII levels. Cancer incidence was significantly higher in this group (750/100,000 person-years) than in groups with less active gastritis. Furthermore, cancer incidence for this group was significantly higher in the subgroup with high H. pylori antibody titers than in the low-titer subgroup. Meanwhile, endoscopic findings revealed that 11.7% of subjects showed RHG reflecting localized highly active inflammation, and cancer risk was significantly higher in patients with RHG than in patients without. Combining the two serum tests and endoscopic examination for RHG allowed identification of subjects with more active gastritis and higher cancer risk. No cancer development was observed in these high-risk subjects after H. pylori eradication. Subjects with highly active gastritis identified by the two serological tests and endoscopic RHG constitute a group at high risk of cancer development with H. pylori-infected nonatrophic stomach. Copyright © 2012 UICC.

Helicobacter pylori in the gastric mucosa of dead children Helicobacter pylori en la mucosa gástrica de cadáveres de niños

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John Jairo Duque Alzate

1999-03-01

Full Text Available 23 children under the age of 12 years who died violently without receiving any treatment, had their gastric mucosa studied by means of he Warthin-Starry stain and immunohistochemistry in search for Helicobacter pylori. It was found that 60.9% (14 cases were positive; of them 64,3% belonged to a low social class and 35,7% to the middle one. Of the positive cases, 9 had acute gastritis, 1 had chronic gastritis and only 4 had normal gastric mucosa. A clear association between Helicobacter pylory and changes in gastritis was observed. En 23 niños menores de 12 años que murieron en forma violenta sin haber recibido tratamiento, se estudiaron para Helicobacter pylori las mucosas gástricas con las coloraciones de hematoxilina eosina, Warthin Starry e inmunohistoquímica. Se encontró que 14 casos (60,9% fueron positivos para esta bacteria, de los cuales 9 (64,3% pertenecían a un estrato social bajo y 5 (35,7% a uno medio. De los casos positivos para H. pylori, 9 tenían gastritis aguda, 1 gastritis crónica y sólo en 4 la mucosa gástrica era normal. Se observó una clara asociación entre H. pylori y cambios de gastritis.

Immune Responses to "Helicobacter pylori" Infection in Children with Intellectual Disabilities

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Douraghi, Masoumeh; Goudarzi, Hossein; Rostami, Mahmoud Nateghi; Nikmanesh, Bahram

2012-01-01

Infection with "Helicobacter pylori" was assessed through serum "H. pylori" IgG antibody in children with intellectual disabilities (ID). The sero-status of cytotoxin-associated gene A (CagA) was determined as a risk determinant for severe "H. pylori"-associated diseases. In total, 210 children with ID were included…

Detection of Helicobacter pylori CagA and VacA genotypes from ...

African Journals Online (AJOL)

Background: Helicobacter pylori(H. Pylori) is one of the most common pathogens affecting human kind, infecting more than 50% of the world's population. Invasive and non- invasive methods have been used to diagnose H. pylori infection. The polymerase chain reaction (PCR) has been broadly and successfully used to ...

Helicobacter pylori - a seasoned pathogen by any other name

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Ahmed Niyaz

2009-12-01

Full Text Available Abstract Helicobacter pylori is a well known inhabitant of human stomach which is linked to peptic ulcer disease and gastric adenocarcinoma. It was recently shown in several studies that H. pylori can be harnessed as a surrogate marker of human migration and that its population structure and stratification patterns exactly juxtapose to those of Homo sapiens. This is enough a testimony to convey that H. pylori may have coevolved with their host. Several protective effects of H. pylori colonization have been considered as evidence of a presumed symbiotic relationship. Contrary to this assumption is the presence of a strong virulence apparatus within H. pylori; why a co-evolved parasite would try inflicting its host with serious infection and even causing cancer? The answer is perhaps embedded in the evolutionary history of both the bacterium and the host. We discuss a hypothetical scenario wherein H. pylori may have acquired virulence genes from donors within its environment that varied with change in human history and ecology. The H. pylori genomes sequenced to date portray fairly high abundance of such laterally acquired genes which have no assigned functions but could be linked to inflammatory responses or other pathogenic attributes. Therefore, the powerful virulence properties and survival strategies of Helicobacter make it a seasoned pathogen; thus the efforts to portray it as a commensal or a (harmless 'bacterial parasite' need rethinking.

Helicobacter pylori as a potential target for the treatment of central serous chorioretinopathy

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Antonio Marcelo Barbante Casella

2012-09-01

Full Text Available OBJECTIVES: The objective of this study was to evaluate the relationship between the treatment of Helicobacter pylori gastric infection and changes in best-corrected visual acuity and macular detachment in patients with chronic central serous chorioretinopathy. METHODS: Seventeen patients diagnosed with central serous chorioretinopathy were examined for gastric infection with Helicobacter pylori using the urease test and gastric biopsy. Helicobacter pylory-positive patients were treated with the appropriate medication. The response to therapy was monitored by evaluating the best-corrected visual acuity and optical coherence tomography. The data were analyzed using Student's t-test before and after treatment. RESULTS: Fourteen patients (15 eyes aged 30-56 years (mean 43.4 ± 8.3 years were positive for Helicobacter pylori. Most of the positive patients had gastric symptoms (78.5%; one had bilateral central serous chorioretinopathy. The mean baseline best-corrected visual acuity was 20/98 (logMAR = 0.53 ± 0.28. Three months after starting treatment with antibiotics, the serous detachment had resolved in 14 of 15 eyes, but two cases required laser treatment. The follow-up period ranged from 6 to 27 months. The mean final best-corrected visual acuity differed significantly from baseline. CONCLUSION: Our findings suggest that Helicobacter pylori infection may be present in many chronic central serous chorioretinopathy patients and that treatment for the infection may have a favorable effect on the outcome of chronic central serous chorioretinopathy. Due to the possibility of the spontaneous regression of chronic central serous chorioretinopathy and the high prevalence of the infection in the general population, prospective and masked clinical trials are necessary to confirm that treatment for Helicobacter pylori infection may benefit patients with chronic central serous chorioretinopathy.

Prevalence Of Helicobacter pylori In Gastric Biopsies Of Patients ...

African Journals Online (AJOL)

The prevalence of Helicobacter pylori infection as seen at the University of Benin Teaching Hospital (UBTH) Benin City Nigeria was 16% which was significant using the students T-test (P<0.05). Eighty one gastric biopsy specimens received in the microbiology laboratory were cultured on chocolate agar. Of the H. pylori ...

Epidemiology of Helicobacter pylori infection.

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Burucoa, Christophe; Axon, Anthony

2017-09-01

The study of Helicobacter pylori genetic variability brought us interesting data on the history of mankind. Based on multilocus sequence typing and more recently on whole-genome sequencing, paleomicrobiology still attracts the attention of global researchers in relation to its ancestor roots and coexistence with humans. Three studies determining the prevalence of virulence factors illustrates the controversial results obtained since 30 years by studies trying to associate prevalence of different virulence markers and clinical outcomes of H. pylori infection. Three articles analyzed the prevalence and risk of multiple (genetically distinct isolates) and mixed (susceptible and resistant isolates) infections. A number of studies confirm that H. pylori prevalence is falling worldwide especially in the developed world and in children but that the level of infection is higher in certain ethnic minorities and in Migrants. There is little new in identifying the mode of H. pylori transmission though intrafamilial spread appears to be important. There have, however, been some interesting papers on the presence of the organism in food, water, and the oral cavity. © 2017 John Wiley & Sons Ltd.

The presence of Helicobacter pylori in oral cavities of patients with leukoplakia and oral lichen planus

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Magdalena Kazanowska-Dygdała

2016-02-01

Full Text Available ABSTRACT Objective Helicobacter pylori infection is one of the most common bacterial infections in men. This gastrointestinal pathogen is closely related to gastritis, peptic ulcers, and the increased risk of gastric cancer. Numerous studies have indicated oral cavities as possible Helicobacter pylori reservoirs. Helicobacter pylori has been detected both in supragingival and subgingival plaques, and also in saliva. In addition, the relationship between lesions of oral mucosa and the presence of H. pylori has been evaluated and described in some studies. The aim of this study was to assess the presence of Helicobacter pylori DNA in the oral cavity of patients with oral leukoplakia and oral lichen planus. Material and Methods The study included 54 patients with oral leukoplakia, 72 with oral lichen planus lesions, and 40 healthy controls. The presence of Helicobacter pylori in oral cavity samples was analyzed using a single-step Polymerase Chain Reaction (PCR method. All patients underwent a periodontal examination and the following clinical parameters were collected: pocket depth, bleeding, and plaque indexes. The periodontal status was assessed using the Offenbacher classification. Results In most patients, pathological lesions were in typical sites on the buccal mucosa (leukoplakia in 88%, and oral lichen planus in 93% of patients. The DNA of the Helicobacter pylori was present in 20% of patients with leukoplakia and 23% of patients with lichen planus. We did not find the DNA of H. pylori in healthy controls. The periodontal status described by periodontal indices was worse in the investigated group than in the control group. Conclusion These findings suggest that the H. pylori presence in oral cavities may be related with leukoplakia and lichen planus oral lesions.

The presence of Helicobacter pylori in oral cavities of patients with leukoplakia and oral lichen planus.

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Kazanowska-Dygdała, Magdalena; Duś, Irena; Radwan-Oczko, Małgorzata

2016-01-01

Helicobacter pylori infection is one of the most common bacterial infections in men. This gastrointestinal pathogen is closely related to gastritis, peptic ulcers, and the increased risk of gastric cancer. Numerous studies have indicated oral cavities as possible Helicobacter pylori reservoirs. Helicobacter pylori has been detected both in supragingival and subgingival plaques, and also in saliva. In addition, the relationship between lesions of oral mucosa and the presence of H. pylori has been evaluated and described in some studies. The aim of this study was to assess the presence of Helicobacter pylori DNA in the oral cavity of patients with oral leukoplakia and oral lichen planus. The study included 54 patients with oral leukoplakia, 72 with oral lichen planus lesions, and 40 healthy controls. The presence of Helicobacter pylori in oral cavity samples was analyzed using a single-step Polymerase Chain Reaction (PCR) method. All patients underwent a periodontal examination and the following clinical parameters were collected: pocket depth, bleeding, and plaque indexes. The periodontal status was assessed using the Offenbacher classification. In most patients, pathological lesions were in typical sites on the buccal mucosa (leukoplakia in 88%, and oral lichen planus in 93% of patients). The DNA of the Helicobacter pylori was present in 20% of patients with leukoplakia and 23% of patients with lichen planus. We did not find the DNA of H. pylori in healthy controls. The periodontal status described by periodontal indices was worse in the investigated group than in the control group. These findings suggest that the H. pylori presence in oral cavities may be related with leukoplakia and lichen planus oral lesions.

Evaluation of Salivary Antibodies to Detect Infection with Helicobacter pylori

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Mark B Loeb

1997-01-01

Full Text Available Helicobacter pylori infection is an important cause of peptic ulcer disease and chronic gastritis. Infection with this bacterium stimulates the production of immunoglobulin (Ig G antibody. Salivary IgG antibody tests to detect H pylori infection offer a convenient and noninvasive method of diagnosis. To evaluate an IgG salivary antibody kit, saliva was collected from 157 out-patients with dyspepsia referred for endoscopy to a tertiary centre. A salivary IgG ELISA antibody assay was performed using the Helisal Helicobacter pylori (IgG assay kit, and at least four gastric biopsies were obtained. H pylori infection was confirmed by demonstration of the organism on Warthin-Starry silver stain (sensitivity 85%, specificity 55%. The prevalence of infection with H pylori was 30%. When the analysis was redone, excluding those treated with eradication therapy, the results were similar (sensitivity 86%, specificity 58%. The positive predictive value of the assay was 45% and the negative predictive value was 90%. Despite the ease of sampling, the assay used has limited diagnostic utility, lacking the predictive value to indicate which patients referred with dyspeptic symptoms to a tertiary care setting are infected with H pylori.

Rosacea and Helicobacter pylori: links and risks

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Lazaridou E

2017-08-01

Full Text Available Elizabeth Lazaridou,1 Chrysovalantis Korfitis,2 Christina Kemanetzi,1 Elena Sotiriou,1 Zoe Apalla,1 Efstratios Vakirlis,1 Christina Fotiadou,1 Aimilios Lallas,1 Demetrios Ioannides1 1First Department of Dermatology and Venereology, Aristotle University Medical School, Thessaloniki, Greece; 2Department of Dermatology, 401 General Army Hospital, Athens, Greece Abstract: Rosacea is a chronic skin disease characterized by facial erythema and telangiectasia. Despite the fact that many hypotheses have been proposed, its etiology remains unknown. In the present review, the possible link and clinical significance of Helicobacter pylori in the pathogenesis of rosacea are being sought. A PubMed and Google Scholar search was performed using the terms “rosacea”, “H.pylori”, “gastrointestinal disorders and H.pylori”, “microorganisms and rosacea”, “pathogenesis and treatment of rosacea”, and “risk factors of rosacea”, and selected publications were studied and referenced in text. Although a possible pathogenetic link between H. pylori and rosacea is advocated by many authors, evidence is still interpreted differently by others. We conclude that further studies are needed in order to fully elucidate the pathogenesis of rosacea. Keywords: eradication, Helicobacter pylori, pathogenesis, rosacea

Immune Evasion Strategies and Persistence of Helicobacter pylori.

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Mejías-Luque, Raquel; Gerhard, Markus

Helicobacter pylori infection is commonly acquired during childhood, can persist lifelong if not treated, and can cause different gastric pathologies, including chronic gastritis, peptic ulcer disease, and eventually gastric cancer. H. pylori has developed a number of strategies in order to cope with the hostile conditions found in the human stomach as well as successful mechanisms to evade the strong innate and adaptive immune responses elicited upon infection. Thus, by manipulating innate immune receptors and related signaling pathways, inducing tolerogenic dendritic cells and inhibiting effector T cell responses, H. pylori ensures low recognition by the host immune system as well as its persistence in the gastric epithelium. Bacterial virulence factors such as cytotoxin-associated gene A, vacuolating cytotoxin A, or gamma-glutamyltranspeptidase have been extensively studied in the context of bacterial immune escape and persistence. Further, the bacterium possesses other factors that contribute to immune evasion. In this chapter, we discuss in detail the main evasion and persistence strategies evolved by the bacterium as well as the specific bacterial virulence factors involved.

Helicobacter pylori impairs murine dendritic cell responses to infection.

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Ya-Hui Wang

Full Text Available BACKGROUND: Helicobacter pylori, a human pathogen associated with chronic gastritis, peptic ulcer and gastric malignancies, is generally viewed as an extracellular microorganism. Here, we show that H. pylori replicates in murine bone marrow derived-dendritic cells (BMDCs within autophagosomes. METHODOLOGY/PRINCIPAL FINDINGS: A 10-fold increase of CFU is found between 2 h and 6 h p.i. in H. pylori-infected BMDCs. Autophagy is induced around the bacterium and participates at late time points of infection for the clearance of intracellular H. pylori. As a consequence of infection, LC3, LAMP1 and MHC class II molecules are retained within the H. pylori-containing vacuoles and export of MHC class II molecules to cell surface is blocked. However, formalin-fixed H. pylori still maintain this inhibitory activity in BMDC derived from wild type mice, but not in from either TLR4 or TLR2-deficient mice, suggesting the involvement of H. pylori-LPS in this process. TNF-alpha, IL-6 and IL-10 expression was also modulated upon infection showing a TLR2-specific dependent IL-10 secretion. No IL-12 was detected favoring the hypothesis of a down modulation of DC functions during H. pylori infection. Furthermore, antigen-specific T cells proliferation was also impaired upon infection. CONCLUSIONS/SIGNIFICANCE: H. pylori can infect and replicate in BMDCs and thereby affects DC-mediated immune responses. The implication of this new finding is discussed for the biological life cycle of H. pylori in the host.

Helicobacter Pylori Infections

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... the stomach. It is the main cause of peptic ulcers, and it can also cause gastritis and stomach ... inflammation. This can lead to gastritis or a peptic ulcer. Researchers aren't sure how H. pylori spreads. ...

Helicobacter pylori moves through mucus by reducing mucin viscoelasticity

OpenAIRE

Celli, Jonathan P.; Turner, Bradley S.; Afdhal, Nezam H.; Keates, Sarah; Ghiran, Ionita; Kelly, Ciaran P.; Ewoldt, Randy H.; McKinley, Gareth H.; So, Peter; Erramilli, Shyamsunder; Bansil, Rama

2009-01-01

The ulcer-causing gastric pathogen Helicobacter pylori is the only bacterium known to colonize the harsh acidic environment of the human stomach. H. pylori survives in acidic conditions by producing urease, which catalyzes hydrolysis of urea to yield ammonia thus elevating the pH of its environment. However, the manner in which H. pylori is able to swim through the viscoelastic mucus gel that coats the stomach wall remains poorly understood. Previous rheology studies on gastric mucin, the key...

Helicobacter Pylori: Vías de transmisión

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Martín Alonso Bayona Rojas

2017-09-01

Full Text Available La importancia de Helicobacter pylori como agente etiológico en diversas patologías se asocia con una alta tasa de morbimortalidad y genera un fuerte impacto en nuestra sociedad y en los sistemas de salud. En ese sentido, la presente revisión de literatura pretende analizar y comprender la ruta de transmisión de este patógeno con el objeto de prevenir su propagación. El conocimiento de la epidemiología y el modo de transmisión permite prevenir la propagación e identificar poblaciones de alto riesgo, especialmente en áreas que tienen altas tasas de linfoma gástrico, cáncer gástrico y úlcera gástrica. Helicobacter Pylori: Transmission RoutesAbstractThe importance of Helicobacter pylori as an etiological agent in several pathologies is associated with a high rate of morbi mortality, which generates a strong impact in our society and in the health systems. The present literature review sought to analize and understand the route of transmission of this pathogen to prevent its spread. Knowledge of the epidemiology and mode of transmission of this pathogen is important to prevent its spread and be useful in identifying high-risk populations, especially in areas with high rates of gastric lymphoma, gastric cancer, and gastric ulcer

Interaction between Helicobacter pylori and latent toxoplasmosis and demographic variables on cognitive function in young to middle-aged adults.

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Gale, Shawn D; Erickson, Lance D; Brown, Bruce L; Hedges, Dawson W

2015-01-01

Helicobacter pylori and latent toxoplasmosis are widespread diseases that have been associated with cognitive deficits and Alzheimer's disease. We sought to determine whether interactions between Helicobacter pylori and latent toxoplasmosis, age, race-ethnicity, educational attainment, economic status, and general health predict cognitive function in young and middle-aged adults. To do so, we used multivariable regression and multivariate models to analyze data obtained from the United States' National Health and Nutrition Examination Survey from the Centers for Disease Control and Prevention, which can be weighted to represent the US population. In this sample, we found that 31.6 percent of women and 36.2 percent of men of the overall sample had IgG Antibodies against Helicobacter pylori, although the seroprevalence of Helicobacter pylori varied with sociodemographic variables. There were no main effects for Helicobacter pylori or latent toxoplasmosis for any of the cognitive measures in models adjusting for age, sex, race-ethnicity, educational attainment, economic standing, and self-rated health predicting cognitive function. However, interactions between Helicobacter pylori and race-ethnicity, educational attainment, latent toxoplasmosis in the fully adjusted models predicted cognitive function. People seropositive for both Helicobacter pylori and latent toxoplasmosis - both of which appear to be common in the general population - appear to be more susceptible to cognitive deficits than are people seropositive for either Helicobacter pylori and or latent toxoplasmosis alone, suggesting a synergistic effect between these two infectious diseases on cognition in young to middle-aged adults.

Interaction between Helicobacter pylori and latent toxoplasmosis and demographic variables on cognitive function in young to middle-aged adults.

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Shawn D Gale

Full Text Available Helicobacter pylori and latent toxoplasmosis are widespread diseases that have been associated with cognitive deficits and Alzheimer's disease. We sought to determine whether interactions between Helicobacter pylori and latent toxoplasmosis, age, race-ethnicity, educational attainment, economic status, and general health predict cognitive function in young and middle-aged adults. To do so, we used multivariable regression and multivariate models to analyze data obtained from the United States' National Health and Nutrition Examination Survey from the Centers for Disease Control and Prevention, which can be weighted to represent the US population. In this sample, we found that 31.6 percent of women and 36.2 percent of men of the overall sample had IgG Antibodies against Helicobacter pylori, although the seroprevalence of Helicobacter pylori varied with sociodemographic variables. There were no main effects for Helicobacter pylori or latent toxoplasmosis for any of the cognitive measures in models adjusting for age, sex, race-ethnicity, educational attainment, economic standing, and self-rated health predicting cognitive function. However, interactions between Helicobacter pylori and race-ethnicity, educational attainment, latent toxoplasmosis in the fully adjusted models predicted cognitive function. People seropositive for both Helicobacter pylori and latent toxoplasmosis - both of which appear to be common in the general population - appear to be more susceptible to cognitive deficits than are people seropositive for either Helicobacter pylori and or latent toxoplasmosis alone, suggesting a synergistic effect between these two infectious diseases on cognition in young to middle-aged adults.

