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. 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.
['Bagheri|Nader|N|', 'Azadegan-Dehkordi|Fatemeh|F|', 'Shirzad|Hedayatollah|H|', 'Rafieian-Kopaei|Mahmoud|M|', 'Rahimian|Ghorbanali|G|', 'Razavi|Alireza|A|']
D005753:Gastric Mucosa D016481:Helicobacter Infections D016480:Helicobacter pylori D054884:Host-Pathogen Interactions D006801:Humans D007108:Immune Tolerance D007249:Inflammation D020381:Interleukin-17
Helicobacter pylori Gastritis Peptic ulcers Gastric cancer Interleukin-17