The Role of Interleukin-17 in the Helicobacter pylori Induced Infection and Immunity

Abstract

Helicobacter pylori infection is regarded as the major cause of various gastric diseases and induces the production of several cytokines including interleukin-17 (IL-17) recently recognized as an important player in the mammalian immune system. This review deals with the role of IL-17 on the H. pylori-induced infection and immunity in humans and experimental animals. H. pylori infection increases IL-17 in the gastric mucosa of humans and experimental animals. In humans, IL-17 induces the secretion of IL-8 by activating the ERK 1/2 MAP kinase pathway and the released IL-8 attracts neutrophils promoting inflammation. IL-23 is increased in patients with H. pylori-related gastritis and regulates IL-17 secretion via STAT3 pathway. Studies in H. pylori-infected mice indicate that IL-17 is primarily associated with gastric inflammation. The early events in the immune response of immunized and challenged mice include the recruitment of T cells and the production of IL-17. Neutrophil attracting chemokines are released, and the bacterial load is considerably reduced. IL-17 plays a dual role in infection and vaccination. In infection, T regulatory cells (Tregs) suppress the inflammatory reaction driven by IL-17 thereby favoring bacterial persistence. Immunization produces Helicobacter-specific memory T-helper cells that can possibly alter the ratio between T-helper 17 and Treg responses so that the IL-17-driven inflammatory reaction can overcome the Treg response leading to bacterial clearance. IL-17 plays an important role in H. pylori-related gastritis and in the reduction of Helicobacter infection in mice following immunization.