14C-urea breath test for the detection of Helicobacter pylori

International Nuclear Information System (INIS)

Veldhuyzen van Zanten, S.J.; Tytgat, K.M.; Hollingsworth, J.; Jalali, S.; Rshid, F.A.; Bowen, B.M.; Goldie, J.; Goodacre, R.L.; Riddell, R.H.; Hunt, R.H.

1990-01-01

The high urease activity of Helicobacter pylori can be used to detect this bacterium by noninvasive breath tests. We have developed a 14 C-urea breath test which uses 5 microCi 14 C with 50 mg nonradioactive urea. Breath samples are collected at baseline and every 30 min for 2 h. Our study compared the outcome of the breath test to the results of histology and culture of endoscopically obtained gastric biopsies in 84 patients. The breath test discriminated well between the 50 positive patients and the 34 patients negative for Helicobacter pylori: the calculated sensitivity was 100%, specificity 88%, positive predictive value 93%, and negative predictive value 100%. Treatment with bismuth subsalicylate and/or ampicillin resulted in lower counts of exhaled 14 CO 2 which correlated with histological improvement in gastritis. The 14 C-urea breath test is a better gold standard for the detection of Helicobacter pylori than histology and/or culture

Association between Helicobacter pylori seropositivity and Hepatic Encephalopathy

International Nuclear Information System (INIS)

Behroozian, R.; Faramarzpur, M.; Rahimi, E.

2010-01-01

Objective: The knowledge on Helicobacter pylori (H. pylori) contribution in the pathology of the liver and biliary tract diseases in human is very limited. The aim of this study was to assess the probable association between H. pylori seropositivity and hepatic encephalopathy. Methodology: This is a case control study conducted through three groups, cirrhotics with hepatic encephalopathy (HE), cirrhotics without HE and healthy controls. All subjects were examined serologically for determination of IgG class antibodies to H. pylori based on ELISA technique. Results: H. pylori seropositivity was present in 88% cirrhotic patients with hepatic encephalopathy, 86% cirrhotics without hepatic encephalopathy and 66% healthy controls. Conclusion: According to our results, H. pylori seropositivity rate in cirrhotic patients with or without hepatic encephalopathy was higher than healthy controls. But H. pylori seropositivity rate was not significantly different among cirrhotics with hepatic encephalopathy and those without it.

SRS-sensor 13C/12C isotops measurements for detecting Helicobacter Pylori

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Grishkanich, Aleksandr; Chubchenko, Yan; Elizarov, Valentin; Zhevlakov, Aleksandr; Konopelko, Leonid

2018-02-01

We developed SRS-sensor 13C/12C isotops measurements detecting Helicobacter Pylori for medical diagnostics of human health. Measuring of absolute 13C/12C isotope amount ratios allows to explore the topical problems of the modern world, alcoholic beverages and tobacco, medical diagnostics of human health. SRS method is used to measure the ratio of carbon isotopes in the exhaled carbon dioxide, which is used to diagnose the human infection of Helicobacter pylori and the influence of the Helicobacter pylori bacterium on the occurrence of gastritis, gastric and duodenal ulcers. A method for the analysis of human infection with Helicobacter pylori was developed on the basis of measurements of the ratio of 13C / 12C carbon isotopes in human exhaled air with a high level of measurement accuracy. The article reviews the work in the field of provision comparability of absolute 13C/12C isotope amount ratios in the environment and food. The analysis of the technical and metrological characteristics of traditional and perspective instruments for measuring isotope ratios is presented. The provision of comparability of absolute 13C/12C isotope amount ratios is carried by gravimetrically prepared reference standards. The key features and emerging issues are discussed.

Functional dyspepsia and dyspepsia associated with Helicobacter pylori infection: Do they have different clinical characteristics?

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J.L. Rodríguez-García

2016-07-01

Conclusions: The patients with dyspepsia infected with Helicobacter pylori had similar clinical characteristics to the non-infected patients and could not be differentiated a priori. The prevalence of Helicobacter pylori infection in patients with functional dyspepsia was 58% and increased with age.

Anti-Bacterial Properties of Herbs against Helicobacter Pylori Infection: A Review

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Hedieh Yousef-Nezhad

2017-09-01

Full Text Available Helicobacter pylori is a gram-negative bacterium that lives in human stomach. This bacterium is the most important cause of chronic gastritis, peptic and duodenal ulcers and gastric cancer. The therapies include the use of antibiotics and a proton pump inhibitor, but unfortunately, these therapeutic methods are not always responsive due to resistance to antibiotics. In recent years, use of alternative treatment, including medicinal herbs was shown to have anti-H. Pylori properties. So, in this review, anti-H. Pylori features of herbals were investigated including ginger, garlic, cranberry, curcumin, green tea and broccoli sprouts derived through the search in Google Scholar search engine, and PubMed scientific database using English keywords such as Helicobacter pylori, anti-H. pylori, ginger, garlic, cranberry, curcumin, broccoli and green tea, between 1984 -2016. Results showed that ginger, garlic, cranberry, curcumin, broccoli and green tea have antibacterial, antioxidant and anti-inflammatory potential properties, and because of their role in protecting the stomach against H. pylori infection, it seems, they can be an appropriate treatment option for patients with this infection.

Helicobacter pylori infection and nonmalignant diseases.

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Sjomina, Olga; Heluwaert, Frederic; Moussata, Driffa; Leja, Marcis

2017-09-01

A substantial decrease in Helicobacter pylori-associated peptic ulcer disease has been observed during the last decades. Drug-related ulcers as well as idiopathic ulcers are becoming predominant and are more refractory to treatment; however, H. pylori infection still plays an important role in ulcer bleeding and recurrence after therapy. The effect of H. pylori eradication upon functional dyspepsia symptoms has been reviewed in this article and generally confirms the results of previous meta-analyses. Additional evidence suggests a lack of impact upon the quality of life, in spite of improvement in symptoms. The association of H. pylori with gastroesophageal reflux disease and Barrett's esophagus remains controversial with a majority of published studies showing a negative association. Furthermore, a strong inverse relationship between the presence of H. pylori and the esophageal eosinophilia was also reported. Several studies and a review addressed the role of H. pylori in autoimmune gastritis and pernicious anemia. The association of the above still remains controversial. Finally, the necessity of routine endoscopy and H. pylori eradication before bariatric surgery is discussed. Several studies suggest the rationale of preoperative upper endoscopy and H. pylori eradication prior to surgery. However, the prevalence of H. pylori infection prior to surgery in these studies generally reflects the overall prevalence of the infection in the particular geographic area. In addition, results on the role of H. pylori in developing postoperative complications remain controversial. © 2017 John Wiley & Sons Ltd.

Oxidative Stress Resulting From Helicobacter pylori Infection Contributes to Gastric CarcinogenesisSummary

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Lindsay D. Butcher

2017-05-01

Full Text Available Helicobacter pylori is a gram-negative, microaerophilic bacterium that infects the stomach and can lead to, among other disorders, the development of gastric cancer. The inability of the host to clear the infection results in a chronic inflammatory state with continued oxidative stress within the tissue. Reactive oxygen species and reactive nitrogen species produced by the immune and epithelial cells damage the host cells and can result in DNA damage. H pylori has evolved to evoke this damaging response while blunting the host’s efforts to kill the bacteria. This long-lasting state with inflammation and oxidative stress can result in gastric carcinogenesis. Continued efforts to better understand the bacterium and the host response will serve to prevent or provide improved early diagnosis and treatment of gastric cancer. Keywords: AP Endonuclease, DNA Damage, H pylori, Gastric Cancer, Oxidative Stress

Helicobacter pylori infection in children.

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Kalach, Nicolas; Bontems, Patrick; Raymond, Josette

2017-09-01

Helicobacter pylori infection in children differs from that in adults, from the point of view of epidemiology, host response, clinical features, related diseases, and diagnosis, as well as treatment strategies. The prevalence of H. pylori infection, in both children and adults, is decreasing in the Western World as well as in some developing countries, which contrasts with the increase in childhood asthma and allergic diseases. Recurrent abdominal pain is not specific during H. pylori infection in children. The role of H. pylori infection and failure to thrive, children's growth, type I diabetes mellitus (T1DM) and celiac disease remains controversial. The main initial diagnosis is based on upper digestive endoscopy with biopsy-based methods. Nodular gastritis may be a pathognomonic endoscopic finding of childhood H. pylori infection. The infection eradication control is based on validated noninvasive tests. The main cause of treatment failure of H. pylori infection is its clarithromycin resistance. We recommend standard antibiotic susceptibility testing of H. pylori in pediatric patients prior to the initiation of eradication therapy. H. pylori treatment in children should be based on an evaluation of the rate of eradication in the local population, a systematic use of a treatment adapted to the susceptibility profile and a treatment compliance greater than 90%. The last meta-analysis in children did not show an advantage for sequential therapy when compared to a 14-day triple therapy. Finally, the high rate of antibiotic resistance responsible for therapy failure in recent years justifies the necessity of a novel vaccine to prevent H. pylori infection in children. © 2017 John Wiley & Sons Ltd.

Helicobacter pylori-Induced HB-EGF Upregulates Gastrin Expression via the EGF Receptor, C-Raf, Mek1, and Erk2 in the MAPK Pathway

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Niluka Gunawardhana

2018-01-01

Full Text Available Helicobacter pylori is associated with hypergastrinemia, which has been linked to the development of gastric diseases. Although the molecular mechanism is not fully understood, H. pylori is known to modulate the Erk pathway for induction of gastrin expression. Herein we found that an epidermal growth factor (EGF receptor kinase inhibitor significantly blocked H. pylori-induced gastrin promoter activity, suggesting involvement of EGF receptor ligands. Indeed, H. pylori induced mRNA expression of EGF family members such as amphiregulin, EGF, heparin-binding EGF-like growth factor (HB-EGF, and transforming growth factor-α. Of these, specific siRNA targeting of HB-EGF significantly blocked H. pylori-induced gastrin expression. Moreover, H. pylori induced HB-EGF ectodomain shedding, which we found to be a critical process for H. pylori-induced gastrin expression. Thus, we demonstrate a novel role for human mature HB-EGF in stimulating gastrin promoter activity during H. pylori infection. Further investigation using specific siRNAs targeting each isoform of Raf, Mek, and Erk elucidated that the mechanism underlying H. pylori-induced gastrin expression can be delineated as the sequential activation of HB-EGF, the EGF receptor, C-Raf, Mek1, and the Erk2 molecules in the MAPK pathway. Surprisingly, whereas Erk2 acts as a potent activator of gastrin expression, siRNA knockdown of Erk1 induced gastrin promoter activity, suggesting that Erk1 typically acts as a repressor of gastrin expression. Elucidation of the mechanism of gastrin modulation by HB-EGF-mediated EGF receptor transactivation should facilitate the development of therapeutic strategies against H. pylori-related hypergastrinemia and consequently gastric disease development, including gastric cancers.

Helicobacter pylori-Induced HB-EGF Upregulates Gastrin Expression via the EGF Receptor, C-Raf, Mek1, and Erk2 in the MAPK Pathway.

Science.gov (United States)

Gunawardhana, Niluka; Jang, Sungil; Choi, Yun Hui; Hong, Youngmin A; Jeon, Yeong-Eui; Kim, Aeryun; Su, Hanfu; Kim, Ji-Hye; Yoo, Yun-Jung; Merrell, D Scott; Kim, Jinmoon; Cha, Jeong-Heon

2017-01-01

Helicobacter pylori is associated with hypergastrinemia, which has been linked to the development of gastric diseases. Although the molecular mechanism is not fully understood, H. pylori is known to modulate the Erk pathway for induction of gastrin expression. Herein we found that an epidermal growth factor (EGF) receptor kinase inhibitor significantly blocked H. pylori -induced gastrin promoter activity, suggesting involvement of EGF receptor ligands. Indeed, H. pylori induced mRNA expression of EGF family members such as amphiregulin, EGF, heparin-binding EGF-like growth factor (HB-EGF), and transforming growth factor-α. Of these, specific siRNA targeting of HB-EGF significantly blocked H. pylori -induced gastrin expression. Moreover, H. pylori induced HB-EGF ectodomain shedding, which we found to be a critical process for H. pylori -induced gastrin expression. Thus, we demonstrate a novel role for human mature HB-EGF in stimulating gastrin promoter activity during H. pylori infection. Further investigation using specific siRNAs targeting each isoform of Raf, Mek, and Erk elucidated that the mechanism underlying H. pylori -induced gastrin expression can be delineated as the sequential activation of HB-EGF, the EGF receptor, C-Raf, Mek1, and the Erk2 molecules in the MAPK pathway. Surprisingly, whereas Erk2 acts as a potent activator of gastrin expression, siRNA knockdown of Erk1 induced gastrin promoter activity, suggesting that Erk1 typically acts as a repressor of gastrin expression. Elucidation of the mechanism of gastrin modulation by HB-EGF-mediated EGF receptor transactivation should facilitate the development of therapeutic strategies against H. pylori -related hypergastrinemia and consequently gastric disease development, including gastric cancers.

Genotyping of vacA alleles of Helicobacter pylori strains recovered ...

African Journals Online (AJOL)

Genotyping of vacA alleles of Helicobacter pylori strains recovered from some Iranian food items. ... Tropical Journal of Pharmaceutical Research ... Conclusion: The presence of similar genotypes in H. pylori strains of foods and those of human clinical samples suggest that contaminated foods may be the source of bacteria ...

Helicobacter pylori in gastroduodenal perforation

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Bharat B Dogra

2014-01-01

Full Text Available Background:peptic ulcers were earlier believed to be caused by dietary factors, gastric acid, and stress. However, in 1983, Warren and Marshall identified the correlation between Helicobacter pylori (H. pylori and peptic ulcers. It is now well established that most of the peptic ulcers occur as a result of H. pylori infection. But the co-relation between perforated peptic ulcer and H. pylori infection is not yet fully established. Aims and objectives : to study the prevalence of H. pylori infection in patients with perforated peptic ulcer. Materials and methods: this was a prospective study carried out in all cases of perforated peptic ulcer reporting in surgical wards of a medical college during 2008-2010. A total of 50 cases, presenting as acute perforation of duodenum and stomach during this period, formed the study group. After resuscitation, all the cases were subjected to emergency exploratory laparotomy. The exact site of perforation was identified, biopsy was taken from the ulcer margin from 2-3 sites and the tissue was sent for H. pylori culture and histopathological examination. Simple closure of perforation, omentoplasty, thorough peritoneal lavage and drainage was carried out. Results: out of the 50 cases of perforated peptic ulcer, 38 happened to be males, and only 12 were females. The age of the patients ranged from 20 to 70 years. All the patients underwent only emergency laparotomy. As many as 46 cases (92% turned out to be positive for H. pylori and only four cases (8% were negative for this infection. Postoperatively, patients who were found to be positive for H. pylori were put on anti-H. pylori treatment. Conclusion: there was a high prevalence of H. pylori infection in patients with perforated gastroduodenal ulcers.

Helicobacter pylori: From Infection to Cure

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ABR Thomson

1996-01-01

Full Text Available Over 380 abstracts, presentations and posters of recent advances were highlighted at the European and International Helicobacter pylori meeting held July 7 to 9, 1995 in Edinburgh, Scotland. New advances abound, with major interest focusing on the simple, safe, inexpensive new `gold standard’ for H pylori eradication therapy: a single week of tid omeprazole 20 mg, metronidazole 400 mg and clarithromycin 250 mg, or omeprazole 20 mg, amoxicillin 1000 mg and clarithromycin 500 mg. To avoid false negative results, two biopsies must be taken from the antrum and two from the gastric body at least four weeks after completion of eradication therapy, and ideally should be supplemented with at least one further H pylori test such as a biopsy for urease activity or culture, or a urea breath test. While most patients with a gastric or duodenal ulcer (DU who do not consume nonsteroidal anti-inflammatory drugs are infected with H pylori, the association is much less apparent in those with a DU who present with an upper gastrointestinal hemorrhage. H pylori eradication for nonulcer dyspepsia is not widely recommended, and the patient with a DU given effective H pylori eradication who presents with dyspepsia likely has erosive esophagitis rather than recurrent DU or H pylori. Gastroenterologists are at increased risk of H pylori infection, particularly older gastroenterologists who are very busy endoscopists.

Sero-prevalence and associated factors of Helicobacter pylori ...

African Journals Online (AJOL)

Department of Internal medicine, Weill Bugando School of Medicine, P.O.Box 1464, Mwanza, Tanzania. 2. Department of .... Data was entered in the computer using excel software ..... study of Helicobacter pylori infection in Mexico. Journal.

Helicobacter pylori Type IV Secretion System and Its Adhesin Subunit, CagL, Mediate Potent Inflammatory Responses in Primary Human Endothelial Cells

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Mona Tafreshi

2018-02-01

Full Text Available The Gram-negative bacterium, Helicobacter pylori, causes chronic gastritis, peptic ulcers, and gastric cancer in humans. Although the gastric epithelium is the primary site of H. pylori colonization, H. pylori can gain access to deeper tissues. Concurring with this notion, H. pylori has been found in the vicinity of endothelial cells in gastric submucosa. Endothelial cells play crucial roles in innate immune response, wound healing and tumorigenesis. This study examines the molecular mechanisms by which H. pylori interacts with and triggers inflammatory responses in endothelial cells. We observed that H. pylori infection of primary human endothelial cells stimulated secretion of the key inflammatory cytokines, interleukin-6 (IL-6 and interleukin-8 (IL-8. In particular, IL-8, a potent chemokine and angiogenic factor, was secreted by H. pylori-infected endothelial cells to levels ~10- to 20-fold higher than that typically observed in H. pylori-infected gastric epithelial cells. These inflammatory responses were triggered by the H. pylori type IV secretion system (T4SS and the T4SS-associated adhesin CagL, but not the translocation substrate CagA. Moreover, in contrast to integrin α5β1 playing an essential role in IL-8 induction by H. pylori upon infection of gastric epithelial cells, both integrin α5β1 and integrin αvβ3 were dispensable for IL-8 induction in H. pylori-infected endothelial cells. However, epidermal growth factor receptor (EGFR is crucial for mediating the potent H. pylori-induced IL-8 response in endothelial cells. This study reveals a novel mechanism by which the H. pylori T4SS and its adhesin subunit, CagL, may contribute to H. pylori pathogenesis by stimulating the endothelial innate immune responses, while highlighting EGFR as a potential therapeutic target for controlling H. pylori-induced inflammation.

Invasive Tests for Helicobacter Pylori in Children

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Hien Q Huynh

2005-01-01

Full Text Available One of the primary indications for upper gastrointestinal (GI endoscopy in children is the presence of persistent and severe upper abdominal symptoms. Upper GI endoscopies are performed to allow the physician to confirm or rule out upper GI pathology. Additionally, upper GI endoscopies with mucosal biopsies are the gold standard for the diagnosis of Helicobacter pylori infection and its complications in children. The gastric biopsies can be used for the rapid urease test, histological examination and bacterial culture to determine antibiotic sensitivity. DNA extracted in these biopsies can also be subjected to genotyping using molecular methods to determine the presence of H pylori infection, antibiotic resistance mutations and H pylori virulence factors.

Helicobacter pylori virulence factors in development of gastric carcinoma.

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Wang, Ming-Yi; Liu, Xiao-Fei; Gao, Xiao-Zhong

2015-01-01

Helicobacter pylori plays a vital role in the pathogenesis of gastric carcinoma. However, only a relatively small proportion of individuals infected with H. pylori develop gastric carcinoma. Differences in the incidence of gastric carcinoma among infected individuals can be explained, at least partly, by the different genotypes of H. pylori virulence factors. Thus far, many virulence factors of H. pylori, such as Cag PAI, VacA, OMPs and DupA, have been reported to be involved in the development of gastric cancer. The risk of developing gastric cancer during H. pylori infection is affected by specific host-microbe interactions that are independent of H. pylori virulence factors. In this review, we discuss virulence factors of H. pylori and their role in the development of gastric carcinoma that will provide further understanding of the biological interactions of H. pylori with the host.

Anti-ulcer and anti-Helicobacter pylori potentials of the ethyl acetate fraction of Physalis alkekengi L. var. franchetii (Solanaceae) in rodent.

