Bacterial factors and immune pathogenesis in H. pylori infection

First Department of Internal Medicine, Hirosaki University School of Medicine, Japan.
Gut (Impact Factor: 14.66). 08/1998; 43 Suppl 1:S2-5.
Source: PubMed


Virulent Helicobacter pylori strains which have been clinically associated with severe outcome induce increased gastric mucosal immune responses. Although several bacterial pathogenic factors have been shown to have a considerable role in H pylori infection, variability in host immune responses may also contribute to mucosal damage in H pylori associated gastritis.

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Available from: Tadashi Shimoyama, Dec 27, 2013
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    • "IL-8 secretion by host cells -H. pylori leads to increased production by the epithelium of the proinflammatory cytokine IL-8 when in close contact with the gastric mucosa (Shimoyama & Crabtree 1998). Because waterexposed H. pylori were able to adhere to epithelial cells, we studied the capability of H. pylori to induce inflammation by evaluating the secretion levels of IL-8 from AGS cells infected with H. pylori inocula exposed to water for different time periods (Fig. 3). "
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    ABSTRACT: While the influence of water in Helicobacter pylori culturability and membrane integrity has been extensively studied, there are little data concerning the effect of this environment on virulence properties. Therefore, we studied the culturability of water-exposed H. pylori and determined whether there was any relation with the bacterium’s ability to adhere, produce functional components of pathogenicity and induce inflammation and alterations in apop- tosis in an experimental model of human gastric epithelial cells. H. pylori partially retained the ability to adhere to epithelial cells even after complete loss of culturability. However, the microorganism is no longer effective in elicit- ing in vitro host cell inflammation and apoptosis, possibly due to the non-functionality of the cag type IV secretion system. These H. pylori-induced host cell responses, which are lost along with culturability, are known to increase epithelial cell turnover and, consequently, could have a deleterious effect on the initial H. pylori colonisation pro- cess. The fact that adhesion is maintained by H. pylori to the detriment of other factors involved in later infection stages appears to point to a modulation of the physiology of the pathogen after water exposure and might provide the microorganism with the necessary means to, at least transiently, colonise the human stomach.
    Memórias do Instituto Oswaldo Cruz 07/2014; 109(4). DOI:10.1590/0074-0276140024 · 1.59 Impact Factor
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    • "About 50-70% of H. pylori strains produce two types of cytotoxins: 1) VacA, whose action is increased by acid pH, which itself results in the degeneration of the epithelial cells of gastric mucosa and 2) CagA, which is a surface protein forming the chief infectious part of H. pylori and is related to a vaster spread. H. pylori strains have the ability to stimulate cytokine production, particularly IL-8 and to induce secretion of lymphocyte chemotactic factors,[9] that possibly causes a specific T-lymphocyte response.[10] The way this bacterium is transmitted is not yet quite clear. "
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    ABSTRACT: Microbial factors may play a role in the pathogenesis of recurrent aphthous stomatitis (RAS). Because of similarities in the characteristics of peptic ulcers and oral aphthous ulcers, it seems reasonable to hypothesize that Helicobacter pylori (H. pylori) could play a role in the development of RAS. The aim of the present study was to determine the relationship between H. pylori and RAS using the results obtained in other related studies. In the present systematic review, all of the relevant papers up to December 2011 were screened. The search was done using PubMed and the Cochrane library and out of 33, 9 articles were selected via the keywords of stomatitis, aphthous and H. pylori. Nine of the studies met the inclusion criteria. Among the selected articles, 6 were inconsistent with the association of H. pylori infection and RAS and 3 agreed to this assumption. The results of the literature indicate that there is no association between H. pylori infection and recurrent aphthous stomatitis.
    Dental research journal 12/2011; 8(Suppl1):S2-S8.
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    • "IL- 1RN*2/*2 genotype may be beneficial in the immune defense against infection by promoting a prolonged Th1 cell-mediated immune response. The T helper cell response towards H. pylori is generally considered to be of the Th1 phenotype, leading to a cell-mediated immune response (Shimoyama and Crabtree, 1998; Ernst, 1999). But prolonged Th1 cell mediated immunity is a causing Pachathundikandi et al. 1061 factor for inflammatory conditions and having more evidence that H. pylori induced Th1 response contributes to cancer development (Ernst and Gold, 2000). "

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