The biological functions of IL-17 in different clinical expressions of Helicobacter pylori-infection

Microbial Pathogenesis
Nader BagheriAlireza Razavi

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 fun...Continue Reading

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Citations

Feb 9, 2016·Immunological Investigations·Nader BagheriHedayatollah Shirzad
Nov 26, 2015·Genetic Testing and Molecular Biomarkers·Yunjie LuChuanyong Zhang
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