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Wang, Yong; Wang, Sui Lou; Zhang, Jiong Yi; Song, Xiao Ning; Zhang, Zhi Yong; Li, Jing Feng; Li, Song

2018-01-30

Physalis alkekengi L. var. franchetii (Solanaceae) has been widely used in Chinese folk medicine due to its wide distribution throughout the country, for the treatment of a wide range of diseases including heat and cold, sore throat, fever, fungal infection, inflammation, toothache, rheumatism, burn, analgesic, ulcer and urinary diseases. However, the effect of P. alkekengi var. franchetii on ulcer and Helicobacter pylori infection has not been reported to date. This study was designed to investigate the anti-inflammatory, anti-ulcer, anti-Helicobacter pylori and analgesic properties of ethyl acetate fraction of the crude aqueous methanolic extract from the aerial parts of the plant P. alkekengi L. var. franchetii in rodents. Acute toxicity of the crude extract of P. alkekengi L. var. franchetii (PAF) was evaluated in rats. The petroleum ether fraction (PEF), butanol fraction (BF), ethyl acetate fraction (EAF) and aqueous fraction (AF) of crude aqueous methanolic extract from PAF were screened for anti-inflammatory and anti-ulcer potential at doses of 100, 250 and 500mg/kg (p.o.), using carrageenin-induced hind paw edema and ethanol-induced gastric lesions test in rats. In vitro anti-Helicobacter pylori activity of EAF was assayed subsequently. In addition, three doses of EAF were evaluated for analgesic activity using hot plate and writhing tests, respectively. Finally, we performed a phytochemical analysis of EAF. Four fractions of crude extract from PAF significantly reduced the paw volume in carrageenin-induced hind paw edema model at different doses (100, 250 and 500mg/kg, p.o.). The fraction EAF at a dose of 500mg/kg exhibited the highest (75.92%) (0.150 ± 0.045***, ***p < 0.001) anti-inflammatory potential, which is similar to indomethacin (***P < 0.001)（0.120 ± 0.014***, 80.74% inhibition of inflammation） at 5mg/kg. Pretreatment with EAF (500mg/kg, p.o.) significantly reduced the intensity of gastric mucosal damage and showed higher gastroprotective

ANTIMICROBIAL ACTIVITY OF GYMNOSPERMA GLUTINOSUM (SPRENG.) LESS. (ASTERACEAE) METHANOL EXTRACTS AGAINST HELICOBACTER PYLORI

OpenAIRE

Gomez-Flores, Ricardo; Espinosa-Ramos, David; Quintanilla-Licea, Ramiro; Barr?n-Gonzalez, Mar?a Porfiria; Tamez-Guerra, Patricia; Tamez-Guerra, Reyes; Rodriguez-Padilla, Cristina

2016-01-01

Background: Prolonged use of antibiotics may lead to the selection of drug-resistant bacteria; as a result, efforts are being made to identify new and effective antimicrobial agents, particularly, from medicinal plants, against bacterial infections. Antimicrobial activity of Gymnosperma glutinosum against Helicobacter pylori has not yet been reported. Materials and methods: The antibacterial in vitro effect of Gymnosperma glutinosum methanol leaf extracts against Helicobacter pylori (ATCC 435...

Helicobacter Pylori Seropostivity of Colon Cancer

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F. Tugba Kos

2014-03-01

Full Text Available Aim: Until now many researches have showed that Helicobacter pylori infection may be etiological factor of colorectal cancer. The aim of current study was to investigate the frequency of H.pylori infection seropositivity of colorectal cancer patients and compare the clinicopathological features of H.pylori positive patients with negative ones. Material and Method: Seventy four colorectal patients were included in study. Retrospectively, patients clinical features, surgery history and pathological characteristics were screened. Patients group serum samples were collected. H.pylori Ig G level were quantitatively measured with ELISA method and levels above 5 arbU/ml were accepted as seropositive. Results: Patients median age was 60.5 ( range 26-83 and 56.8% (n=42 were male. H.pylori Ig G was positive in 37.8% (n=28 and negative in 62.2% (n=46 of patient group. H.pylori serpositive and negative patients median age of diagnosis were 56 and 64 respectively (p=0.01. There were no significant difference between H.pylori seropositive group when compared with negative group according to age, level of CEA and Ca 19-9, stage, lymph node involvement, perineural and vascular invasion, presence of polyps, differantion, localisation of tumours. Discussion: H.pylori seropositive patients were diagnosed at younger age. Association of this finding with etiology was confusing. Further studies with healthy controls may provide detailed information about whether H.pylori seropositivity is associated with colorectal cancer etiology.

Chemokines and antimicrobial peptides have a cag-dependent early response to Helicobacter pylori infection in primary human gastric epithelial cells.

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Mustapha, Pascale; Paris, Isabelle; Garcia, Magali; Tran, Cong Tri; Cremniter, Julie; Garnier, Martine; Faure, Jean-Pierre; Barthes, Thierry; Boneca, Ivo G; Morel, Franck; Lecron, Jean-Claude; Burucoa, Christophe; Bodet, Charles

2014-07-01

Helicobacter pylori infection systematically causes chronic gastric inflammation that can persist asymptomatically or evolve toward more severe gastroduodenal pathologies, such as ulcer, mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric cancer. The cag pathogenicity island (cag PAI) of H. pylori allows translocation of the virulence protein CagA and fragments of peptidoglycan into host cells, thereby inducing production of chemokines, cytokines, and antimicrobial peptides. In order to characterize the inflammatory response to H. pylori, a new experimental protocol for isolating and culturing primary human gastric epithelial cells was established using pieces of stomach from patients who had undergone sleeve gastrectomy. Isolated cells expressed markers indicating that they were mucin-secreting epithelial cells. Challenge of primary epithelial cells with H. pylori B128 underscored early dose-dependent induction of expression of mRNAs of the inflammatory mediators CXCL1 to -3, CXCL5, CXCL8, CCL20, BD2, and tumor necrosis factor alpha (TNF-α). In AGS cells, significant expression of only CXCL5 and CXCL8 was observed following infection, suggesting that these cells were less reactive than primary epithelial cells. Infection of both cellular models with H. pylori B128ΔcagM, a cag PAI mutant, resulted in weak inflammatory-mediator mRNA induction. At 24 h after infection of primary epithelial cells with H. pylori, inflammatory-mediator production was largely due to cag PAI substrate-independent virulence factors. Thus, H. pylori cag PAI substrate appears to be involved in eliciting an epithelial response during the early phases of infection. Afterwards, other virulence factors of the bacterium take over in development of the inflammatory response. Using a relevant cellular model, this study provides new information on the modulation of inflammation during H. pylori infection. Copyright © 2014, American Society for Microbiology. All Rights Reserved.

Treatment of Helicobacter pylori infection favourably affects gastric mucosal superoxide dismutases

NARCIS (Netherlands)

Götz, J. M.; Thio, J. L.; Verspaget, H. W.; Offerhaus, G. J.; Biemond, I.; Lamers, C. B.; Veenendaal, R. A.

1997-01-01

Excessive production of reactive oxygen metabolites (ROMs) by phagocytic cells is thought to contribute to the mucosal pathology of Helicobacter pylori infection. Previously, H pylori infection was shown to have a differential effect on some gastric mucosal scavenger enzymes of ROMs-namely,

Fisiopatología molecular en la infección por Helicobacter pylori

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Franklin Torres Jiménez

2016-01-01

Full Text Available La infección por Helicobacter pylori es el proceso de colonización bacteriana más común a nivel mundial. En 1994 la Agencia Internacional para la Investigación en Cáncer ( IARC catalogó al Helicobacter Pylori como un carcinógeno tipo I. La infección por esta bacteria incrementa el riesgo de padecer cáncer gástrico hasta 6 veces más que los individuos que no presentan la infección. Colombia tiene una prevalencia de infección por Helicobacter pylori del 86 % en adultos mayores de 20 años y del 80% en niños mayores de 8 años. La infección persistente y recidivante de la mucosa gástrica puede generar una respuesta inflamatoria, o procesos silentes, que en el peor de los casos puede progresar a un adenocarcinoma gástrico tipo difuso o intestinal. Existen múltiples factores que influyen en las consecuencias clínicas de la infección por Helicobacter pylori: en mención: predisposición genética del huésped, inmunorregulación genética del paciente infectado, factores ambientales y heterogeneidad de los factores de virulencia de las diversas cepas. Por lo anterior se infiere que las patolo - gías gástricas, en especial la gastritis y el adenocarcinoma, son padecimientos de etiología multifactorial que pueden originarse por diversas causas o condiciones. En esta revisión se analizarán los principales aspectos relacionados con la fisiopatología molecular en la infección por Helicobacter pylori , en particular tópicos correspondientes a los factores de virulencia.

H. Pylori Positivity and Various Pathological, Endoscopic and Clinical Features Correlated with Each Other

International Nuclear Information System (INIS)

Coskun, A.; Yukselen, V.; Yasa, M. H.; Karaoglu, A. O.; Meteoglu, I.; Ergin, F.; Kadikoylu, G.

2015-01-01

Objective: To investigate the relationship between dyspepsia symptom scores and endoscopic appearances, and histopathological findings and helicobacter pylori positivity in patients having dyspepsia symptom. Methods: The study was conducted at the gastroenterology outpatient clinic of Adnan Menderes University, School of Medicine, Aydin, Turkey from April 2012 to July 2012 and comprised patients between 18-65 years of age who were admitted with dyspepsia. Glasgow dyspepsia severity scoring was done with questions posed orally to the patients. In histopathological evaluation of biopsy specimens according to Sydney criteria, chronic inflammation, activity, atrophy, intestinal metaplasia and helicobacter pylori parameters were used. Total number of eosinophils and number of mast cells were recorded. Results: Of the 60 patients with dyspepsia, 38(63.3 percent) were female and 22(36.7 percent) were male. The degree of activation and severity of inflammation increased significantly with increasing helicobacter pylori positivity(r=0.459'p<0.0001; r=0.475'p<0.0001). A significant relationship was found between inflammation, activation and the number of mast cells (p<0.05).There was no relationship between helicobacter pylori intensity and the eosinophil count (r=0.171; p=0.093). There was also a statistically significant correlation between severity of inflammation and activation and the number of eosinophils (r=0.313;p=0.002;r=0.245;p=0.016). Conclusion: Mast cell density was seen to have a role in the inflammatory processes of helicobacter pylori infection. (author)

CCR2 mediates Helicobacter pylori-induced immune tolerance and contributes to mucosal homeostasis.

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Sun, Xia; Zhang, Min; El-Zaatari, Mohamad; Huffnagle, Gray B; Kao, John Y

2017-04-01

We previously demonstrated that H. pylori infection leads to increased induction of regulatory T cells in local and systemic immune compartments. Here, we investigate the role of CCR2 in the tolerogenic programing of dendritic cells in a mouse model of H. pylori infection. CCR2 deficient (CCR2KO) mice and wild-type (Wt) mice infected with H. pylori SS1 strain were analyzed by qPCR and FACS analysis. In vitro, bone marrow-derived DC on day 6 from CCR2KO and Wt mice cocultured with or without H. pylori were examined to determine the impact of CCR2 signaling on dendritic cells function by qPCR, ELISA, and FACS analyses. Acute H. pylori infection was associated with a threefold increase in CCR2 mRNA expression in the gastric mucosa. H. pylori-infected CCR2KO mice exhibited a higher degree of mucosal inflammation, that is, increased gastritis scores and pro-inflammatory cytokine mRNA levels, but lower degree of H. pylori gastric colonization compared to infected Wt mice. Peripheral H. pylori-specific immune response measured in the CCR2KO spleen was characterized by a higher Th17 response and a lower Treg response. In vitro, CCR2KO bone marrow-derived DC was less mature and shown a lower Treg/Th17 ratio. Moreover, blockade of CCR2 signaling by MCP-1 neutralizing antibody inhibited H. pylori-stimulated bone marrow-derived DC maturation. Our results indicate that CCR2 plays an essential role in H. pylori-induced immune tolerance and shed light on a novel mechanism of CCR2-dependent DC Treg induction, which appears to be important in maintaining mucosal homeostasis during H. pylori infection. © 2016 John Wiley & Sons Ltd.

Effects of prolonged chlorine exposures upon PCR detection of Helicobacter pylori DNA.

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The effect of low doses of free chlorine on the detection by qPCR of Helicobacter pylori (H. pylori) cells by qPCR in tap water was monitored. H. pylori target sequences (within suspended, intact cells at densities of 102 to 103 cells /ml) were rendered undetectable by qPCR an...

Clinical characteristics of Helicobacter pylori-negative drug-negative peptic ulcer bleeding.

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Chung, Woo Chul; Jeon, Eun Jung; Kim, Dae Bum; Sung, Hea Jung; Kim, Yeon-Ji; Lim, Eun Sun; Kim, Min-Ah; Oh, Jung Hwan

2015-07-28

To investigate the clinical characteristics and outcomes of idiopathic Helicobacter pylori (H. pylori)-negative and drug-negative] peptic ulcer bleeding (PUB). A consecutive series of patients who experienced PUB between 2006 and 2012 was retrospectively analyzed. A total of 232 patients were enrolled in this study. The patients were divided into four groups according to the etiologies of PUB: idiopathic, H. pylori-associated, drug-induced and combined (H. pylori-associated and drug-induced) types. We compared the clinical characteristics and outcomes between the groups. When the silver stain or rapid urease tests were H. pylori-negative, we obtained an additional biopsy specimen by endoscopic re-examination and performed an H. pylori antibody test 6-8 wk after the initial endoscopic examination. For a diagnosis of idiopathic PUB, a negative result of an H. pylori antibody test was confirmed. In all cases, re-bleeding was confirmed by endoscopic examination. For the risk assessment, the Blatchford and the Rockall scores were calculated for all patients. For PUB, the frequency of H. pylori infection was 59.5% (138/232), whereas the frequency of idiopathic cases was 8.6% (20/232). When idiopathic PUB was compared to H. pylori-associated PUB, the idiopathic PUB group showed a higher rate of re-bleeding after initial hemostasis during the hospital stay (30% vs 7.4%, P = 0.02). When idiopathic PUB was compared to drug-induced PUB, the patients in the idiopathic PUB group showed a higher rate of re-bleeding after initial hemostasis upon admission (30% vs 2.7%, P ulcer (77% vs 49%, P < 0.01). However, the Blatchford and the Rockall scores were not significantly different between the two groups. Among the patients who experienced drug-induced PUB, no significant differences were found with respect to clinical characteristics, irrespective of H. pylori infection. Idiopathic PUB has unique clinical characteristics such as re-bleeding after initial hemostasis upon admission

Vitamin B12 status and its association with Helicobacter pylori infection in alcohol dependent patients

NARCIS (Netherlands)

van Oijen, Martijn G. H.; Laheij, Robert J. F.; de Jong, Cor A. J.; Peters, Wilbert H. M.; Jansen, Jan B. M. J.

2004-01-01

Both infection with Helicobacter pylori and alcohol abuse have been associated with low vitamin B12 serum levels. The interaction between both risk factors is unknown. The aim of this study was to determine whether Helicobacter pylori infection is associated with low vitamin B12 levels in alcohol

Serum TNF-α levels and Helicobacter pylori cagA and vacA genes

Science.gov (United States)

Siregar, G. A.; Halim, S.; Sitepu, R. R.; Darmadi

2018-03-01

Helicobacter pylori is associated with higher virulence. TNF-α has an important role in host defense against H. pylori infection. The aim of this study was to investigate the relationship between TNF-α serum levels with cagA and vacA genes in H. pylori infection. This was a cross-sectional study involving 80 patients that consecutively admitted to endoscopy unit. Diagnosis of H. pylori infection was based on rapid urease test. Serum samples werecollected to determine circulating TNF-α level. Polymerase chain reaction was done to examine H. pylori vacA and cagA genes. Data analysis was carriedout using SPSS version 22 with 95%CI and p<0.05 was considered statistically significant. About 45 (56.3%) patients infected with Helicobacter pylori. There were 33 (73.3%) patients with H. pylori cagA positive. Serum TNF-α levels in patients with the H. pylori positive were significantly higher compared to H. pylori negative. Serum level of TNF-α was significantly higher in cagA positive than negative. Subjects with H. pylori cagA gene positive were more likely to have ahigher level of serum TNF-α than H. pylori cagA gene negative.

Treatment of Helicobacter pylori infection 2011.

LENUS (Irish Health Repository)

O'Connor, Anthony

2012-02-01

This article reviews the literature published pertaining to Helicobacter pylori eradication over the last year. The general perception among clinicians and academics engaged in research on H. pylori has been that eradication rates for first-line therapies are falling, although some data published this year have cast doubt on this. The studies published this year have therefore focussed on developing alternative strategies for the first-line eradication of H. pylori. In this regard, clear evidence now exists that both levofloxacin and bismuth are viable options for first-line therapy. The sequential and "concomitant" regimes have also been studied in new settings and may have a role in future algorithms also. In addition, data have emerged that the probiotic Saccharomyces boulardii may be a useful adjunct to antibiotic therapy. Other studies promote individualized therapies based on host polymorphisms, age, and other such demographic factors.

Seroprevalence of Helicobacter pylori in Korea: A multicenter, nationwide study conducted in 2015 and 2016.

Science.gov (United States)

Lee, Jeong Hoon; Choi, Kee Don; Jung, Hwoon-Yong; Baik, Gwang Ho; Park, Jong Kyu; Kim, Sung Soo; Kim, Byung-Wook; Hong, Su Jin; Lim, Hyun; Shin, Cheol Min; Lee, Si Hyung; Jeon, Seong Woo; Kim, Ji Hyun; Choi, Cheol Woong; Jung, Hye-Kyung; Kim, Jie-Hyun; Choi, Suck Chei; Cho, Jin Woong; Lee, Wan Sik; Na, Soo-Young; Sung, Jae Kyu; Song, Kyung Ho; Chung, Jun-Won; Yun, Sung-Cheol

2018-04-01

The Korean College of Helicobacter and Upper Gastrointestinal Research has studied Helicobacter pylori (H. pylori) prevalence since 1998 and found a dynamic change in its prevalence in Korea. The aim of this study was to determine the recent H. pylori prevalence rate and compare it with that of previous studies according to socioeconomic variables. We planned to enroll 4920 asymptomatic Korean adults from 21 centers according to the population distribution of seven geographic areas (Seoul, Gyeonggi, Gangwon, Chungcheong, Kyungsang, Cholla, and Jeju). We centrally collected serum and tested H. pylori serum IgG using a chemiluminescent enzyme immunoassay. We analyzed 4917 samples (4917/4920 = 99.9%) from January 2015 to December 2016. After excluding equivocal serologic results, the H. pylori seropositivity rate was 51.0% (2414/4734). We verified a decrease in H. pylori seroprevalence compared with previous studies performed in 1998, 2005, and 2011 (P pylori seroprevalence rate differed by area: Cholla (59.5%), Chungcheong (59.2%), Kyungsang (55.1%), Jeju (54.4%), Gangwon (49.1%), Seoul (47.4%), and Gyeonggi (44.6%). The rate was higher in those older than 40 years (38.1% in those aged 30-39 years and 57.7% in those aged 40-49 years) and was lower in city residents than in noncity residents at all ages. Helicobacter pylori seroprevalence in Korea is decreasing and may vary according to population characteristics. This trend should be considered to inform H. pylori-related policies. © 2018 The Authors. Helicobacter Published by John Wiley & Sons Ltd.

Role of Helicobacter pylori in stomach cancer after partial gastrectomy for benign ulcer disease Papel del Helicobacter pylori en el cáncer gástrico tras gastrectomía parcial por úlcera benigna

Directory of Open Access Journals (Sweden)

A. Seoane

2005-11-01

Full Text Available Objective: to determine the prevalence of Helicobacter pylori infection in patients having undergone gastrectomy for non-neoplastic disease who later developed gastric stump cancer. Material and methods: retrospective study of all patients with partial gastrectomy for non-malignant peptic disease who were submitted to an endoscopic exploration between 1995 and 2001. A comparison was made of major clinical and histological characteristics, and the presence of Helicobacter pylori among patients with and without gastric cancer in the stomach remnant. Results: a total of 73 patients were studied in this period. Fifteen patients (20.5% had remnant-stump gastric cancer. All but one were adenocarcinomas (71% intestinal and 29% diffuse, respectively. The average time between diagnosis of gastric cancer and previous gastrectomy was 32 (14-48 years. There was a higher detection rate of Helicobacter pylori in patients with cancer in the gastric remnant (100 vs. 81.5%, respectively, p Objetivo: determinar la prevalencia de la infección por Helicobacter pylori en pacientes gastrectomizados por enfermedad no neoplásica, y que han desarrollado posteriormente cáncer gástrico. Material y métodos: estudio retrospectivo con reclutamiento de todos los pacientes con gastrectomía parcial por enfermedad péptica benigna que han sido sometidos a una exploración endoscópica entre 1995-2001. Se ha realizado una comparación de las principales características clínicas e histológicas y de la presencia de Helicobacter pylori en los pacientes con y sin cáncer del remanente gástrico. Resultados: se han estudiado un total de 73 pacientes en este periodo. Se han encontrado 15 pacientes (20,5% con cáncer en el remanente gástrico, 14 adenocarcinomas (71% tipo intestinal y 29% tipo difuso y un linfoma. El tiempo transcurrido entre el diagnóstico de cáncer gástrico y la gastrectomía previa ha sido de 32 (14-48 años. Se ha detectado un alto porcentaje de infecci

The Helicobacter pylori theory and duodenal ulcer disease. A case study of the research process

DEFF Research Database (Denmark)

Christensen, A H; Gjørup, T

1995-01-01

should be selected for H. pylori eradication treatment. CONCLUSION: Descriptive clinical studies and laboratory studies of disease mechanisms were the prevailing types of research about H. pylori. Comparatively few therapeutic intervention studies were done; this fact may have hampered the acceptance......OBJECTIVES: To describe the medical research process from the time of the generation of a new theory to its implementation in clinical practice. The Helicobacter pylori (H. pylori) theory, i.e. the theory that H. pylori plays a significant causal role in duodenal ulcer disease was chosen as a case....... MATERIAL: Abstracts from 1984 to 1993, identified in the CD-Rom, Medline system, ("Silverplatter"), using the search terms Campylobacter pylori and Helicobacter pylori, and reviews and editorials about H. pylori in some of the most widespread clinical journals. RESULTS: 2204 papers on H. pylori were...

