The Biological Functions of Il-17 in Different Clinical Expressions of Helicobacter Pylori-Infection Publisher Pubmed



Bagheri N¹ ; Azadegandehkordi F² ; Shirzad H² ; Rafieiankopaei M³ ; Rahimian G⁴ ; Razavi A¹
Source: Microbial Pathogenesis Published:2015

Abstract

Helicobacter pylori (H.pylori) infection is regarded as the major cause of various gastric diseases (gastritis, peptic ulcers and gastric cancer) and induces the production of several cytokines. Interleukin-17 (IL-17) is recently recognized as an important player in the pathophysiology of infectious and immune-mediated gastrointestinal diseases. H.pylori infection increases IL-17 in the gastric mucosa of humans. IL-17 usually causes secretion of IL-8 through activation of ERK 1/2 MAP kinase pathway. The released IL-8 attracts neutrophils promoting inflammation. T regulatory cells (Tregs) suppress the inflammatory reaction driven by IL-17, there by favoring bacterial persistence in H.pylori-infection. The pathogenesis of H.pylori-induced inflammation is not well understood. Inflammation is promoted by both host factors and H.pylori factors, such as the proteins cytotoxin associated gene A (cagA) and vacuolating cytotoxin A (vacA). IL-1β, IL-6, tumor necrosis factor (TNF)-α, TGF-β1, IL-17, IL-18, IL-21 and IL-22 have been reported to be involved in H.pylori-induced gastric mucosal inflammation, but the details and relation to different patterns of inflammation remain unclear. Numerous studies have demonstrated important functions of IL-17 in acute and chronic inflammatory processes. This paper reviews the role of IL-17 in gastritis, peptic ulcers and gastric cancer related to H.pylori. © 2015 Elsevier Ltd.