Gastric T lymphocyte responses to Helicobacter pylori in patients with H pylori colonisation.

Fan, X. J.; Chua, Andrew Seng Boon; Shahi, C. N.; McDevitt, Joseph; Keeling, P. W. N.; Kelleher, Dermot

doi:10.1136/gut.35.10.1379

Cited by 132 publications

(97 citation statements)

References 27 publications

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“…In a study the expression of FasL mRNA was higher in T-cells of infected patients versus healthy subjects, which suggests that local T-cells may induce apoptosis through Fas/FasL (71). In addition, the …”

Section: A Link Between H Pylori Apoptosis and Cell Proliferationmentioning

confidence: 99%

Helicobacter pylori infection and gastric mucosal epithelial cell apoptosis

Olivares

Gisbert

2005

Rev. esp. enferm. dig.

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Section: A Link Between H Pylori Apoptosis and Cell Proliferationmentioning

confidence: 99%

Helicobacter pylori infection and gastric mucosal epithelial cell apoptosis

Olivares

Gisbert

2005

Rev. esp. enferm. dig.

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“…Upregulation of proinflammatory molecule expression during H. pylori infection correlates with disease severity IFN-g has been shown to upregulate NOD1 expression via IRF1 in intestinal epithelial cells (20), and previous studies have reported that these three factors (IFN-g, NOD1, and IRF1), may be critical for the development of gastritis and Th1-type adaptive immune responses during H. pylori infection (1,3,49,50). We therefore examined the existence of a possible positive feedback mechanism between these factors, chemokine production and disease severity using gastric biopsies (Tables II, III) from subjects infected or not with H. pylori.…”

Section: H Pylori Induces Irf1 Transcription In a Cagpai-and Nod1-dementioning

confidence: 99%

Nucleotide Oligomerization Domain 1 Enhances IFN-γ Signaling in Gastric Epithelial Cells during Helicobacter pylori Infection and Exacerbates Disease Severity

Allison

Ferrand

McLeod

et al. 2013

The Journal of Immunology

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Virulent Helicobacter pylori strains that specifically activate signaling in epithelial cells via the innate immune molecule, nucleotide oligomerization domain 1 (NOD1), are more frequently associated with IFN-γ–dependent inflammation and with severe clinical outcomes (i.e., gastric cancer and peptic ulceration). In cell culture models, we showed that H. pylori activation of the NOD1 pathway caused enhanced proinflammatory signaling in epithelial cells in response to IFN-γ stimulation through the direct effects of H. pylori on two components of the IFN-γ signaling pathway, STAT1 and IFN regulatory factor 1 (IRF1). Specifically, H. pylori activation of the NOD1 pathway was shown to increase the levels of STAT1-Tyr701/Ser727 phosphorylation and IRF1 expression/synthesis in cells, resulting in enhanced production of the NOD1- and IFN-γ–regulated chemokines, IL-8– and IFN-γ–induced protein 10, respectively. Consistent with the notion that heightened proinflammatory signaling in epithelial cells may have an impact on disease severity, we observed significantly increased expression levels of NOD1, CXCL8, IRF1, and CXCL10 in human gastric biopsies displaying severe gastritis, when compared with those without gastritis (p < 0.05, p < 0.001, p < 0.01, and p < 0.05, respectively). Interestingly, NOD1, CXCL8, and IRF1 expression levels were also significantly upregulated in gastric tumor tissues, when compared with paired nontumor samples (p < 0.0001, p < 0.05, and p < 0.05, respectively). Thus, we propose that cross-talk between NOD1 and IFN-γ signaling pathways contribute to H. pylori–induced inflammatory responses, potentially revealing a novel mechanism whereby virulent H. pylori strains promote more severe disease.

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“…Furthermore, H. pylori may evade host responses through the inhibition of Ag-specific T cell proliferation. Early reports have suggested that T cells exposed to H. pylori are impaired in their ability to proliferate (9,14,19,20). More recently, Koyama and colleagues (21) have reported that gastric T cells express Fas ligand (FasL) and undergo apoptosis in situ.…”

mentioning

confidence: 99%

Negative Selection of T Cells byHelicobacter pylorias a Model for Bacterial Strain Selection by Immune Evasion

Wang

Brooks

Bamford

et al. 2001

The Journal of Immunology

102

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The majority of humans infected with Helicobacter pylori maintain a lifelong infection with strains bearing the cag pathogenicity island (PAI). H. pylori inhibits T cell responses and evades immunity so the mechanism by which infection impairs responsiveness was investigated. H. pylori caused apoptotic T cell death, whereas Campylobacter jejuni did not. The induction of apoptosis by H. pylori was blocked by an anti-Fas Ab (ZB4) or a caspase 8 inhibitor. In addition, a T cell line with the Fas rendered nonfunctional by a frame shift mutation was resistant to H. pylori-induced death. H. pylori strains bearing the cag PAI preferentially induced the expression of Fas ligand (FasL) on T cells and T cell death, whereas isogenic mutants lacking these genes did not. Inhibiting protein synthesis blocked FasL expression and apoptosis of T cells. Preventing the cleavage of FasL with a metalloproteinase inhibitor increased H. pylori-mediated killing. Thus, H. pylori induced apoptosis in Fas-bearing T cells through the induction of FasL expression. Moreover, this effect was linked to bacterial products encoded by the cag PAI, suggesting that persistent infection with this strain may be favored through the negative selection of T cells encountering specific H. pylori Ags.

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Gastric T lymphocyte responses to Helicobacter pylori in patients with H pylori colonisation.

Cited by 132 publications

References 27 publications

Helicobacter pylori infection and gastric mucosal epithelial cell apoptosis

Helicobacter pylori infection and gastric mucosal epithelial cell apoptosis

Nucleotide Oligomerization Domain 1 Enhances IFN-γ Signaling in Gastric Epithelial Cells during Helicobacter pylori Infection and Exacerbates Disease Severity

Negative Selection of T Cells byHelicobacter pylorias a Model for Bacterial Strain Selection by Immune Evasion

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