Anti-inflammatory effects of IL-17A on Helicobacter pylori-induced gastritis

作者：Otani Koji^*; Watanabe Toshio; Tanigawa Tetsuya; Okazaki Hirotoshi; Yarnagami Hirokazu; Watanabe Kenji; Tominaga Kazunari; Fujiwara Yasuhiro; Oshitani Nobuhide; Arakawa Tetsuo

来源：Biochemical and Biophysical Research Communications, 2009, 382(2): 252-258.

DOI：10.1016/j.bbrc.2009.02.107

• Helicobacter pylori
• IL-17A
• Mouse

Helicobacter pylori-induced immune responses are skewed toward a T helper (Th) I phenotype. IL-17-producing Th17 cells have recently been discovered, and we examined the role of IL-17A in H. pylori-induced gastritis. Six months after inoculation with H. pylori, the mice received an intraperitoneal injection of recombinant IL-17A, anti-IL-17A antibody or irrelevant IgG(2a) for 3 days. H. pylon infection markedly increased mRNA for IL-17A. Double immunofluorescence studies showed that IL-17A proteins were expressed on CD(4+) T cells, macrophages, and dendritic cells. H. pylori infection elevated mRNAs for IL-12, IFN-gamma, and TNF-alpha with increase in myeloperoxidase activity, whereas it did not affect mRNAs for IL-4 and IL-5. Neutralization of IL-17A elevated mRNAs for IFN-gamma and TNF-alpha, and myeloperoxidase activity, whereas recombinant IL-17A had a tendency to reduce these parameters. In conclusion, IL-17A exerts anti-inflammatory effects on H. pylori-induced gastritis through suppression of Th1 differentiation.

• 出版日期2009-5-1