IL‐17 is Involved in Helicobacter pylori‐Induced Gastric Inflammatory Responses in a Mouse Model

Abstract

Background: Helicobacter pylori ( H. pylori ) is the major cause of chronic active gastritis and peptic ulcer disease. Recent studies have shown that H. pylori produces various cytokines that are related to neutrophil or mononuclear cell accumulation. Interleukin-17 (IL-17) is the founding member of an emerging family of inflammatory cytokines whose biological activities remain incompletely defined. In this study, the contributions of IL-17 to the induction of gastric inflammation and to the protection from H. pylori infection were investigated using IL-17 gene-knockout

Coinfection with Enterohepatic Helicobacter Species Can Ameliorate or Promote Helicobacter pylori-Induced Gastric Pathology in C57BL/6 Mice

“…In contrast, higher mRNA levels of gastric Il-17A in HhHp mice than in mono-H. pyloriinfected mice were noted. Previous studies have established a role of a proinflammatory Th17 pathway in the development of H. pylori-induced gastric disease in mouse and gerbil models (9,42,46). Our results indicate that the H. hepaticus-associated accentuation of H. pylori-induced gastric pathology was not mediated by upregulation of the Th1 response but instead resulted from a robust Th17 response to HhHp infection.…”

“…It was previously reported that expression of Il-17A by proinflammatory Th17 cells was significantly increased in H. pylori-colonized human gastric mucosa (30). Experimental H. pylori infection in mice and gerbils also upregulated mRNA levels of gastric Il-17A (42,46). We measured and compared mRNA levels of gastric Il-17A among the infection groups in this study as well as in samples from our previous study (sham control, mono-H. pylori-infected, HbHp, and H. bilis-infected mice) (Fig.…”

Cytokine BAFF Released byHelicobacter pylori–Infected Macrophages Triggers the Th17 Response in Human Chronic Gastritis

“…Many data support the idea that the Th17 response favors the bacterial growth in mice and contributes to the inflammation both in mice and in humans (3)(4)(5), although its role is probably not essential because IFN-g has the largest effect (2). Along with this evidence, other data suggest that this response may exert a regulatory effect rather than a proinflammatory one (6).…”

The CD4+ T Cell-Mediated IFN-γ Response to Helicobacter Infection Is Essential for Clearance and Determines Gastric Cancer Risk

“…In addition (or alternatively) to IFN-␥, another proinflammatory cytokine, IL-17, has recently been assigned an important function in the mucosal response to Helicobacter infection, in particular in neutrophil recruitment. IL-17 levels are increased in the human-infected mucosa (69) as well as in vaccinated mice (59), and this seems to initiate acute inflammation in the mouse model (70). However, a conclusive functional role for IL-17 in Helicobacter control has not yet been found; on the contrary, IL-17 Ϫ/Ϫ mice seem to be less colonized than wildtype mice (70).…”

“…IL-17 levels are increased in the human-infected mucosa (69) as well as in vaccinated mice (59), and this seems to initiate acute inflammation in the mouse model (70). However, a conclusive functional role for IL-17 in Helicobacter control has not yet been found; on the contrary, IL-17 Ϫ/Ϫ mice seem to be less colonized than wildtype mice (70). Data on vaccine studies in IL-17 Ϫ/Ϫ mice are not yet available, but will hopefully clarify soon whether IL-17 is important in vaccine-induced protection.…”