The Role of Interleukin-17 in the Helicobacter pylori Induced Infection and Immunity

Kabir, Shahjahan

doi:10.1111/j.1523-5378.2010.00812.x

Cited by 79 publications

(71 citation statements)

References 57 publications

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“…While we did not find IL-17 to be a protective innate immune response against SchuS4 infection, in a Helicobacter pylori infection model, IL-17 can be dispensable or detrimental to innate immunity, whereas vaccination can induce a protective IL-17 response (33). In our work here, we show that oral LVS vaccination provides equivalent, partial protection against morbidity and mortality following pulmonary challenge with SchuS4 in both wild-type and IL-17R␣ Ϫ/Ϫ mice.…”

Section: Discussionmentioning

confidence: 53%

Interleukin-17 Protects against the Francisella tularensis Live Vaccine Strain but Not against a Virulent F. tularensis Type A Strain

et al. 2013

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e Francisella tularensis is a highly infectious intracellular bacterium that causes the zoonotic infection tularemia. While much literature exists on the host response to F. tularensis infection, the vast majority of work has been conducted using attenuated strains of Francisella that do not cause disease in humans. However, emerging data indicate that the protective immune response against attenuated F. tularensis versus F. tularensis type A differs. Several groups have recently reported that interleukin-17 (IL-17) confers protection against the live vaccine strain (LVS) of Francisella. While we too have found that IL-17R␣ ؊/؊ mice are more susceptible to F. tularensis LVS infection, our studies, using a virulent type A strain of F. tularensis (SchuS4), indicate that IL-17R␣ ؊/؊ mice display organ burdens and pulmonary gamma interferon (IFN-␥) responses similar to those of wild-type mice following infection. In addition, oral LVS vaccination conferred equivalent protection against pulmonary challenge with SchuS4 in both IL-17R␣؊/؊ and wild-type mice. While IFN-␥ was found to be critically important for survival in a convalescent model of SchuS4 infection, IL-17 neutralization from either wild-type or IFN-␥ ؊/؊ mice had no effect on morbidity or mortality in this model. IL-17 protein levels were also higher in the lungs of mice infected with the LVS rather than F. tularensis type A, while IL23p19 mRNA expression was found to be caspase-1 dependent in macrophages infected with LVS but not SchuS4. Collectively, these results demonstrate that IL-17 is dispensable for host immunity to type A F. tularensis infection, and that induced and protective immunity differs between attenuated and virulent strains of F. tularensis.

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Section: Discussionmentioning

confidence: 53%

Interleukin-17 Protects against the Francisella tularensis Live Vaccine Strain but Not against a Virulent F. tularensis Type A Strain

et al. 2013

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“…We proposed that this Th1-independent gastritis might be attributable to IL-17 upregulation in the absence of Th1 T cells (27). Other laboratories have also suggested that IL-17 may contribute to gastritis due to H. pylori, and evidence to suggest that IL-17 does, in fact, have a role is accumulating (32)(33)(34), although the suggestion has been made that it may be regulatory rather than proinflammatory (35).…”

mentioning

confidence: 86%

“…One goal of this study was to investigate proinflammatory cytokines that may contribute to gastritis in the absence of IFN-␥-producing T cells. Our preliminary data (not shown) suggested that IL-17 was upregulated in the gastric mucosa of H. pylori-infected recipients of IFN-␥-KO CD4 T cells with gastritis, and some investigators have suggested that IL-17 is an inflammatory cytokine that promotes gastritis (32,34). In order to determine if IL-17A contributes to gastritis, we used our simple infection model to compare gastritis severity and gastric cytokine production in C57BL/6, IFN-␥ KO, IL-17A KO, and DKO mice.…”

Section: Cd25mentioning

confidence: 99%

Complex T Cell Interactions Contribute to Helicobacter pylori Gastritis in Mice

et al. 2013

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Disease due to the gastric pathogen Helicobacter pylori varies in severity from asymptomatic to peptic ulcer disease and cancer. Accumulating evidence suggests that one source of this variation is an abnormal host response. The goal of this study was to use a mouse model of H. pylori gastritis to investigate the roles of regulatory T cells (Treg) as well as proinflammatory T cells (Th1 and Th17) in gastritis, gastric T cell engraftment, and gastric cytokine production. Our results support published data indicating that severe gastritis in T cell recipient mice is due to failure of Treg engraftment, that Treg ameliorate gastritis, and that the proinflammatory response is attributable to interactions between several cell subsets and cytokines. We confirmed that gamma interferon (IFN-␥) is essential for induction of gastritis but showed that IFN-␥-producing CD4 T cells are not necessary. Interleukin 17A (IL-17A) also contributed to gastritis, but to a lesser extent than IFN-␥. Tumor necrosis factor alpha (TNF-␣) and IL-17F were also elevated in association with disease. These results indicate that while H. pylori-specific CD4 ؉ T cells and IFN-␥ are both essential for induction of gastritis due to H. pylori, IFN-␥ production by T cells is not essential. It is likely that other proinflammatory cytokines, such as IL-17F and TNF-␣, shown to be elevated in this model, also contribute to the induction of disease. We suggest that gastritis due to H. pylori is associated with loss of immunoregulation and alteration of several cytokines and cell subsets and cannot be attributed to a single immune pathway.

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“…On the other hand, elevated levels of IL21 and IL23 expression in gastric mucosa induce and sustain IL17 production [66] . Recently, a new clue for the pathogenesis of H. pylorirelated gastric inflammation and GC is impairment of ghrelin synthesis in H. pyloricolonized stomach.…”

Section: Cytokines Secretionmentioning

confidence: 99%

“…IL17 can enhance expression of IL8 in epithelial cells [66] . On the other hand, elevated levels of IL21 and IL23 expression in gastric mucosa induce and sustain IL17 production [66] .…”

Section: Cytokines Secretionmentioning

confidence: 99%

Role ofHelicobacter pyloriinfection in pathogenesis of gastric carcinoma

Zhang

Fan

Chen

2016

WJGP

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Gastric cancer (GC) is one of the most common carcino ma and the second leading cause of cancerrelated deaths worldwide. Helicobacter pylori (H. pylori ) infection causes a series of precancerous lesions like gastritis, atrophy, intestinal metaplasia and dysplasia, and is the strongest known risk factor for GC, as supported by epidemiological, preclinical and clinical studies. However, the mechanism of H. pylori developing gastric carcinoma has not been well defined. Among infected individuals, approximately 10% develop severe gastric lesions such as peptic ulcer disease, 1%3% progresses to GC.

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The Role of Interleukin-17 in the Helicobacter pylori Induced Infection and Immunity

Abstract: IL-17 plays an important role in H. pylori-related gastritis and in the reduction of Helicobacter infection in mice following immunization.

Cited by 79 publications

References 57 publications

Interleukin-17 Protects against the Francisella tularensis Live Vaccine Strain but Not against a Virulent F. tularensis Type A Strain

Interleukin-17 Protects against the Francisella tularensis Live Vaccine Strain but Not against a Virulent F. tularensis Type A Strain

Complex T Cell Interactions Contribute to Helicobacter pylori Gastritis in Mice

Role ofHelicobacter pyloriinfection in pathogenesis of gastric carcinoma

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