Prevalence of Helicobacter pylori in children by noninvasive stool ...

African Journals Online (AJOL)

Prevalence of Helicobacter pylori in children by noninvasive stool Antigen Enzyme Immunoassay. Augustine O. Ebonyi, Emeka Ejeliogu, Stanley T. Odigbo, Martha Omoo Ochoga, Stephen Oguche, Anejo-Okopi A. Joseph ...

Emerging Role of Probiotics in the Management of Helicobacter pylori Infection: Histopathologic Perspectives.

Science.gov (United States)

Emara, Mohamed H; Elhawari, Soha A; Yousef, Salem; Radwan, Mohamed I; Abdel-Aziz, Hesham R

2016-02-01

There is growing evidence from preclinical and clinical studies that emphasizes the efficacy of probiotics in the management of Helicobacter (H) pylori infection; it increased the eradication rate, improved patient clinical manifestations and lowered treatment associated side effects. In this review we documented the potential ability of probiotics to ameliorate H. pylori induced histological features. We searched the available literature for full length articles focusing the role of probiotics on H. pylori induced gastritis from histologic perspectives. Probiotics lowered H. pylori density at the luminal side of epithelium, improved histological inflammatory and activity scores both in the gastric corpus and antrum. This effect persists for long period of time after discontinuation of probiotic supplementation and this is probably through an immune mechanism. The current evidence support the promising role of probiotics in improving H. pylori induced histopathological features both in gastric antrum and corpus and for long periods of time. Because increased density of H. pylori on the gastric mucosa is linked to more severe gastritis and increased incidence of peptic ulcers, we can infer that a reduction of the density might help to decrease the risk of developing pathologies, probably the progression toward atrophic gastritis and gastric adenocarcinoma. These effects together with improving the H. pylori eradication rates and amelioration of treatment related side effects might open the door for probiotics to be added to H. pylori eradication regimens. © 2015 John Wiley & Sons Ltd.

Mechanisms of disease: Helicobacter pylori virulence factors.

Science.gov (United States)

Yamaoka, Yoshio

2010-11-01

Helicobacter pylori plays an essential role in the development of various gastroduodenal diseases; however, only a small proportion of people infected with H. pylori develop these diseases. Some populations that have a high prevalence of H. pylori infection also have a high incidence of gastric cancer (for example, in East Asia), whereas others do not (for example, in Africa and South Asia). Even within East Asia, the incidence of gastric cancer varies (decreasing in the south). H. pylori is a highly heterogeneous bacterium and its virulence varies geographically. Geographic differences in the incidence of gastric cancer can be explained, at least in part, by the presence of different types of H. pylori virulence factor, especially CagA, VacA and OipA. However, it is still unclear why the pathogenicity of H. pylori increased as it migrated from Africa to East Asia during the course of evolution. H. pylori infection is also thought to be involved in the development of duodenal ulcer, which is at the opposite end of the disease spectrum to gastric cancer. This discrepancy can be explained in part by the presence of H. pylori virulence factor DupA. Despite advances in our understanding of the development of H. pylori-related diseases, further work is required to clarify the roles of H. pylori virulence factors.

Development of gastric cancer associated with Helicobacter pylori infection.

Science.gov (United States)

Sugiyama, Toshiro

2004-09-01

Helicobacter pylori infection is associated with histological gastritis, gastric atrophy, gastric cancer and mucosa-associated lymphoid tissue lymphoma in the stomach. However, gastric cancer only develops in a minority of infected individuals. Such clinical diversity is caused by variations in the interactions between H. pylori pathogenicity, host susceptibility, and environmental factors. Based on evidence from three prospective epidemiological studies, the International Agency for Research on Cancer and the World Health Organization (IARC/WHO) concluded in 1994 that H. pylori has a causal linkage to gastric carcinogenesis and is a definite carcinogen in humans. Two large-scale, prospective, epidemiological studies have recently been reported in Japan and have confirmed that H. pylori infection constitutes a high risk factor for the development of gastric cancer, at least in males. In order to obtain evidence that eradication of H. pylori leads to a reduction in the occurrence of gastric cancer, reversibility of precancerous lesions, gastric atrophy or intestinal metaplasia should be proven after eradication treatment. A biopsy specimen from the lesser curvature of the corpus is the most sensitive for evaluating the regression of gastric atrophy on histology, and the evaluation needs be conducted at least 13 months after treatment. In a Mongolian gerbil model with or without low-dose chemical carcinogens, it has been demonstrated that H. pylori can lead to the development of gastric cancer. Experimental studies have elucidated that virulence factors of H. pylori interact with gastric epithelial cell signaling related to carcinogenesis. The cag pathogenicity island (cagPAI) is a major virulence gene cluster; it encodes the type IV secretion machinery system forming a cylinder-like structure. The CagA protein is translocated into target cells via this secretion system and induces a hummingbird phenotype, a growth factor-like effect. The other gene products are

Association of Vac A- and Cag A-specific Helicobacter pylori strain infection with spontaneous preterm birth.

Science.gov (United States)

Yang, Seung Woo; Kwon, Han Sung; Sohn, In Sook; Kim, Young Ju; Hwang, Han Sung

2017-04-01

To better understand the correlation between Helicobacter pylori (H. pylori) seropositivity and spontaneous preterm birth. A total of 320 pregnant women were classified into two groups: normal control singleton pregnant group (n = 264) and singleton spontaneous preterm birth group (n = 56). Blood samples were collected at the time of delivery, and the H. pylori IgG, various virulence factors and systemic inflammation status were compared between the two groups. Between the two groups, the serum H. pylori IgG, Cytotoxin-associated agntigen A (Cag A), Vacuolating cytotoxin A (Vac A) significantly increased in spontaneous preterm birth group than in the control group. Also, in preterm group, highly sensitive C-reactive protein (hsCRP) as a systemic inflammatory marker is statistically elevated at inflammatory status range. Whereas in the term pregnant group, hsCRP was normal range even though high incidence of H. pylori IgG seropositivity. Also, in the seropositive group, hsCRP is statistically correlated with H. pylori IgG, Cag A and Vac A. There is an association between the presence of antibodies against H. pylori in maternal serum and the development of preterm birth. Furthermore, serology type of H. pylori with Vac A, Cag A relates to preterm birth even though high H. pylori prevalence rate.

High prevalence of Helicobacter pylori infection in Malaysian Parkinson's disease patients

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Nafisah WY

2013-11-01

Full Text Available WY Nafisah,1 A Hamdi Najman,1 R Hamizah,1 S Azmin,1 R Rabani,1 SA Shah,2 MI Norlinah11Department of Medicine, 2Department of Community Health, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur, MalaysiaBackground: Studies have reported a higher prevalence of Helicobacter pylori (H. pylori infection in Parkinson's disease.Objectives: To determine the frequency of H. pylori in patients with Parkinson's disease compared to controls and its effect on symptom severity and quality of life.Methods: A cross-sectional comparative study involving 29 Parkinson's disease patients and 23 controls. The 13C-urea breath test was used to diagnose H. pylori. Symptom severity and quality of life were assessed using the Unified Parkinson's Disease Rating Scale (UPDRS and 39-item Parkinson's Disease Questionnaire (PDQ-39, respectively.Results: The frequency of H. pylori infection was 48.3% in the Parkinson's disease group and 21.7% in controls (P=0.048. This became more significant (P=0.012 when we excluded relatives of H. pylori-positive patients from the control group. There was no association between Hoehn and Yahr stages, UPDRS and PDQ-39 scores, and H. pylori.Conclusion: H. pylori infection is more prevalent in the Malaysian Parkinson's disease population compared to controls (48.3% versus 21.7%. However, symptom severity and quality of life was not related to H. pylori infection.Keywords: Parkinson's disease, Helicobacter pylori, prevalence, 13C-urea breath test

Helicobacter pylori colonization of the oral cavity: A milestone discovery

Science.gov (United States)

Yee, John KC

2016-01-01

Over the past several years, the severity of Helicobacter pylori (H. pylori) infections has not significantly diminished. After successful eradication, the annual H. pylori recurrence rate is approximately 13% due to oral H. pylori infection. Established clinical diagnostic techniques do not identify an oral etiologic basis of H. pylori prior to gastric infection. There has been disagreement as to whether oral infection of H. pylori exists or not, with no definite conclusion. In medical practice, negative results with the urea breath test suggest that the stomach infection of H. pylori is cured in these patients. In fact, patients can present negative urea breath test results and yet exhibit H. pylori infection due to oral infection. The present paper provides evidence that H. pylori oral infection is nonetheless present, and the oral cavity represents a secondary site for H. pylori colonization. PMID:26811613

Distribution of the incidence and location of the Helicobacter pylori according to age and gender in patients who undergone endoscopy

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Levent Demirtas

2014-09-01

Full Text Available Objective:The aim of this study was to define the distribution of the incidence and location of Helicobacter pylori in terms of the age and gender in the gastritis patients undergone endoscopy. Methods:Endoscopy and pathology reports of 1,405 patients who undergone biopsy of upper gastrointestinal system endoscopy were retrospectively examined. The frequency and location of Helicobacter pylori infection were evaluated according to the locations, gender and age groups. Based on the Sydney classification, the patients were scored as none (-, low (+, medium (++ and high (+++. Results: A total of 1405 patients (58.6% females, 41.4% males who had both antrum and corpus biopsies were included. Mean age was 48.58±16.96 (15-94 years. The Helicobacter pylori positivity was significantly higher in males than in the female patients (p=0.012. Helicobacter pylori positivity both in corpus and antrum was 1,101 (78.4%, Helicobacter pylori was negative in 304 (21.6% patients. Although, females had higher positivity rate, no significant difference was found between the age and gender groups. In 1,064 patients (75.7% Helicobacter pylori was positive while it was found as negative in 341 (24.3% biopsies taken from the antrum. While in 572 (40.7% of the biopsy outcomes taken from the corpus Helicobacter pylori was found as positive, it was found as negative in 833 (59.3%. No statistically significant differences were found between the age groups in terms of the positivity of Helicobacter pylori both in antrum and in corpus. Conclusion: In our study, the frequency of the Helicobacter pylori positivity was 78.4%. This can be accepted as a serious public health problem in terms of the associated diseases.

empiric treatment based on helicobacter pylori serology cannot ...

African Journals Online (AJOL)

EMPIRIC TREATMENT BASED ON. HELICOBACTER PYLORI SEROLOGY. CANNOT SUBSTITUTE FOR EARLY. ENDOSCOPY IN THE. MANAGEMENT OF DYSPEPTIC. RURAL BLACK AFRICANS. Stephen JD O'Keefe, B Salvador, J Nainkin, S Majikir H. Stevens, A Atherstone. Background_ Evidence that chronic gastric ...

Kyoto global consensus report on Helicobacter pylori gastritis

NARCIS (Netherlands)

K. Sugano (Kentaro); J. Tack (Jan); E.J. Kuipers (Ernst); D.Y. Graham (David Y.); E. El-Omar; S. Miura (Soichiro); K. Haruma (Ken); M. Asaka (Masahiro); N. Uemura (Naomi); P. Malfertheiner

2015-01-01

textabstractObjective To present results of the Kyoto Global Consensus Meeting, which was convened to develop global consensus on (1) classification of chronic gastritis and duodenitis, (2) clinical distinction of dyspepsia caused by Helicobacter pylori from functional dyspepsia, (3) appropriate

Helicobacter pylori Infection is a Significant Factor Risk for Hyperhomocysteinemia in the Patients with Coronary Artery Disease

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Soudabeh Fallah

2016-01-01

Full Text Available ABSTRACT This work aimed to determine whether seropositivity to Helicobacter pylori infection was an independent risk factor for hyperhomocysteinemia patients with cardiovascular disease. The H. pylori IgG, IgA and homocystein levels in 96 patients with cardiovascular disease and 64 participants free of cardiovascular disease as control subjects were determined by ELISA assay. The results showed that seropositivity to H. pylori IgG and IgA levels of coronary artery disease (CADpatients was significantly higher than the controls and CAD patients with H. pylori IgG and IgA negative antibodies. A significant correlation was found between the seropositivity to H. pylori IgG and homocysteine levels of CAD patients in comparison with the controls and CAD patients with seronegativity to H. pylori IgG and IgA (r=0.233, P= 0.019 . The involvement of H. pylori infection in atherosclerosis process was based on the chronic inflammation, which might facilitate the CAD-related pathologies. The effect of the presence of H. pylori infection on homocysteine levels elevation in the CAD patients (as a risk factor independent of other traditional factors was remarkable.

Using Nuclear Techniques to Detect Helicobacter Pylori Infection

International Nuclear Information System (INIS)

Slater, Christine

2014-01-01

Helicobacter pylori (H. pylori) is present in all countries the world over. More than 50% of the world’s population harbour H. pylori in their upper gastrointestinal tract. It can negatively influence nutrition by affecting the uptake of iron and zinc and by increasing susceptibility to diarrhoeal disease. Beyond that, H. pylori is also a major cause of stomach diseases like chronic gastritis, and elevates the risk of developing stomach cancer. The carbon-13 urea breath test is a quick and non-invasive diagnostic test to detect the presence of H. pylori. The patient drinks urea labelled with stable carbon isotopes ( 13 C) that is dissolved in orange juice or citric acid to make sure it coats the entire surface of the stomach, thereby improving the test’s accuracy. If H. pylori is present, it metabolizes the urea and, after 30 minutes, produces carbon dioxide labelled with the stable carbon isotope ( 13 CO 2 ), which can be detected in the breath analysis

Clustering of Helicobacter pylori VacA in lipid rafts, mediated by its receptor, receptor-like protein tyrosine phosphatase beta, is required for intoxication in AZ-521 Cells

DEFF Research Database (Denmark)

Nakayama, Masaaki; Hisatsune, Jyunzo; Yamasaki, Eiki

2006-01-01

Helicobacter pylori vacuolating cytotoxin, VacA, induces multiple effects on epithelial cells through different cellular events: one involves pore formation, leading to vacuolation, mitochondrial damage, and apoptosis, and the second involves cell signaling, resulting in stimulation of proinflamm......Helicobacter pylori vacuolating cytotoxin, VacA, induces multiple effects on epithelial cells through different cellular events: one involves pore formation, leading to vacuolation, mitochondrial damage, and apoptosis, and the second involves cell signaling, resulting in stimulation...

In vitro anti-Helicobacter pylori action of 30 Chinese herbal medicines used to treat ulcer diseases.

Science.gov (United States)

Li, Yang; Xu, Chen; Zhang, Qiang; Liu, Jun Yan; Tan, Ren Xiang

2005-04-26

Infection by Helicobacter pylori has been ascertained to be an important etiologic impetus leading usually to chronic active gastritis and gastric ulcer with growing incidences worldwide. Utilizing as the test pathogen a standard and five clinic strains of Helicobacter pylori, the antibacterial action was assessed in vitro with ethanol extracts of 30 Chinese herbal medicines which have been frequently prescribed since ancient times for treating gastritis-like disorders. Among the 30 tested materials, the ethanol extracts of Abrus cantoniensis (Fabaceae), Saussurea lappa (Asteraceae) and Eugenia caryophyllata (Myrtaceae) were strongly inhibitory to all test strains (MICs: approximately 40 microg/ml), and Hippophae rhamnoides (Elaeagnaceae), Fritillaria thunbergii (Liliaceae), Magnolia officinalis and Schisandra chinensis (Magnoliaceae), Corydalis yanhusuo (Papaveraceae), Citrus reticulata (Rutaceae), Bupleurum chinense and Ligusticum chuanxiong (Apiaceae) substantially active with MICs close to 60.0 microg/ml. As to antibacterial actions of the aqueous extracts of the same drugs, those derived from Cassia obtusifolia (Fabaceae), Fritillaria thunbergii and Eugenia caryophyllata were remarkably inhibitory against all the six Helicobacter pylori strains (MICs: approximately 60 microg/ml). The work compared almost quantitatively the magnitude of the anti-Helicobacter pylori actions of the 30 most prescribed gastritis-treating Chinese herbal drugs, and located as well some source plants where potent anti-Helicobacter pylori phytochemicals could be characterized.

Dietary Factors in Relation to Helicobacter pylori Infection

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Seyyed Ali Mard

2014-01-01

Full Text Available Background and Aim. Helicobacter pylori (HP and diet are both risk factors for gastric cancer. The aim of this study was to evaluate the Helicobacter pylori infection and dietary habits common in Khuzestan province. Methods. This cross-sectional study was conducted in 2011–2013 on 374 patients. Participants were interviewed using a food frequency questionnaire and tissue sample of the antrum was sent for pathology lab. The histopathological major variables were graded on a scale of 3 (mild, moderate, and severe and data analyzed using nonparametric tests. Results. In this study, of 160 patients (43% that were determined, 8.1 percent had severe contamination. Among dietary patterns, relationship between energy intake and carbohydrate with H. pylori was significant. A direct association was found between mean daily intakes of sausage (P=0.001 and burgers (P<0.05 with HP infection. Low intake of fresh vegetables and fruits was the most significant risk factors (P<0.05. Conclusion. There is a possibility that some dietary factors such as consumption of fast foods and low intake of fresh vegetables may increase the chance of HP and severity of this infection.

Seroprevalence of Helicobacter pylori in Hispanics living in Puerto Rico: A population-based study.

Science.gov (United States)

González-Pons, María; Soto-Salgado, Marievelisse; Sevilla, Javier; Márquez-Lespier, Juan M; Morgan, Douglas; Pérez, Cynthia M; Cruz-Correa, Marcia

2018-02-01

Helicobacter pylori is an important etiologic factor for peptic ulcers and gastric cancer, one of the top ten leading causes of cancer death in Puerto Rico. However, the prevalence of H. pylori infections in this population was previously unknown. The aim of this study was to examine the seroprevalence of H. pylori and its associated risk factors in Puerto Rico. A cross-sectional study was designed using an existing population-based biorepository. Seropositivity was determined using the Premier ™ H. pylori immunoassay. Helicobacter pylori seroprevalence was estimated with 95% confidence using marginal standardization following logistic regression. To assess the risk factors associated with H. pylori seropositivity, a multivariable log-binomial model was fitted to estimate the prevalence ratio (PR) and its 95% confidence interval (95% CI). A total of 528 population-based serum samples were analyzed. The mean age of the study population was 41 ± 12 years, of whom 55.3% were females. The overall seroprevalence of H. pylori was 33.0% (95% CI = 28.3%-38.1%). Increasing age and having Puerto Rico. The H. pylori seroprevalence observed in Puerto Rico is similar to the seroprevalence reported in the overall population of the United States. The association between H. pylori seroprevalence and the risk factors analyzed offers insight into the epidemiology of gastric cancer in Puerto Rico and warrants further investigation. © 2017 The Authors. Helicobacter Published by John Wiley & Sons Ltd.

Controversies in the Helicobacter pylori/duodenal ulcer story.

Science.gov (United States)

Hobsley, Michael; Tovey, Frank I; Holton, John

2008-12-01

In patients with Helicobacter pylori-positive duodenal ulcer (DU), the organism must be eradicated to achieve rapid, stable healing. However, evidence is against much else that is commonly accepted. (1) Does H. pylori cause the ulcer? Evidence against includes archaeopathology, geographical prevalence, temporal relationships and H. pylori-negative DU patients. DU can recur after eradication of H. pylori infection, and DUs may remain healed after reduction of acid secretion despite persistent infection. The faster healing of ulcers when H. pylori has been eradicated is due to the organism's interference with neoangiogenesis and the healing of wounded epithelial cells. (2) Does H. pylori infection persist until pharmacologically eradicated? Studies based on current infection show that H. pylori infection is a labile state that can change in 3 months. High rates of gastric acid secretion result in spontaneous cure, whereas low rates permit re-infection. Hydrochloric acid, necessary for producing a DU, is strongly associated with the likelihood of an ulcer. At the start, patients owe their ulcer to gastric hypersecretion of hydrochloric acid; approximately 60% may be H. pylori-negative. If acid is suppressed, the less acid milieu encourages invasion by H. pylori, especially if the strain is virulent.

