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

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. Helicobacter 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 Helicobacter pylori-infection. The pathogenesis of Helicobacter pylori-induced inflammation is not well understood. Inflammation is promoted by both host factors and Helicobacter pylori factors, such as the proteins cytotoxin associated gene A (cagA) and vacuolating cytotoxin A (vacA). IL-1 beta, IL-6, tumor necrosis factor (TNF)-alpha, TGF-beta 1, IL-17, IL-18, IL-21 and IL-22 have been reported to be involved in Helicobacter 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 Helicobacter pylori. (C) 2015 Elsevier Ltd. All rights reserved.