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

• Helicobacter pylori infection is regarded as the major cause of various gastric diseases.
• Inflammation is promoted by host factors and H. pylori factors.
• VacA and cagA are important virulence factor involving in gastric diseases.
• IL-17 is recognized as an important player in infectious diseases.
• IL-17 has been reported to be involved in various gastric diseases.

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.