Infection with Helicobacter pylori is associated with protection against tuberculosis.

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Sharon Perry

2010-01-01

Full Text Available Helicobacter pylori, a lifelong and typically asymptomatic infection of the stomach, profoundly alters gastric immune responses, and may benefit the host in protection against other pathogens. We explored the hypothesis that H. pylori contributes to the control of infection with Mycobacterium tuberculosis.We first examined M. tuberculosis-specific IFN-gamma and H. pylori antibody responses in 339 healthy Northern Californians undergoing routine tuberculin skin testing. Of 97 subjects (29% meeting criteria for latent tuberculosis (TB infection (LTBI, 45 (46% were H. pylori seropositive. Subjects with LTBI who were H. pylori-seropositive had 1.5-fold higher TB antigen-induced IFN-gamma responses (p = 0.04, ANOVA, and a more Th-1 like cytokine profile in peripheral blood mononuclear cells, compared to those who were H. pylori seronegative. To explore an association between H. pylori infection and clinical outcome of TB exposure, we evaluated H. pylori seroprevalence in baseline samples from two high risk TB case-contact cohorts, and from cynomolgus macaques experimentally challenged with M. tuberculosis. Compared to 513 household contacts who did not progress to active disease during a median 24 months follow-up, 120 prevalent TB cases were significantly less likely to be H. pylori infected (AOR: 0.55, 95% CI 0.0.36-0.83, p = 0.005, though seroprevalence was not significantly different from non-progressors in 37 incident TB cases (AOR: 1.35 [95% CI 0.63-2.9] p = 0.44. Cynomolgus macaques with natural H. pylori infection were significantly less likely to progress to TB 6 to 8 months after M. tuberculosis challenge (RR: 0.31 [95% CI 0.12-0.80], p = 0.04.H. pylori infection may induce bystander effects that modify the risk of active TB in humans and non-human primates. That immunity to TB may be enhanced by exposure to other microbial agents may have important implications for vaccine development and disease control.

[Helicobacter pylori -- 2010].

Science.gov (United States)

Buzás, György Miklós

2010-12-05

Helicobacter pylori, discovered 27 years ago, has remained the most prevalent infectious agent in the world. In the author's hypothesis, the increase of peptic ulcer prevalence in the 19-20th century could be attributable to the extended worldwide use of gastric tubes for secretory testing which led to the iatrogenic transmission of pathogenic strains. Helicobacter pylori outer membrane proteins (OMP), and duodenal ulcer promoting (dupA) proteins were identified as novel virulence factors, leading to the production of pro-inflammatory cytokines, which could be future targets of therapy. There is no ideal first-line eradication of the infection and according to expert's opinion, the efficiency of these regimens has fallen gradually in recent years to unacceptably low levels; however, in the author's opinion this is a multifactorial phenomenon which can not be generalized. As alternative drugs, the efficiency of levofloxacin, furazolidone and rifabutin has been proven by meta-analyses. Sequential and bismuth-free quadruple therapies, although highly efficient, are not yet used on a large scale. The recurrence of the infection is 2.27%/year in developed and of 13.0%/year in developing countries. Spontaneous eradication occurred in 8-20% of the children and 5-11% of adults. The prevalence of clarithromycin resistance is increasing worldwide. In Hungary, it has reached 10.9% in county cities, according to a national survey. In a district of Budapest called Ferencváros, the prevalence between 2005 and 2009 was 16-22%, with no increasing trend. The development of enzymatic inhibitors (urease, carbonic anhydrase and gamma-glutamyl transpeptidase), modified antibiotics and efflux pump inhibitors seem promising ways because these compounds do not lead to resistance; however, none have yet been used in humans.

Helicobacter pylori: recent advances in the study of its pathogenicity and prevention Helicobacter pylori: avances recientes en el estudio de su prevención y patogenicidad

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Germán R. Aguilar

2001-06-01

Full Text Available Helicobacter pylori has acquired great importance during the last two decades, after being recognized as an important pathogen that infects a great portion of the human population. This microorganism is recognized as the main causal agent of chronic gastritis and duodenal ulcers, and it is associated with the subsequent development of gastric carcinoma. The pathogenic mechanisms of H. pylori and their relation to gastric ailments have not been clearly defined. However, at present it is well established that urease, vacuolating cytotoxin VacA, and the pathogenicity island (cag PAI gene products, are the main factors of virulence of this organism. Thus, individuals infected with strains that express these virulence factors probably develop a severe local inflammation that may induce the development of peptic ulcer and gastric cancer. The way the infection spreads throughout the world suggests the possibility that there are multiple pathways of transmission. Due to the importance that H. pylori has acquired as a human pathogen, laboratories worldwide are attempting to develop a vaccine that confers long-term immunological protection against infection by this microorganism. Hence, the objective of this review is to present the most relevant findings of the biology of H. Pylori and its interaction with the human host. The full version of this paper is available too at: http://www.insp.mx/salud/index.htmlHelicobacter pylori ha adquirido gran importancia durante las últimas dos décadas, al ser reconocido como un importante patógeno que infecta una gran porción de la población humana. Este microrganismo es reconocido como el principal agente que causa la gastritis crónica y la úlcera duodenal, además de que se ha asociado con el subsecuente desarrollo del carcinoma gástrico. Los mecanismos patogénicos de H. pylori y su relación con los padecimientos gástricos no se han definido en forma clara. Sin embargo, actualmente está bien establecido

ANTIBIOTIC RESISTANCE OF HELICOBACTER PYLORI AMONG CHILDREN AND THERAPY SELECTION

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Ye.A. Kornienko

2006-01-01

Full Text Available The reason for the low therapy efficiency of many gastrobduodenal diseases is the increasing resistance to the antibiotics helicobacter pylori (Н. pylori, which is conditioned by the mutations of its various genes. The most practical importance is attributed to the 23s RRNA mutations, underlying resistance to claritromicin. According to the international consensus maastrichtb3, the scheme of treatment with the inhibitor of the proton pump, claritromicin and metronidasol is recommended as the 1st line therapy. The present work assesses the resistance of Н. pylori to claritromicin aided by pcrbdiagnostics of the 23s RRNA mutation of rna in the biopsy material of the mucous coat of stomach and standard treatment scheme efficiency if compared with the onebantibiotic scheme – amoxicillin, bismuth and inhibitor of the proton pump. 68 children with Н. pylori bassociated diseases have been examined. The frequency of resistance of Н. pylori to claritromicin made up 28%. The standard 10bday long scheme of treatment was efficient among 14% of the patients, the 7bday long schemes with amoxicillin, bismuth and omeprazole were efficient among 40% of the patients, the 10bday long schemes with amoxicillin, bismuth and omeprazole were efficient among 75% of the patients; with omeprazole replaced by esomeprazole the efficiency was observed among 83% of the patients along with the good treatment tolerance.Key words: helicobacter pylori, antibiotic resistance, eradication.

Prevalence of Helicobacter Pylori in Gastric Fluid in the Surgical Patient

Science.gov (United States)

1998-05-01

highest rates of H. pylori infection occur in areas with the highest rates of stomach cancer, such as China, Japan, Peru and Scotland. However, even in the...Mahoney, D.H. (1997). Helicobacter pylori gastritis in a child with sickle cell anemia and recurrent abdominal pain. Journal of Hematology and

Helicobacter pylori Peptidyl Prolyl Isomerase Expression Is Associated with the Severity of Gastritis.

Science.gov (United States)

Oghalaie, Akbar; Saberi, Samaneh; Esmaeili, Maryam; Ebrahimzadeh, Fatemeh; Barkhordari, Farzaneh; Ghamarian, Abdolreza; Tashakoripoor, Mohammad; Abdirad, Afshin; Eshagh Hosseini, Mahmoud; Khalaj, Vahid; Mohammadi, Marjan

2016-12-01

Helicobacter pylori secretory peptidyl prolyl isomerase, HP0175, is progressively identified as a pro-inflammatory and pro-carcinogenic protein, which serves to link H. pylori infection to its more severe clinical outcomes. Here, we have analyzed host HP0175-specific antibody responses in relation to the severity of gastritis. The HP0175 gene fragment was PCR-amplified, cloned, expressed and purified by Ni-NTA affinity chromatography. Serum antigen-specific antibody responses of non-ulcer dyspeptic patients (N = 176) against recombinant HP0175 were detected by western blotting. The infection status of these subjects was determined by rapid urease test, culture, histology, and serology. The grade of inflammation and stage of atrophy were scored blindly according to the OLGA staging system. The recombinant HP0175 (rHP0175) was expressed as a ~35 kDa protein and its identity was confirmed by western blotting using anti-6X His tag antibody and pooled H. pylori-positive sera. Serum IgG antibodies against rHP0175 segregated our patients into two similar-sized groups of sero-positives (90/176, 51.1 %) and sero-negatives (86/176, 48.9 %). The former presented with higher grades of gastric inflammation (OR = 4.4, 95 % CI = 1.9-9.9, P = 0.001) and stages of gastric atrophy (OR = 18.3, 95 %CI = 1.4-246.6, P = 0.028). Our findings lend further support to the pro-inflammatory nature of H. pylori peptidyl prolyl isomerase (HP0175) and recommends this antigen as a non-invasive serum biomarker of the severity of H. pylori-associated gastritis.

Cell-cycle inhibition by Helicobacter pylori L-asparaginase.

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Claudia Scotti

Full Text Available Helicobacter pylori (H. pylori is a major human pathogen causing chronic gastritis, peptic ulcer, gastric cancer, and mucosa-associated lymphoid tissue lymphoma. One of the mechanisms whereby it induces damage depends on its interference with proliferation of host tissues. We here describe the discovery of a novel bacterial factor able to inhibit the cell-cycle of exposed cells, both of gastric and non-gastric origin. An integrated approach was adopted to isolate and characterise the molecule from the bacterial culture filtrate produced in a protein-free medium: size-exclusion chromatography, non-reducing gel electrophoresis, mass spectrometry, mutant analysis, recombinant protein expression and enzymatic assays. L-asparaginase was identified as the factor responsible for cell-cycle inhibition of fibroblasts and gastric cell lines. Its effect on cell-cycle was confirmed by inhibitors, a knockout strain and the action of recombinant L-asparaginase on cell lines. Interference with cell-cycle in vitro depended on cell genotype and was related to the expression levels of the concurrent enzyme asparagine synthetase. Bacterial subcellular distribution of L-asparaginase was also analysed along with its immunogenicity. H. pylori L-asparaginase is a novel antigen that functions as a cell-cycle inhibitor of fibroblasts and gastric cell lines. We give evidence supporting a role in the pathogenesis of H. pylori-related diseases and discuss its potential diagnostic application.

Presence of Helicobacter pylori in a Mexican Pre-Columbian Mummy

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Cerbón Marco A

2008-07-01

Full Text Available Abstract Background Recent studies showed that Helicobacter pylori existed in the New World prior to the arrival of Columbus. The purpose of the present study was to detect the presence of Helicobacter pylori in pre-Columbian mummies from Northern Mexico. Methods Six samples were studied (four samples of gastric remains, tongue-soft palate, and brain remained as negative controls from two of the six naturally mummified corpses studied (adult male and infant male. Samples were taken from tissues suitable for DNA amplification by Polymerase chain reaction (PCR. DNA was extracted and H. pylori detection was carried out by PCR and hybridized with the pHp probe from 16S rRNA gene. The purified PCR products were cloned and sequenced in both directions. DNA sequences were analyzed with ALIGN and BLAST software. A second amplification was performed using ureB gene by real-time PCR. Results From four samples of gastric remnant, only two were H. pylori-positive for amplification of a 109 bp DNA fragment; the remaining two were negative, as were the tongue-soft palate and the brain biopsies as well. These PCR products were hybridized with a pHp probe. Nucleotide sequence analysis showed homology with H. pylori in 98 of 99% when compared with the gene bank nucleotide sequence. Only one sample of gastric remnant H. pylori-positive with 16S rRNA gene was also positive for ureB gene from H. pylori. Conclusion This data supported infection with H. pylori in Mexican pre-Columbian mummies dating from approximately 1,350 AC.

In situ targeted MRI detection of Helicobacter pylori with stable magnetic graphitic nanocapsules

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Li, Yunjie; Hu, Xiaoxiao; Ding, Ding; Zou, Yuxiu; Xu, Yiting; Wang, Xuewei; Zhang, Yin; Chen, Long; Chen, Zhuo; Tan, Weihong

2017-06-01

Helicobacter pylori infection is implicated in the aetiology of many diseases. Despite numerous studies, a painless, fast and direct method for the in situ detection of H. pylori remains a challenge, mainly due to the strong acidic/enzymatic environment of the gastric mucosa. Herein, we report the use of stable magnetic graphitic nanocapsules (MGNs), for in situ targeted magnetic resonance imaging (MRI) detection of H. pylori. Several layers of graphene as the shell effectively protect the magnetic core from corrosion while retaining the superior contrast effect for MRI in the gastric environment. Boronic-polyethylene glycol molecules were synthesized and modified on the MGN surface for targeted MRI detection. In a mouse model of H. pylori-induced infection, H. pylori was specifically detected through both T2-weighted MR imaging and Raman gastric mucosa imaging using functionalized MGNs. These results indicated that enhancement of MRI using MGNs may be a promising diagnostic and bioimaging platform for very harsh conditions.

One-week triple therapy for eradication of helicobacter pylori

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Shah, N.H.; Shah, M.S.; Khan, I.; Hameed, K.

2002-01-01

Objective: The optimum therapy for Helicobacter pylori infection is yet to be defined in Pakistan despite a high prevalence of helicobacter associated diseases in this community. The most popular and effective regimen was therefore chosen among the currently recommended combinations used worldwide to document its efficacy in our symptomatic Helicobacter positive dyspeptic patients. Design: It was a prospective, non-randomized study. Place and duration of Study: The study lasted from January 1998 till June 1999 at the Postgraduate Institute, Government Lady Reading Hospital and Fauji Foundation Hospital, Peshawar. Subjects and Methods: Consecutive dyspeptic patients with peptic ulcer disease as well as non ulcer dyspepsia with a positive H. pylori status on histology from the specimens obtained from the antral region of the stomach, who consented to take part in the study were enrolled. They were given omeprazole 20 mg bd, clarithromycin 500 mg bd. And amoxycillin 1 gm bd for one week. One group comprised patients with confirmed peptic ulcer disease while the second group comprised patients with macroscopic/microscopic antral gastritis. Patients with peptic ulcer disease were given additional course of omerprazol for another 4 weeks to ensure healing of their ulcers. All patients were re scoped after stopping all drugs and their H. pylori status re-assessed on histology. Results: A total of 84 patients consented to enter the study. Fifty-nine were males and twenty-five were females. Fifty-eight patients completed the study while others were lost followup. There were no dropouts due to side effects of the drugs. Sixteen patients had peptic ulcer disease while 68 had macroscopic/microscopic active antral gastric only. The Helicobacter pylori eradication has been successful in only 12 patients giving a cure rate of 20.60% as determined per protocol analysis. The eradication rates were disappointingly low in both groups. Conclusion: The results are extremely

ASSESSING THE EFFECTIVENESS OF LOW PRESSURE ULTRAVIOLET LIGHT FOR INACTIVATING HELICOBACTER PYLORI

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Three strains of Helicobacter pylori were exposed to ultraviolet (UV) light from a low-pressure source to determine log inactivation versus applied fluence. Results indicate that H. pylori is readily inactivated at UV fluences typically used in water treatment r...

Novel and Effective Therapeutic Regimens for Helicobacter pylori in an Era of Increasing Antibiotic Resistance

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Yi Hu

2017-05-01

Full Text Available Helicobacter pylori (H. pylori is a common gastrointestinal bacterial strain closely associated with the incidence of chronic gastritis, peptic ulcers, gastric mucosa-associated lymphoid tissue lymphoma, and gastric cancer. A current research and clinical challenge is the increased rate of antibiotic resistance in H. pylori, which has led to a decreased H. pylori eradication rate. In this article, we review recent H. pylori infection and reinfection rates and H. pylori resistance to antibiotics, and we discuss the pertinent treatments. A PubMed literature search was performed using the following keywords: Helicobacter pylori, infection, reinfection, antibiotic resistance, bismuth, proton pump inhibitors, vonoprazan, susceptibility, quintuple therapy, dual therapy, and probiotic. The prevalence of H. pylori has remained high in some areas despite the decreasing trend of H. pylori prevalence observed over time. Additionally, the H. pylori reinfection rate has varied in different countries due to socioeconomic and hygienic conditions. Helicobacter pylori monoresistance to clarithromycin, metronidazole or levofloxacin was common in most countries. However, the prevalence of amoxicillin and tetracycline resistance has remained low. Because H. pylori infection and reinfection present serious challenges and because H. pylori resistance to clarithromycin, metronidazole or levofloxacin remains high in most countries, the selection of an efficient regimen to eradicate H. pylori is critical. Currently, bismuth-containing quadruple therapies still achieve high eradication rates. Moreover, susceptibility-based therapies are alternatives because they may avoid the use of unnecessary antibiotics. Novel regimens, e.g., vonoprazan-containing triple therapies, quintuple therapies, high-dose dual therapies, and standard triple therapies with probiotics, require further studies concerning their efficiency and safety for treating H. pylori.

Regulation of the actin cytoskeleton in Helicobacter pylori-induced migration and invasive growth of gastric epithelial cells

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Rieder Gabriele

2011-11-01

Full Text Available Abstract Dynamic rearrangement of the actin cytoskeleton is a significant hallmark of Helicobacter pylori (H. pylori infected gastric epithelial cells leading to cell migration and invasive growth. Considering the cellular mechanisms, the type IV secretion system (T4SS and the effector protein cytotoxin-associated gene A (CagA of H. pylori are well-studied initiators of distinct signal transduction pathways in host cells targeting kinases, adaptor proteins, GTPases, actin binding and other proteins involved in the regulation of the actin lattice. In this review, we summarize recent findings of how H. pylori functionally interacts with the complex signaling network that controls the actin cytoskeleton of motile and invasive gastric epithelial cells.

Vacuolating Cytotoxin of Helicobacter pylori Plays a Role during Colonization in a Mouse Model of Infection

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Salama, Nina R.; Otto, Glen; Tompkins, Lucy; Falkow, Stanley

2001-01-01

Helicobacter pylori, the causative agent of gastritis and ulcer disease in humans, secretes a toxin called VacA (vacuolating cytotoxin) into culture supernatants. VacA was initially characterized and purified on the basis of its ability to induce the formation of intracellular vacuoles in tissue culture cells. H. pylori strains possessing different alleles of vacA differ in their ability to express active toxin. Those strains expressing higher toxin levels are correlated with more severe gast...

IL-17a and IL-22 Induce Expression of Antimicrobials in Gastrointestinal Epithelial Cells and May Contribute to Epithelial Cell Defense against Helicobacter pylori.

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Beverly R E A Dixon

Full Text Available Helicobacter pylori colonization of the human stomach can lead to adverse clinical outcomes including gastritis, peptic ulcers, or gastric cancer. Current data suggest that in addition to bacterial virulence factors, the magnitude and types of immune responses influence the outcome of colonization. Specifically, CD4+ T cell responses impact the pathology elicited in response to H. pylori. Because gastritis is believed to be the initiating host response to more detrimental pathological outcomes, there has been a significant interest in pro-inflammatory T cell cytokines, including the cytokines produced by T helper 17 cells. Th17 cells produce IL-17A, IL-17F, IL-21 and IL-22. While these cytokines have been linked to inflammation, IL-17A and IL-22 are also associated with anti-microbial responses and control of bacterial colonization. The goal of this research was to determine the role of IL-22 in activation of antimicrobial responses in models of H. pylori infection using human gastric epithelial cell lines and the mouse model of H. pylori infection. Our data indicate that IL-17A and IL-22 work synergistically to induce antimicrobials and chemokines such as IL-8, components of calprotectin (CP, lipocalin (LCN and some β-defensins in both human and primary mouse gastric epithelial cells (GEC and gastroids. Moreover, IL-22 and IL-17A-activated GECs were capable of inhibiting growth of H. pylori in vitro. While antimicrobials were activated by IL-17A and IL-22 in vitro, using a mouse model of H. pylori infection, the data herein indicate that IL-22 deficiency alone does not render mice more susceptible to infection, change their antimicrobial gene transcription, or significantly change their inflammatory response.

Empiric treatment based on Helicobacter Pylori serology cannont ...

African Journals Online (AJOL)

Background: Evidence that chronic gastric Helicobacter pylori (HP) infection is an aetiological factor in dyspepsia, peptic ulcer disease, gastric carcinoma and lymphoma has led to the suggestion that all serologically positive dyspeptic patients should be treated empirically with antibiotics to eradicate the infection, without ...

Foveolar cells phagocytose apoptotic neutrophils in chronic active Helicobacter pylori gastritis.

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Caruso, R A; Fedele, F; Di Bella, C; Mazzon, E; Rigoli, L

2012-11-01

The recognition and removal of apoptotic inflammatory cells by tissue macrophages and non-professional phagocytes, in a process called efferocytosis, is required for resolution of inflammation and is actively anti-inflammatory. We have previously demonstrated phagocytosis of apoptotic neutrophils by tumor cells in human gastric carcinoma, but to date, there have been no studies investigating this process in chronic active Helicobacter pylori gastritis. Biopsy specimens from 28 subjects with or without H. pylori infection and active inflammation were examined and graded according to the updated Sydney system. Light microscopy, electron microscopy, and Terminal Deoxynucleotidyltransferase-Mediated UTP End Labeling staining were used to identify apoptosis. H. pylori infection was detected by histology and by molecular assay in 16 out of 28 cases. DNA from paraffin-embedded gastric biopsies was amplified using primers specific for cagA, for the cag "empty site" as well as for the s and m alleles of vacA. The more virulent cagA-positive strains were found in five out of nine patients with chronic active gastritis. The vacA s1/m1 and s2/m1 genotypes were more common in nine patients with chronic active gastritis, while the vacA s2/m2 genotype was more frequent in seven patients with chronic inactive gastritis. Apoptotic neutrophils were also detected within the cytoplasmic vacuoles of the foveolar cells of nine cases with chronic active gastritis. Transmission electron micrographs revealed further apoptotic neutrophils within spacious phagosomes of foveolar cells in a similar manner to those described in late-phase efferocytosis both in vivo and in vitro. These new observations expand the morphological spectrum of gastritis in patients infected with more virulent H. pylori strains, compatible with an anti-inflammatory role for the gastric epithelial cells in their removal of apoptotic neutrophils during active chronic gastritis.

Detection of helicobacter pylori in nasal polyps using rapid urease test and ELISA

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Masood Kaviani

2009-01-01

Full Text Available Introduction: Nasal polyposis is an inflammatory condition of unknown etiology. Recently concerns regarding gastroesophageal reflux or helicobacter pylori as a possible pathologic cause of nasal polyps have been increasing. The present study was planned to investigate the presence of helicobacter pylori in nasal polyps. Materials and Methods: This case-control study was undertaken enrolling 37 patients with nasal polyps who had undergone nasal endoscopic sinus surgery and 38 control subjects. Biopsy specimens of nasal polyps and inferior turbinates were assessed by rapid urease test. Blood samples of both study and control subjects were evaluated for anti H.pylori IgG by ELISA. H. pylori status was regarded positive, if both tests were positive. Results: Seropositivity was more common in the patients with nasal polyps (66.2% than control subjects (36.8% (P

Helicobacter pylori in First Nations and Recent Immigrant Populations in Canada

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Nicola L Jones

2012-01-01

Full Text Available The diminishing prevalence of Helicobacter pylori infection among most segments of the Canadian population has led to changes in the etiologies and patterns of associated upper gastrointestinal diseases, including fewer peptic ulcers and their complications. Canadian Aboriginals and recent immigrants are among populations in which the prevalence of H pylori infection remains high and, therefore, the health risks imposed by H pylori remain a significant concern. Population-based strategies for H pylori eradication in groups with a low prevalence of infection are unlikely to be cost effective, but such measures are attractive in groups in which the prevalence rates of infection remain substantial. In addition to a lower prevalence of peptic ulcers and dyspepsia, the public health value of eradication may be particularly important if this leads to a reduction in the prevalence of gastric cancer in high prevalence groups. Therefore The Canadian Helicobacter Study Group held a conference that brought together experts in the field to address these issues, the results of which are reviewed in the present article. Canadians with the highest prevalence of H pylori infection are an appropriate focus for considering the health advantages of eradicating persistent infection. In Canadian communities with a high prevalence of both H pylori and gastric cancer, there remains an opportunity to test the hypothesis that H pylori infection is a treatable risk factor for malignancy.

Prevalence of Helicobacter pylori and parasites in symptomatic children examined for Helicobacter pylori antibodies, antigens, and parasites in Yemen.

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Bin Mohanna, Mabrook A; Al-Zubairi, Lutf M; Sallam, Abdul K

2014-11-01

To estimate the prevalence of Helicobacter pylori (H. pylori) and parasites in symptomatic children examined for H. pylori antibodies, antigens, and parasites in Yemen. A record-based study was carried out at Specialized Sam Pediatric Center in Sana'a, Yemen for 3 years between 2011-2013. Out of the 43,200 patients seen for different causes through that period, 1008 (2.3%) (females: 675 [67%]; males: 333 [33%]) had gastric complaints, and were subjected to an examination of blood and stool for H. pylori and parasites. Data regarding age and gender was also collected. The age of the patients ranged from 3-15 years. The prevalence of H. pylori among children examined for H. pylori was 65%, 30% of them were males, and 35% were females (chi square [I2]=142, p<0.01]). The prevalence in the 6-8 years age group was 83%, and it was 52% in the age group of 12-15 years. The prevalence of giardiasis was 10%, and amoebiasis was 25%. Prevalence of H. pylori infection among children was high, and was more prevalent in the age group of 6-8 years than in the other age groups. Females were more affected than males. Parasites (amoebiasis and giardiasis) infestation was less prevalent.

Expression and Antigenic Evaluation of VacA Antigenic Fragment of Helicobacter Pylori

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Hasanzadeh, Leila; Ghaznavi-Rad, Ehsanollah; Soufian, Safieh; Farjadi, Vahideh; Abtahi, Hamid

2013-01-01

Objective(s) : Helicobacter pylori, a human specific gastric pathogen is a causative agent of chronic active gastritis. The vacuolating cytotoxin (VacA) is an effective virulence factor involved in gastric injury. The aim of this study was to construct a recombinant protein containing antigenic region of VacA gene and determine its antigenicity. Materials and Methods: The antigenic region of VacA gene was detected by bioinformatics methods. The polymerase chain reaction method was used to amplify a highly antigenic region of VacA gene from chromosomal DNA of H. pylori. The eluted product was cloned into the prokaryotic expression vector pET32a. The target protein was expressed in the Escherichia coli BL21 (DE3) pLysS. The bacteria including pET32a-VacA plasmids were induced by IPTG. The antigenicity was finally studied by western blotting using sera of 15 H. pylori infected patients after purification. Results: Enzyme digestion analysis, PCR and DNA sequencing results showed that the target gene was inserted correctly into the recombinant vector. The expressed protein was purified successfully via affinity chromatography. Data indicated that antigenic region of VacA protein from Helicobacter pylori was recognized by all 15 patient’s sera. Conclusion : Our data showed that antigenic region of VacA protein can be expressed by in E. co.li. This protein was recognized by sera patients suffering from H. pylori infection. the recombinant protein has similar epitopes and close antigenic properties to the natural form of this antigen. Recombinant antigenic region of VacA protein also seems to be a promising antigen for protective and serologic diagnosis . PMID:23997913

Expression and Antigenic Evaluation of VacA Antigenic Fragment of Helicobacter Pylori

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Leila Hasanzadeh

2013-07-01

Full Text Available Objective(s: Helicobacter pylori, a human specific gastric pathogen is a causative agent of chronic active gastritis. The vacuolating cytotoxin (VacA is an effective virulence factor involved in gastric injury. The aim of this study was to construct a recombinant protein containing antigenic region of VacA gene and determine its antigenicity.   Materials and Methods: The antigenic region of VacA gene was detected by bioinformatics methods. The polymerase chain reaction method was used to amplify a highly antigenic region of VacA gene from chromosomal DNA of H. pylori. The eluted product was cloned into the prokaryotic expression vector pET32a. The target protein was expressed in the Escherichia coli BL21 (DE3 pLysS. The bacteria including pET32a-VacA plasmids were induced by IPTG. The antigenicity was finally studied by western blotting using sera of 15 H. pylori infected patients after purification. Results: Enzyme digestion analysis, PCR and DNA sequencing results showed that the target gene was inserted correctly into the recombinant vector. The expressed protein was purified successfully via affinity chromatography. Data indicated that antigenic region of VacA protein from Helicobacter pylori was recognized by all 15 patient’s sera. Conclusion : Our data showed that antigenic region of VacA protein can be expressed by in E. co.li. This protein was recognized by sera patients suffering from H. pylori infection. the recombinant protein has similar epitopes and close antigenic properties to the natural form of this antigen. Recombinant antigenic region of VacA protein also seems to be a promising antigen for protective and serologic diagnosis .

The prevalence of Helicobacter pylori gastritis in newly diagnosed children with inflammatory bowel disease.

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Roka, Kleoniki; Roubani, Aikaterini; Stefanaki, Kalliopi; Panayotou, Ioanna; Roma, Eleftheria; Chouliaras, Giorgos

2014-10-01

Recent studies have shown that patients with inflammatory bowel disease (IBD) are less likely to be infected with Helicobacter pylori compared with non-IBD patients. We aimed to study the prevalence of H. pylori-positive and H. pylori-negative gastritis in newly diagnosed children with IBD in comparison to those with non-IBD in Greece. All children who underwent first esophagogastroduodenal endoscopy between 2002 and 2011 were retrospectively included. Four groups were studied: patients with Crohn's disease (CD), ulcerative colitis (UC), IBD unclassified (IBDU), and non-IBD individuals (non-IBD). Helicobacter pylori infection was defined by positive culture or by positive histology and CLO test. Those children with negative or not available culture and only one positive test (histology or CLO) were further evaluated by urea breath test, and the positives were also included in the infected group. We studied 159 patients with IBD (66 CD, 34 UC, and 59 IBDU) and 1209 patients in non-IBD individuals. Helicobacter pylori gastritis was less frequent in the IBD group (3.8% vs 13.2% in the control group, p gastritis were 3.3 times more likely to belong in the IBD group compared with H. pylori-positive patients (p = .006). Occurrence of H. pylori gastritis is less frequent in children with IBD compared with controls. Our study confirms an inverse association between H. pylori and IBD. Future studies are needed to distinguish between a true protective role of H. pylori and a confounding effect due to previous antibiotic use in children with IBD. © 2014 John Wiley & Sons Ltd.

A study on the effect of Helicobacter pylori infection on p53 expression in gastric cancer and gastritis tissues.

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Salih, Barik A; Gucin, Zuhal; Bayyurt, Nizamettin

2013-09-16

Helicobacter pylori cause damage to gastric epithelial cells and alterations in the p53 gene that lead to cancer development. This study aimed to determine the correlation of p53 expression with H. pylori using immunohistochemistry, RFLP-PCR, and histopathology. Gastric biopsy samples from gastric cancer (GC) (n = 54) and gastritis (n = 31) patients were examined for histopathological changes and expression of p53 protein by immunohistochemistry. Immunohistochemical analysis of p53 protein expression in H. pylori-positive GC sections showed an average of 44.3% positive cells in tumors and 6.9% in normal tissues, as compared to 16.4% and 4.4% in H. pylori-negative sections. P53 expression showed significant association with H. pylori (P = 0.005), invasion depth (P = 0.029) and inflammation reaction (P = 0.008). In gastritis sections, no difference in the average p53 staining in H. pylori-positive or -negative sections was seen. PCR-RFLP results also showed no difference in genotype frequencies of p53 in H. pylori-positive or -negative gastritis sections. Histopathology study of H. pylori-positive GC sections showed that 97.2% were the intestinal type and 2.8% the diffuse type, while in H. pylori-negative sections 35.2% were the intestinal type and 64.8% the diffuse type. Biopsy sections from H. pylori-positive gastritis patients revealed more severe inflammation than those of H. pylori-negative patients. Our results show that H. pylori infection affects p53 expression in GC. The average p53 expression was significantly higher in tumor than in normal tissues. In gastritis sections p53 expression was significantly associated with H. pylori.

The association between Helicobacter pylori infection and the risk of advanced colorectal neoplasia may differ according to age and cigarette smoking.

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Park, Hyunsung; Park, Jae Jun; Park, Yoo Mi; Baik, Su Jung; Lee, Hyun Ju; Jung, Da Hyun; Kim, Jie-Hyun; Youn, Young Hoon; Park, Hyojin

2018-03-29

The association between Helicobacter pylori infection and advanced colorectal neoplasia (ACN) remains controversial. This study aimed to clarify the association between H. pylori infection and ACN according to age groups. We retrospectively analyzed the association between H. pylori infection and ACN in patients aged Helicobacter pylori positivity was determined by the results of serum anti-H. pylori immunoglobulin G or rapid urease test, if the anti-H. pylori immunoglobulin G was in the borderline range. Among the 19 337 patients who were included, 56.2% and 3.4% were positive for H. pylori and ACN, respectively. Helicobacter pylori infection independently increased the risk of ACN in patients aged pylori infection and ACN was affected by smoking history. When stratified by age and smoking history, H. pylori infection conferred an increased risk of ACN in patients aged pylori infection and a history of smoking than in those without (69.3% vs 54.4%, respectively; P = .031). Helicobacter pylori infection confers an increased risk of ACN, but the association may differ according to age and smoking history. © 2018 John Wiley & Sons Ltd.

Virulence factors and treatment of Helicobacter pylori infections

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Talebibezminabadi, A.

2013-01-01

Helicobacter pylori is a Gram-negative, spiral shaped bacterium that colonizes the epithelial mucosa of the human stomach of more than 50% of the worlds population. Colonization typically occurs during early childhood, and if left untreated it usually lasts for life. The long-term persistence of H.

The accuracy of the Helicobacter pylori stool antigen test in diagnosing H-pylori in treated and untreated patients

NARCIS (Netherlands)

Arents, NL; van Zwet, AA; Thijs, JC; de Jong, A; Pool, MO; Kleibeuker, JH

Objective and design To evaluate the performance of the Helicobacter pylori stool antigen test (HpSA test) in detecting H. pylori infection and monitoring the effect of treatment. This was done in two separate studies using either a biopsy or the C-13-urea breath test based 'gold standard' (in

Helicobacter pylori vacA and cagA genotypes in patients from northeastern Brazil with upper gastrointestinal diseases

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Meyssa Quezado de Figueiredo Cavalcante

2012-06-01

Full Text Available Helicobacter pylori causes chronic gastric inflammation and significantly increases the risk of duodenal and gastric ulcer disease and distal gastric carcinoma. In this study, we evaluated the Helicobacter pylori vacA and cagA genotypes in patients from a Brazilian region where there is a high prevalence of gastric cancer. Polymerase chain reaction (PCR was used to investigate vacA mosaicism and cagA status in the gastric mucosa of 134 H. pylori-positive patients, including 76 with gastritis: 28 with peptic ulcer disease and 30 with gastric cancer. The s1m1 variant was the predominant vacA genotype observed, whereas the s1 allele was more frequently observed in patients with more severe diseases associated with H. pylori infection [p = 0.03, odds ratio (OR = 5.72, 95% confidence interval (CI = 1.15-38.60]. Furthermore, all of the s1 alleles were s1b. Mixed vacA m1/m2 strains were found more frequently in patients with gastric cancer and a cagA-positive status was significantly associated with gastric cancer (p = 0.016, OR = 10.36, 95% CI = 1.35-217.31. Patients with gastric cancer (21/21, 100%, p = 0.006 or peptic ulcers (20/21, 95%, p = 0.02 were more frequently colonised by more virulent H. pylori strains compared to gastritis patients (41/61, 67.2%. In conclusion, in the northeastern of Brazil, which is one of the regions with the highest prevalence of gastric cancer in the country, infection with the most virulent H. pylori strains, carrying the cagA gene and s1m1 vacA alleles, predominates and is correlated with more severe H. pylori-associated diseases.

Linezolid susceptibility in Helicobacter pylori, including strains with multidrug resistance.

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Boyanova, Lyudmila; Evstatiev, Ivailo; Gergova, Galina; Yaneva, Penka; Mitov, Ivan

2015-12-01

Only a few studies have evaluated Helicobacter pylori susceptibility to linezolid. The aim of the present study was to assess linezolid susceptibility in H. pylori, including strains with double/multidrug resistance. The susceptibility of 53 H. pylori strains was evaluated by Etest and a breakpoint susceptibility testing method. Helicobacter pylori resistance rates were as follows: amoxicillin, 1.9%; metronidazole, 37.7%; clarithromycin, 17.0%; tetracycline, 1.9%; levofloxacin, 24.5%; and linezolid (>4 mg/L), 39.6%. The linezolid MIC50 value was 31.2-fold higher than that of clarithromycin and 10.5-fold higher than that of levofloxacin; however, 4 of 11 strains with double/multidrug resistance were linezolid-susceptible. The MIC range of the oxazolidinone agent was larger (0.125-64 mg/L) compared with those in the previous two reports. The linezolid resistance rate was 2.2-fold higher in metronidazole-resistant strains and in strains resistant to at least one antibiotic compared with the remaining strains. Briefly, linezolid was less active against H. pylori compared with clarithromycin and levofloxacin, and linezolid resistance was linked to resistance to metronidazole as well as to resistance to at least one antibiotic. However, linezolid activity against some strains with double/multidrug resistance may render the agent appropriate to treat some associated H. pylori infections following in vitro susceptibility testing of the strains. Clinical trials are required to confirm this suggestion. Copyright © 2015 Elsevier B.V. and the International Society of Chemotherapy. All rights reserved.

Helicobacter pylori stool antigen test (HpSA) for the diagnosis of gastric infection

International Nuclear Information System (INIS)

Faruqui, A.N.; Majid, U.; Ahmed, L.; Khalil, M.; Hussan, M.U.

2007-01-01

To determine the accuracy of Helicobacter pylori Stool Antigen test (HpSA), compared with endoscopic histopathology for the diagnosis of gastric Helicobecter pylori infection. A total of 50 patients underwent endoscopy for gastric antral mucosal tissue biopsy for histopathology of H.pylori and advised for HpSA. Patient's information including age, gender, past history, presenting signs and symptoms, results of HpSA and histopathology were recorded. Sensitivity analysis was performed to calculate sensitivity, specificity, and predictive values of HpSA. Among 50 patients, 48% males and 52% females (M: F 1: 1.08), a total of 27 (54%) were true positive while 20 (40%) were true negative. Two patients were false negative and only one was false positive. Sensitivity of HpSA was, therefore, 93.1%, specificity 95% and positive and negative predictive values were 96.42% and 90.9% respectively. Helicobacter pylori stool antigen was an accurate and reliable test for the diagnosis of gastric H. pylori infection. (author)

Lactoferrin Adsorbed onto Biomimetic Hydroxyapatite Nanocrystals Controlling - In Vivo - the Helicobacter pylori Infection

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Fulgione, Andrea; Nocerino, Nunzia; Iannaccone, Marco; Roperto, Sante; Capuano, Federico; Roveri, Norberto; Lelli, Marco; Crasto, Antonio; Calogero, Armando; Pilloni, Argenia Paola; Capparelli, Rosanna

2016-01-01

Background The resistance of Helicobacter pylori to the antibiotic therapy poses the problem to discover new therapeutic approaches. Recently it has been stated that antibacterial, immunomodulatory, and antioxidant properties of lactoferrin are increased when this protein is surface-linked to biomimetic hydroxyapatite nanocrystals. Objective Based on these knowledge, the aim of the study was to investigate the efficacy of lactoferrin delivered by biomimetic hydroxyapatite nanoparticles with cell free supernatant from probiotic Lactobacillus paracasei as an alternative therapy against Helicobacter pylori infection. Methods Antibacterial and antinflammatory properties, humoral antibody induction, histopathological analysis and absence of side effects were evaluated in both in vitro and in vivo studies. Results The tests carried out have been demonstrated better performance of lactoferrin delivered by biomimetic hydroxyapatite nanoparticles combined with cell free supernatant from probiotic Lactobacillus paracasei compared to both lactoferrin and probiotic alone or pooled. Conclusion These findings indicate the effectiveness and safety of our proposed therapy as alternative treatment for Helicobacter pylori infection. PMID:27384186

No evidence of a role for mitochondrial complex I in Helicobacter pylori pathogenesis.

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Ng, Garrett Z; Ke, Bi-Xia; Laskowski, Adrienne; Thorburn, David R; Sutton, Philip

2017-06-01

Complex I is the first enzyme complex in the mitochondrial respiratory chain, responsible for generating a large fraction of energy during oxidative phosphorylation. Recently, it has been identified that complex I deficiency can result in increased inflammation due to the generation of reactive oxygen species by innate immune cells. As a reduction in complex I activity has been demonstrated in human stomachs with atrophic gastritis, we investigated whether complex I deficiency could influence Helicobacter pylori pathogenesis. Ndufs6 gt/gt mice have a partial complex I deficiency. Complex I activity was quantified in the stomachs and immune cells of Ndufs6 gt/gt mice by spectrophotometric assays. Ndufs6 gt/gt mice were infected with H. pylori and bacterial colonization assessed by colony-forming assay, gastritis assessed histologically, and H. pylori -specific humoral response quantified by ELISA. The immune cells and stomachs of Ndufs6 gt/gt mice were found to have significantly decreased complex I activity, validating the model for assessing the effects of complex I deficiency in H. pylori infection. However, there was no observable effect of complex I deficiency on either H. pylori colonization, the resulting gastritis, or the humoral response. Although complex I activity is described to suppress innate immune responses and is decreased during atrophic gastritis in humans, our data suggest it does not affect H. pylori pathogenesis. © 2017 John Wiley & Sons Ltd.

Clinical Manifestations of Helicobacter pylori-Negative Gastritis.

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Shiota, Seiji; Thrift, Aaron P; Green, Linda; Shah, Rajesh; Verstovsek, Gordana; Rugge, Massimo; Graham, David Y; El-Serag, Hashem B

2017-07-01

There are data to suggest the existence of non-Helicobacter pylori gastritis. However, the risk factors and clinical course for H pylori-negative gastritis remain unclear. We aimed to examine the prevalence and determinants of H pylori-negative gastritis in a large multiethnic clinical population. We conducted a cross-sectional study among patents scheduled for an elective esophagastroduodenoscopy or attending selected primary care clinics and eligible for screening colonoscopy at a single Veterans Affairs medical center. We identified cases of H pylor-negative gastritis, H pylori-positive gastritis, and H pylori-negative nongastritis, where gastritis was defined by the presence of neutrophils and/or mononuclear cells. Risk factors for H pylori-negative gastritis were analyzed in logistic regression models. A total of 1240 patients had information from all biopsy sites, of whom 695 (56.0%) had gastritis. H pylori-negative gastritis was present in 123 patients (9.9% of all study subjects and 17.7% of all patients with gastritis). Among all patients with gastritis, African Americans were statistically significantly less likely than non-Hispanic whites to have H pylori-negative gastritis (odds ratio, 0.25; 95% confidence interval, 0.14-0.43). Conversely, PPI users were more likely to have H pylori-negative gastritis than H pylori-positive gastritis compared with nonusers (odds ratio, 2.02; 95% confidence interval, 1.17-3.49). The cumulative incidence of gastric erosions and ulcers were higher in patients with H pylori-negative gastritis than H pylori-negative nongastritis. We found that H pylori-negative gastritis was present in approximately 18% of patients with gastritis. The potential for H pylori-negative gastritis to progress or the risk of gastric cancer of those with gastric mucosal atrophy/intestinal metaplasia remains unclear. Copyright © 2017 AGA Institute. Published by Elsevier Inc. All rights reserved.

Helicobacter pylori Infection Causes Characteristic DNA Damage Patterns in Human Cells

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Max Koeppel

2015-06-01

Full Text Available Infection with the human pathogen Helicobacter pylori (H. pylori is a major risk factor for gastric cancer. Since the bacterium exerts multiple genotoxic effects, we examined the circumstances of DNA damage accumulation and identified regions within the host genome with high susceptibility to H. pylori-induced damage. Infection impaired several DNA repair factors, the extent of which depends on a functional cagPAI. This leads to accumulation of a unique DNA damage pattern, preferentially in transcribed regions and proximal to telomeres, in both gastric cell lines and primary gastric epithelial cells. The observed pattern correlates with focal amplifications in adenocarcinomas of the stomach and partly overlaps with known cancer genes. We thus demonstrate an impact of a bacterial infection directed toward specific host genomic regions and describe underlying characteristics that make such regions more likely to acquire heritable changes during infection, which could contribute to cellular transformation.

Helicobacter pylori infection and atrophic gastritis | Ebule | African ...

African Journals Online (AJOL)

Background: Helicobacter pylori-infection associated gastritis is known to be a significant risk factor of gastric cancer. Serum levels of Gastrin-17 and Pepsinogen1which are respectively biomarkers of gastric antral and corpus mucosal activity are well known parameters of atrophic gastritis. Objectives: To determine the ...

Asymptomatic gastric heterotopia in the rectum with Helicobacter pylori infection.

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Swatek, Jarosław; Wronecki, Lech; Ciechanek, Roman; Szumiło, Justyna

2015-12-01

Gastric heterotopia is very rare in the rectum - less than 50 cases have been reported so far. Only in six of them Helicobacter pylori has been observed in heterotopic mucosa. We report a case of a 58-year-old woman with asymptomatic gastric heterotopia in the rectum, incidentally revealed during colonoscopy as a small, sessile polyp. The presence of H. pylori was confirmed by immunohistochemistry. This finding supports the opinion that H. pylori may pass along the gastrointestinal tract in a viable form and that the fecal-oral route of transmission is possible.

Effect of specimen collection techniques, transport media, and incubation of cultures on the detection rate of Helicobacter pylori

NARCIS (Netherlands)

van der Hulst, R. W.; Verheul, S. B.; Weel, J. F.; Gerrits, Y.; ten Kate, F. J.; Dankert, J.; Tytgat, G. N.

1996-01-01

Culture and histologic examination are considered "gold standard" methods for the detection of Helicobacter pylori, but discrepancies may occur with either method. Failure to detect Helicobacter pylori may be due to sampling error, inappropriate transport or culture media, or insufficient duration

dupA polymorphisms and risk of Helicobacter pylori-associated diseases.

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Queiroz, Dulciene M M; Rocha, Gifone A; Rocha, Andreia M C; Moura, Sílvia B; Saraiva, Ivan E B; Gomes, Luciana I; Soares, Taciana F; Melo, Fabrício F; Cabral, Mônica M D A; Oliveira, Celso A

2011-03-01

The dupA of Helicobacter pylori has been suggested as a virulence marker associated with the development of duodenal ulcer disease. However, the studies performed in different geographical areas have shown that there are variations in the prevalence of dupA and its association with H. pylori clinical outcomes. Our group did not observe associations between the presence of dupA and H. pylori clinical outcomes in Brazil. On the other hand, we observed 2 mutations in the sequence of dupA that lead to stop codons: a deletion of an adenine at position 1311 and an insertion of an adenine at position 1426 of the gene. Our aim was to evaluate associations of the presence of dupA with duodenal ulcer and gastric cancer, considering dupA-positive only those H. pylori strains that do not have the mutations in the gene sequence. We also evaluated the effect of infection with a strain carrying an intact dupA on the gastric mucosa histology and IL-8 gastric levels. Colonization with strains that had the intact dupA was negatively associated with gastric carcinoma (p=0.001, OR=0.32, 95% CI=0.16-0.66). The presence of dupA was also associated with an increased degree of antral mucosa inflammation (p=0.01) and with decreased corpus atrophy (pdupA without the stop codon polymorphisms is associated with a lower risk of development of gastric carcinoma in Brazilian subjects. Copyright © 2010 Elsevier GmbH. All rights reserved.

Changing epidemiology of Helicobacter pylori in Japan.

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Inoue, Manami

2017-03-01

Helicobacter pylori (H. Pylori) is known as the most important cause of gastric cancer. The prevalence of H. pylori infection varies widely by geographic area, age, and socioeconomic status. In Japan, H. pylori infection has been highly correlated with the incidence rate of gastric cancer, and a reduction in H. pylori infection is therefore crucial for decreasing the incidence of gastric cancer, especially at the population level. Infection occurs during childhood, commonly before 5 years of age. In Japan, where gastric cancer has ranked as the most common cancer by incidence and mortality for the last several decades, the prevalence of H. pylori infection has dramatically declined by birth cohort effect, mainly due to improvements in the general hygiene environment in childhood. Older generations born before around 1950 show a high prevalence of around 80-90 %, decreasing with age to reach around 10 % or less in those born around the 1990s, and less than 2 % for children born after the year 2000. This change will have generational effects on gastric cancer prevention strategies, both primary and secondary. The risk-stratified approach to gastric cancer prevention should be considered in Japan and other countries which have similarly experienced rapid economic development.

[The influence of Helicobacter pylori infection on the occurance of gastroesophageal reflux in patients with renal insufficiency].

Science.gov (United States)

Stolić, Radojica; Jovanović, Aleksandar; Perić, Vladan; Trajković, Goran; Zivić, Ziva; Stolić, Dragica; Lazarević, Tatjana; Sovtić, Sasa

2007-12-01

Gastric acid is a key factor in the pathophysiology of gastroesophageal reflux disease. A plausible mechanism by which the Helicobacter pylori infection might protect against reflux disease is by its propensity to produce atrophic gastritis. The aim of the study was to establish the influence of Helicobacter pylori infection on the occurrence of gastroesophageal reflux in patients with different stages of renal insufficiency. The examination was organized as a prospective, clinical study and involved 68 patients--33 patients with preterminal stage of renal failure and 35 patients with terminal renal insufficiency. Due to dyspeptic difficulties, in all the patients there was preformed upper esophagogastroscopy and Helicobacter pylori infection was found by ureasa test. The patients with preterminal renal insufficiency were significantly younger than patients with terminal renal failure (53.4 +/- 11.1 vs. 65.4 +/- 12.3 years; p = 0.014). There was found a statistically significant difference between the groups in Helicobacter pylori infection (p = 0.03), hiatal hernia (p = 0.008), gastroesophageal reflux disease (p = 0.007), and duodenal ulcer (p = 0.002). Using the multiple non-parametric correlative analysis there was confirmed a negative correlation between Helicobacter pylori infection and gastro-esophageal reflux disease (Kendal tauB = -0.523; p = 0.003) and hiatal hernia (Kendal tauB = 0.403; p = 0.021), while there was found a positive correlation between gastro-esophageal reflux disease and hiatal hernia (Kendal tauB = 0.350; p = 0.044). Helicobacter pylori infection is a significant protective parameter of the incidence of gastro-esophageal reflux disease in patients with both pre-terminal and terminal renal insufficiency.

The influence of Helicobacter pylori infection on the occurrence of gastroesophageal reflux in patients with renal insufficiency

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Stolić Radojica

2007-01-01

Full Text Available Introduction/Aim. Gastric acid is a key factor in the pathophysiology of gastroesophageal reflux disease. A plausible mechanism by which the Helicobacter pylori infection might protect against reflux disease is by its propensity to produce atrophic gastritis. The aim of the study was to establish the influence of Helicobacter pylori infection on the occurrence of gastroesophageal reflux in patients with different stages of renal insufficiency. Methods. The examination was organized as a prospective, clinical study and involved 68 patients − 33 patients with preterminal stage of renal failure and 35 patients with terminal renal insufficiency. Due to dyspeptic difficulties, in all the patients there was preformed upper esophagogastroscopy and Helicobacter pylori infection was found by ureasa test. Results. The patients with preterminal renal insufficiency were significantly younger than patients with terminal renal failure (53.4±11.1 vs. 65.4±12.3 years; p = 0.014. There was found a statistically significant difference between the groups in Helicobacter pylori infection (p = 0.03, hiatal hernia (p = 0.008, gastroesophageal reflux disease (p = 0.007, and duodenal ulcer (p = 0.002. Using the multiple non-parametric correlative analysis there was confirmed a negative correlation between Helicobacter pylori infection and gastro-esophageal reflux disease (Kendal τB = -0.523; p = 0.003 and hiatal hernia (Kendal τB = 0.403; p = 0.021, while there was found a positive correlation between gastro-esophageal reflux disease and hiatal hernia (Kendal τB = 0.350; p = 0.044. Conclusion. Helicobacter pylori infection is a significant protective parameter of the incidence of gastro-esophageal reflux disease in patients with both pre-terminal and terminal renal insufficiency.

Helicobacter pylori in out-patients of a general practitioner

DEFF Research Database (Denmark)

Rothenbacher, D; Bode, G; Winz, T

1997-01-01

Data on prevalence and determinants of Helicobacter pylori infection in well-defined populations are scarce. We investigated the prevalence and determinants of active H. pylori infection in a population of out-patients attending a general practitioner in Southern Germany. Infection status.......4%). Prevalence of H. pylori infection increased with age from 10.8% (95% CI 5.7-18.1%) in the age group 15-29 years to 30.8% (95% CI 22.1-40.6%) in the age group 60-79 years and was 20.3%, 30.4% and 28.2% for the age groups 30-39, 40-49 and 50-59 years, respectively. Education and childhood living conditions...

[The effect of Helicobacter pylori eradication on chronic gastritis].

Science.gov (United States)

Kodama, Masaaki; Murakami, Kazunari; Okimoto, Tadayoshi; Fujioka, Toshio

2013-08-01

Helicobacter pylori (H. pylori) is a major pathogen of chronic atrophic gastritis, intestinal metaplasia, and gastric cancer. Atrophic gastritis and intestinal metaplasia are recognized as precancerous lesion of gastric cancer. Many studies reported that H. pylori eradication had the preventive effect of gastric cancer. Moreover many studies mentioned the improvement of gastric atrophy and/or intestinal metaplasia. Two meta-analysis indicated the improvement of atrophic gastritis but not of intestinal metaplasia. In our study, intestinal metaplasia improved at lesser curvature of the corpus six years after eradication. H. pylori eradication has benefit for gastric cancer prevention provably due to improvement of the precancerous lesion such as atrophic gastritis and intestinal metaplasia. Especially, H. pylori eradication before the appearance of atrophy and intestinal metaplasia has been considered to be effective in inhibiting the development of gastric cancer. Therefore, improvement or elimination of chronic gastritis with H. pylori eradication might have possibility of gastric cancer inhibition.

Helicobacter pylori and gastroduodenal pathology: New threats of the old friend

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Sechi Leonardo A

2005-01-01

Full Text Available Abstract The human gastric pathogen Helicobacter pylori causes chronic gastritis, peptic ulcer disease, gastric carcinoma, and mucosa-associated lymphoid tissue (MALT lymphoma. It infects over 50% of the worlds' population, however, only a small subset of infected people experience H. pylori-associated illnesses. Associations with disease-specific factors remain enigmatic years after the genome sequences were deciphered. Infection with strains of Helicobacter pylori that carry the cytotoxin-associated antigen A (cagA gene is associated with gastric carcinoma. Recent studies revealed mechanisms through which the cagA protein triggers oncopathogenic activities. Other candidate genes such as some members of the so-called plasticity region cluster are also implicated to be associated with carcinoma of stomach. Study of the evolution of polymorphisms and sequence variation in H. pylori populations on a global basis has provided a window into the history of human population migration and co-evolution of this pathogen with its host. Possible symbiotic relationships were debated since the discovery of this pathogen. The debate has been further intensified as some studies have posed the possibility that H. pylori infection may be beneficial in some humans. This assumption is based on increased incidence of gastro-oesophageal reflux disease (GERD, Barrett's oesophagus and adenocarcinoma of the oesophagus following H. pylori eradication in some countries. The contribution of comparative genomics to our understanding of the genome organisation and diversity of H. pylori and its pathophysiological importance to human healthcare is exemplified in this review.

Helicobacter pylori Diversity and Gastric Cancer Risk

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Timothy L. Cover

2016-03-01

Full Text Available Gastric cancer is a leading cause of cancer-related death worldwide. Helicobacter pylori infection is the strongest known risk factor for this malignancy. An important goal is to identify H. pylori-infected persons at high risk for gastric cancer, so that these individuals can be targeted for therapeutic intervention. H. pylori exhibits a high level of intraspecies genetic diversity, and over the past two decades, many studies have endeavored to identify strain-specific features of H. pylori that are linked to development of gastric cancer. One of the most prominent differences among H. pylori strains is the presence or absence of a 40-kb chromosomal region known as the cag pathogenicity island (PAI. Current evidence suggests that the risk of gastric cancer is very low among persons harboring H. pylori strains that lack the cag PAI. Among persons harboring strains that contain the cag PAI, the risk of gastric cancer is shaped by a complex interplay among multiple strain-specific bacterial factors as well as host factors. This review discusses the strain-specific properties of H. pylori that correlate with increased gastric cancer risk, focusing in particular on secreted proteins and surface-exposed proteins, and describes evidence from cell culture and animal models linking these factors to gastric cancer pathogenesis. Strain-specific features of H. pylori that may account for geographic variation in gastric cancer incidence are also discussed.

Metabolic consequences of Helicobacter pylori infection and eradication

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Buzás, György Miklós

2014-01-01

Helicobacter pylori (H. pylori) is still the most prevalent infection of the world. Colonization of the stomach by this agent will invariably induce chronic gastritis which is a low-grade inflammatory state leading to local complications (peptic ulcer, gastric cancer, lymphoma) and remote manifestations. While H. pylori does not enter circulation, these extragastric manifestations are probably mediated by the cytokines and acute phase proteins produced by the inflammed mucosa. The epidemiologic link between the H. pylori infection and metabolic changes is inconstant and controversial. Growth delay was described mainly in low-income regions with high prevalence of the infection, where probably other nutritional and social factors contribute to it. The timely eradication of the infection will lead to a more healthy development of the young population, along with preventing peptic ulcers and gastric cancer An increase of total, low density lipoprotein and high density liporotein cholesterol levels in some infected people creates an atherogenic lipid profile which could promote atherosclerosis with its complications, myocardial infarction, stroke and peripheral vascular disease. Well designed and adequately powered long-term studies are required to see whether eradication of the infection will prevent these conditions. In case of glucose metabolism, the most consistent association was found between H. pylori and insulin resistance: again, proof that eradication prevents this common metabolic disturbance is expected. The results of eradication with standard regimens in diabetics are significantly worse than in non-diabetic patients, thus, more active regimens must be found to obtain better results. Successful eradication itself led to an increase of body mass index and cholesterol levels in some populations, while in others no such changes were encountered. Uncertainities of the metabolic consequences of H. pylori infection must be clarified in the future. PMID:24833852

Treatment of Helicobacter pylori infections: Mitigating factors and ...

African Journals Online (AJOL)

Helicobacter pylori is a Gram-negative, microaerophilic spiral or motile rod that infects about half the world's population with a very high prevalence in the developing world. It is an important aetiological factor in the development of gastritis, peptic ulcer disease, gastric atrophy and B cell mucosa associated lymphoid tissue ...

Confirmation of eradication of Helicobacter pylori infection by 14C-urea breath test

International Nuclear Information System (INIS)

Pathak, C.M.; Bhasin, D.K.; Sharma, B.C.; Roy, P.; Vaiphei, K.

1998-01-01

Helicobacter pylori (H. pylori) is a potent urease producer, a characteristic that has been exploited in the development of the 14 C-urea breath test (UBT). 14 C-UBT is being used as a highly reliable test for the diagnosis of H. pylori infection. There is paucity of reports on the utility of this test to confirm the H. pylori eradication after its treatment. The study was conducted to determine the utility of 14 C-UBT in confirming the eradication of H. pylori

Glutathione peroxidase level in patients with Helicobacter pylori-associated gastritis

Science.gov (United States)

Tala, Z. Z.; Siregar, G. A.; Siregar, G. P.

2018-03-01

Helicobacter pylori (H. pylori) associated with the generation of reactive oxygen species (ROS), with leads to oxidative stress in the gastric mucosa. GPX is one of human antioxidative defense system allows the elimination of excess ROS. A cross-sectional study was in 80 consecutive gastritis patients who came to the endoscopic unit of Adam Malik General Hospital and PermataBunda Hospital in Medan, Indonesia, from May–September 2017, to determine the difference of GPX serum level between positive and negative infected H. pylori. the diagnosis of gastritis used Histopathology. Rapid urease test for diagnosis of H. pylori infection. Serum samples were obtained to determined circulating GPX. It used Univariate and bivariate analysis (Mann Whitney U test). There were 50 patients (62.5%) infected with H. pylori. GPX levels in patients with positive H. pylori gastritis were lower than those of negative H. pylori but did not differ significantly. In conclusion, there were no significant differences in GPX level between positive and negative infected H. pylori patients.

Helicobacter Pylori Infection in the Elderly

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Jyh-Ming Liou

2008-12-01

Full Text Available The elderly often seek medical attention because of gastroduodenal diseases. Helicobacter pylori (H. pylori infection is associated with several gastroduodenal diseases and its prevalence increases with age worldwide. It is estimated that 10–15% of infected patients will have peptic ulcer disease and 1% of patients will have gastric cancer or mucosa-associated lymphoid tissue lymphoma. Notably, the most severe clinical outcomes, i.e., gastric cancer and complicated peptic ulcer diseases, usually occur in elderly patients. Thus the test-and-treatment strategy is not recommended for elderly patients with uninvestigated dyspepsia. However, biopsy specimens for the rapid urease test and histology should be taken from both the antrum and corpus to increase the detection rate in elderly patients, especially in those with atrophic gastritis. The urea breath test may increase the detection rate if the rapid urease test or histology are negative in elderly patients with atrophic gastritis. Standard triple therapy and sequential therapy can achieve satisfactory eradication rates for H. pylori in elderly patients. Elderly patients with peptic ulcers may have a similar benefit from treatment of H. pylori infection as non-elderly patients. Eradication of H. pylori infection may also lead to improvement in histologic grading of gastritis, but the risk of gastric cancer cannot be completely reduced, especially in patients with existing premalignant lesions.

Helicobacter pylori gastritis in a child with sickle cell anemia and recurrent abdominal pain.

Science.gov (United States)

Kennedy, L; Mahoney, D H; Redel, C A

1997-01-01

Recurrent abdominal pain is a common complaint in children with sickle cell disease. Helicobacter pylori gastritis has recently been described in association with recurrent abdominal pain in children. A case report is given of a 16-year-old black male with hemoglobin SS disease presenting with recurrent abdominal pain and hematemesis. Endoscopic exam of the upper gastrointestinal tract revealed gastritis, and biopsy confirmed H. pylori infection. Serology studies demonstrated increased anti-H. pylori antibody titers. The young man responded well to treatment, with resolution of his symptoms. Helicobacter pylori infection is a new diagnostic consideration for children with recurrent abdominal pain and should be included in the differential diagnosis of children with sickle cell disease, especially when abdominal pain is recurrent and accompanied by vomiting. Larger case studies will be necessary to determine the true incidence of H. pylori in children with sickle cell disease and recurrent abdominal pain.

Concurrent proinflammatory and apoptotic activity of a Helicobacter pylori protein (HP986 points to its role in chronic persistence.

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Ayesha Alvi

Full Text Available Helicobacter pylori induces cytokine mediated changes in gastroduodenal pathophysiology, wherein, the activated macrophages at the sub-mucosal space play a central role in mounting innate immune response against the antigens. The bacterium gains niche through persistent inflammation and local immune-suppression causing peptic ulcer disease or chronic gastritis; the latter being a significant risk factor for the development of gastric adenocarcinoma. What favors persistence of H. pylori in the gastric niches is not clearly understood. We report detailed characterization of a functionally unknown gene (HP986, which was detected in patient isolates associated with peptic ulcer and gastric carcinoma. Expression and purification of recombinant HP986 (rHP986 revealed a novel, ∼29 kDa protein in biologically active form which associates with significant levels of humoral immune responses in diseased individuals (p<0.001. Also, it induced significant levels of TNF-α and Interleukin-8 in cultured human macrophages concurrent to the translocation of nuclear transcription factor-κB (NF-κB. Further, the rHP986 induced apoptosis of cultured macrophages through a Fas mediated pathway. Dissection of the underlying signaling mechanism revealed that rHP986 induces both TNFR1 and Fas expression to lead to apoptosis. We further demonstrated interaction of HP986 with TNFR1 through computational and experimental approaches. Independent proinflammatory and apoptotic responses triggered by rHP986 as shown in this study point to its role, possibly as a survival strategy to gain niche through inflammation and to counter the activated macrophages to avoid clearance.

Pleiotropic Actions of Helicobacter pylori Vacuolating Cytotoxin, VacA

OpenAIRE

Isomoto, Hajime; Moss, Joel; Hirayama, Toshiya

2010-01-01

Helicobacter pylori produces a vacuolating cytotoxin, VacA, and most virulent H. pylori strains secrete VacA. VacA binds to two types of receptor-like protein tyrosine phosphatase (RPTP), RPTPα and RPTPβ, on the surface of host cells. VacA bound to RPTPβ, relocates and concentrates in lipid rafts in the plasma membrane. VacA causes vacuolization, membrane anion-selective channel and pore formation, and disruption of endosomal and lysosomal activity in host cells. Secreted VacA is processed in...

Role of microRNAs and Exosomes in Helicobacter pylori and Epstein-Barr Virus Associated Gastric Cancers

Science.gov (United States)

Polakovicova, Iva; Jerez, Sofia; Wichmann, Ignacio A.; Sandoval-Bórquez, Alejandra; Carrasco-Véliz, Nicolás; Corvalán, Alejandro H.

2018-01-01

Emerging evidence suggests that chronic inflammation caused by pathogen infection is connected to the development of various types of cancer. It is estimated that up to 20% of all cancer deaths is linked to infections and inflammation. In gastric cancer, such triggers can be infection of the gastric epithelium by either Helicobacter pylori (H. pylori), a bacterium present in half of the world population; or by Epstein-Barr virus (EBV), a double-stranded DNA virus which has recently been associated with gastric cancer. Both agents can establish lifelong inflammation by evolving to escape immune surveillance and, under certain conditions, contribute to the development of gastric cancer. Non-coding RNAs, mainly microRNAs (miRNAs), influence the host innate and adaptive immune responses, though long non-coding RNAs and viral miRNAs also alter these processes. Reports suggest that chronic infection results in altered expression of host miRNAs. In turn, dysregulated miRNAs modulate the host inflammatory immune response, favoring bacterial survival and persistence within the gastric mucosa. Given the established roles of miRNAs in tumorigenesis and innate immunity, they may serve as an important link between H. pylori- and EBV-associated inflammation and carcinogenesis. Example of this is up-regulation of miR-155 in H. pylori and EBV infection. The tumor environment contains a variety of cells that need to communicate with each other. Extracellular vesicles, especially exosomes, allow these cells to deliver certain type of information to other cells promoting cancer growth and metastasis. Exosomes have been shown to deliver not only various types of genetic information, mainly miRNAs, but also cytotoxin-associated gene A (CagA), a major H. pylori virulence factor. In addition, a growing body of evidence demonstrates that exosomes contain genetic material of viruses and viral miRNAs and proteins such as EBV latent membrane protein 1 (LMP1) which are delivered into

Role of microRNAs and Exosomes in Helicobacter pylori and Epstein-Barr Virus Associated Gastric Cancers

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Iva Polakovicova

2018-04-01

Full Text Available Emerging evidence suggests that chronic inflammation caused by pathogen infection is connected to the development of various types of cancer. It is estimated that up to 20% of all cancer deaths is linked to infections and inflammation. In gastric cancer, such triggers can be infection of the gastric epithelium by either Helicobacter pylori (H. pylori, a bacterium present in half of the world population; or by Epstein-Barr virus (EBV, a double-stranded DNA virus which has recently been associated with gastric cancer. Both agents can establish lifelong inflammation by evolving to escape immune surveillance and, under certain conditions, contribute to the development of gastric cancer. Non-coding RNAs, mainly microRNAs (miRNAs, influence the host innate and adaptive immune responses, though long non-coding RNAs and viral miRNAs also alter these processes. Reports suggest that chronic infection results in altered expression of host miRNAs. In turn, dysregulated miRNAs modulate the host inflammatory immune response, favoring bacterial survival and persistence within the gastric mucosa. Given the established roles of miRNAs in tumorigenesis and innate immunity, they may serve as an important link between H. pylori- and EBV-associated inflammation and carcinogenesis. Example of this is up-regulation of miR-155 in H. pylori and EBV infection. The tumor environment contains a variety of cells that need to communicate with each other. Extracellular vesicles, especially exosomes, allow these cells to deliver certain type of information to other cells promoting cancer growth and metastasis. Exosomes have been shown to deliver not only various types of genetic information, mainly miRNAs, but also cytotoxin-associated gene A (CagA, a major H. pylori virulence factor. In addition, a growing body of evidence demonstrates that exosomes contain genetic material of viruses and viral miRNAs and proteins such as EBV latent membrane protein 1 (LMP1 which are

Elevated interleukin-32 expression is associated with Helicobacter pylori-related gastritis.

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Liu-Sheng Peng

Full Text Available BACKGROUND: Interleukin-32 (IL-32 is a recently discovered proinflammatory cytokine involved in inflammatory diseases. We investigated the expression of IL-32 and its regulation mechanism in the inflammatory response of patients with Helicobacter pylori (H. pylori infection. DESIGN AND METHODS: IL-32 mRNA and protein expression in gastric tissues was detected by quantitative real-time PCR and immunohistochemistry. The regulation of IL-32 in human gastric epithelia cell line AGS was investigated by different cytokine stimulation and different H. pylori strain infection. RESULTS: Gastric IL-32 mRNA and protein expression were elevated in patients with H. pylori infection and positively correlated with gastritis. In H. pylori-infected patients, the mRNA level of IL-32 was also correlated with that of proinflammatory cytokines IL-1β and TNF-α. In vitro IL-1β and TNF-α could upregulate IL-32 mRNA and protein level in AGS cells, which was dependent on NF-κB signal pathway. The regulation of IL-32 expression in response to H. pylori-infection could be weakened by using neutralizing antibodies to block IL-1β and TNF-α. Moreover, H. pylori-infected AGS cells also induced IL-32 mRNA and protein expression, which was dependent on CagA. CONCLUSIONS: IL-32 level is elevated in patients with H. pylori infection and its expression is regulated by proinflammatory stimuli, suggesting that IL-32 may play a role in the pathogenesis of H. pylori-related gastritis.

The prevalence and related symptomatology of Helicobacter pylori in children with recurrent abdominal pain

DEFF Research Database (Denmark)

Wewer, Anne Vibeke; Andersen, L P; Pærregaard, Anders

1998-01-01

in 46/66 by culture and histology. The presence of H. pylori was significantly associated with active or inactive chronic gastritis. The presence of H. pylori was associated with both parents being born in a country with a high prevalence and a low social class. Helicobacter pylori-positive children had...

Association between helicobacter pylori and gastrointestinal symptoms in children

NARCIS (Netherlands)

Spee, Leo A A; Madderom, Marieke B; Pijpers, Maaike; van Leeuwen, Yvonne; Berger, Marjolein Y

OBJECTIVE: Recurrent abdominal pain (RAP) and other gastrointestinal (GI) symptoms are common complaints among children. The role of Helicobacter pylori in the cause of these complaints remains controversial. Nevertheless, there is an increasing pressure on primary care clinicians to screen for H

Association of specific haplotype of TNFα with Helicobacter pylori ...

Indian Academy of Sciences (India)

Home; Journals; Journal of Genetics; Volume 87; Issue 3. Association of specific haplotype of TNF with Helicobacter pylori-mediated duodenal ulcer in eastern Indian population. Meenakshi Chakravorty Dipanjana Datta De Abhijit Choudhury Amal Santra Susanta Roychoudhury. Research Note Volume 87 Issue 3 ...

Genotyping of vacA alleles of Helicobacter pylori strains recovered ...

African Journals Online (AJOL)

commonly detected genotypes in the meat-based foods, viz, vegetable sandwich and ready to eat fish, were vacA ... Keywords: Helicobacter pylori, VacA genotypes, Genotyping, Food items ..... Microbiology and Quality Control, Islamic Azad.

Risks and Benefits of Helicobacter pylori Eradication: Current Status

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Richard H Hunt

2002-01-01

Full Text Available In patients with diseases known to be associated with Helicobacter pylori infection, such as peptic ulcer, treatment of the underlying infection is the standard of care. However, in most major consensus management guidelines, including those published in Canada, widespread testing for H pylori infection is not recommended. This practice is not encouraged because of insufficient evidence of cost-benefit in gastric cancer prevention, the potential for increases in antibiotic resistance and the controversial hypothesis of potential negative effects of eradication in certain clinical entities. For example, there is insufficient evidence to recommend against eradicating H pylori discovered in a patient with symptoms of gastroesophageal reflux disease. The management guidelines designed specifically in Canada should, therefore, continue to be applied, with H pylori diagnosed and treated in appropriately selected patients.

Helicobacter pylori infection and inflammatory bowel disease: Is there a link?

Science.gov (United States)

Papamichael, Konstantinos; Konstantopoulos, Panagiotis; Mantzaris, Gerassimos J

2014-01-01

Helicobacter pylori (H. pylori) infection is one of the most widely spread infectious diseases in humans. It can cause chronic gastritis, peptic ulcer disease and gastric malignancies and has been associated with extra-gastric disorders. H. pylori elicit a chronic systemic inflammatory response which, under certain conditions, may trigger autoimmune reactions and may be implicated in the pathogenesis of autoimmune diseases. Although the pathogenesis of inflammatory bowel disease (IBD) is unknown, it is thought to result from complex interactions between environmental factors and microbiota in the gut of individuals who are genetically susceptible. Several bacterial and viral agents have been implicated in the aetiology of IBD. In theory, H. pylori infection could be involved in the pathogenesis of IBD by inducing alterations in gastric and/or intestinal permeability or by causing immunological derangements resulting in absorption of antigenic material and autoimmunity via various immunological pathways. Similar mechanisms may also be responsible for the co-existence of IBD with other autoimmune diseases and/or extra-intestinal manifestations. However, the epidemiological data fail to support this association. In fact, various studies indicate that the prevalence of H. pylori infection is low in patients with IBD, suggesting a protective role for this infection in the development of IBD. In this report, we aim to shed light on proposed mechanisms and confounding factors underlying the potential link between H. pylori infection and IBD. PMID:24914359

Re-annotation of the genome sequence of Helicobacter pylori 26695

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Resende Tiago

2013-12-01

Full Text Available Helicobacter pylori is a pathogenic bacterium that colonizes the human epithelia, causing duodenal and gastric ulcers, and gastric cancer. The genome of H. pylori 26695 has been previously sequenced and annotated. In addition, two genome-scale metabolic models have been developed. In order to maintain accurate and relevant information on coding sequences (CDS and to retrieve new information, the assignment of new functions to Helicobacter pylori 26695s genes was performed in this work. The use of software tools, on-line databases and an annotation pipeline for inspecting each gene allowed the attribution of validated EC numbers and TC numbers to metabolic genes encoding enzymes and transport proteins, respectively. 1212 genes encoding proteins were identified in this annotation, being 712 metabolic genes and 500 non-metabolic, while 191 new functions were assignment to the CDS of this bacterium. This information provides relevant biological information for the scientific community dealing with this organism and can be used as the basis for a new metabolic model reconstruction.

EGFR tyrosine kinase inhibitory peptide attenuates Helicobacter pylori-mediated hyper-proliferation in AGS enteric epithelial cells

Energy Technology Data Exchange (ETDEWEB)

Himaya, S.W.A. [Marine Bio-Process Research Center, Pukyong National University, Nam-Gu, Busan, 608-737 (Korea, Republic of); Dewapriya, Pradeep [Department of Chemistry, Pukyong National University, Nam-Gu, Busan, 608-737 (Korea, Republic of); Kim, Se-Kwon, E-mail: sknkim@pknu.ac.kr [Marine Bio-Process Research Center, Pukyong National University, Nam-Gu, Busan, 608-737 (Korea, Republic of); Department of Chemistry, Pukyong National University, Nam-Gu, Busan, 608-737 (Korea, Republic of)

2013-06-15

Helicobacter pylori infection is one of the most critical causes of stomach cancer. The current study was conducted to explore the protective effects of an isolated active peptide H-P-6 (Pro-Gln-Pro-Lys-Val-Leu-Asp-Ser) from microbial hydrolysates of Chlamydomonas sp. against H. pylori-induced carcinogenesis. The peptide H-P-6 has effectively suppressed H. pylori-induced hyper-proliferation and migration of gastric epithelial cells (AGS). However, the peptide did not inhibit the viability of the bacteria or invasion into AGS cells. Therefore, the effect of the peptide on regulating H. pylori-induced molecular signaling was investigated. The results indicated that H. pylori activates the EGFR tyrosine kinase signaling and nuclear translocation of the β-catenin. The EGFR activation has led to the up-regulation of PI3K/Akt signaling pathway. Moreover, the nuclear translocation levels of β-catenin were significantly increased as a result of Akt mediated down-regulation of GSK3/β protein levels in the cytoplasm. Both of these consequences have resulted in increased expression of cell survival and migration related genes such as c-Myc, cyclin-D, MMP-2 and matrilysin. Interestingly, the isolated peptide potently inhibited H. pylori-mediated EGFR activation and thereby down-regulated the subsequent P13K/Akt signaling leading to β-catenin nuclear translocation. The effect of the peptide was confirmed with the use of EGFR tyrosine kinase inhibitor AG1487 and molecular docking studies. Collectively this study identifies a potent peptide which regulates the H. pylori-induced hyper-proliferation and migration of AGS cells at molecular level. - Highlights: • Chlamydomonas sp. derived peptide H-P-6 inhibits H. pylori-induced pathogenesis. • H-P-6 suppresses H. pylori-induced hyper-proliferation and migration of AGS cells. • The peptide inhibits H. pylori-induced EGFR activation.

Is raised helicobacter pylori antibody titre enough to decide retreatment

International Nuclear Information System (INIS)

Bibi, S.; Ahmed, W.; Arif, A.; Alam, S.E.

2011-01-01

Background: Helicobacter pylori infection causes a rise in its antibodies which take almost a year to come to baseline following successful eradication treatment. Checking these values in between a year may give falsely high values and many patients may thus be over treated. Aims: To serially determine Helicobacter pylori antibody titres in patients after giving them triple therapy for H. pylori eradication and see how these values drop over time. Study type, Settings and duration: Longitudinal study conducted in Department of Gastroenterology and Hepatology, Pakistan Medical Research Council, Research Centre, Jinnah Post Graduate Medical Centre, Karachi, from May 2006 to April 2010. Subjects and Methods: Over the period of four years, 186 patients who were found positive for campylobacter like organism test during endoscopy were further tested for anti H. pylori IgG titre before being treated for H. pylori. Patients were given triple therapy comprising of Omeprazole (20 mg twice daily), Amoxicillin (1 gm twice daily) and Clarythromycin (500 mg twice daily) for a week and were followed at 1, 3, 6 and 12 months to check symptomatic relief and they were tested again for H.Pylori antibody titres. Data was collected on pre-designed proforma which included patient's demography, symptoms and diagnosis. Results: Out of 186 patients who had a positive campylobacter like organism test, 173 patients consented to participate in the study. Serology for H.Pylori was positive in 119(68%) cases. A decline in mean antibody titres was observed as 11%, 21.5%, 54.7% and 59.2% at 1, 3, 6 and 12 months respectively. Conclusions: Sensitivity of serology for diagnosing H. pylori infection is good but using these as a tool for monitoring response to treatment is doubtful. A slow drop in H.pylori antibodies was seen over 12 months and therefore, physicians are cautioned not to retreat the already treated cases till about one year post treatment. Policy message: H. pylori antibodies should

Anti-Helicobacter pylori activity and immunostimulatory effect of extracts from Byrsonima crassa Nied. (Malpighiaceae

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Vilegas Wagner

2009-01-01

Full Text Available Abstract Background Several in vitro studies have looked at the effect of medicinal plant extracts against Helicobacter pylori (H. pylori. Regardless of the popular use of Byrsonima crassa (B. crassa as antiemetic, diuretic, febrifuge, to treat diarrhea, gastritis and ulcers, there is no data on its effects against H. pylori. In this study, we evaluated the anti-H. pylori of B. crassa leaves extracts and its effects on reactive oxygen/nitrogen intermediates induction by murine peritoneal macrophages. Methods The minimal inhibitory concentration (MIC was determined by broth microdilution method and the production of hydrogen peroxide (H2O2 and nitric oxide (NO by the horseradish peroxidase-dependent oxidation of phenol red and Griess reaction, respectively. Results The methanolic (MeOH and chloroformic (CHCl3 extracts inhibit, in vitro, the growth of H. pylori with MIC value of 1024 μg/ml. The MeOH extract induced the production H2O2 and NO, but CHCl3 extract only NO. Conclusion Based in our results, B. crassa can be considered a source of compounds with anti-H. pylori activity, but its use should be done with caution in treatment of the gastritis and peptic ulcers, since the reactive oxygen/nitrogen intermediates are involved in the pathogenesis of gastric mucosal injury induced by ulcerogenic agents and H. pylori infections.

The Multiple Carbohydrate Binding Specificities of Helicobacter pylori

Science.gov (United States)

Teneberg, Susann

Persistent colonization of the human stomach by Helicobacter pylori is a risk factor for the development of peptic ulcer disease and gastric cancer. Adhesion of microbes to the target tissue is an important determinant for successful initiation, establishment and maintenance of infection, and a variety of different candidate carbohydrate receptors for H. pylori have been identified. Here the different the binding specifities, and their potential role in adhesion to human gastric epithelium are described. Finally, recent findings on the roles of sialic acid binding SabA adhesin in interactions with human neutrophils and erythrocytes are discussed.

The Importance of Urease in Acid Protection for the Gastric-colonising Bacteria Helicobacter pylori and Helicobacter felis sp. nov.

OpenAIRE

Ferrero, R. L.; Lee, A.

2011-01-01

The urease of the gastric pathogen Helicobacter pylori shares numerous characteristics with the urease of a bacterium isolated from cat gastric mucosa, Helicobacter felis sp. nov. The native enzymes have similar apparent molecular weights and, when subjected to SDS-PAGE, disassociate into active subunits of comparable relative mobilities. In contrast, a bacterium (St1) that colonises rodent ileal mucosa, and is related to Helicobacter spp., expresses a distinct urease from those of the gastri...

Does Helicobacter pylori exhibit corkscrew motion while swimming?