Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10766157 | Biochemical and Biophysical Research Communications | 2009 | 7 Pages |
Abstract
Helicobacter pylori-induced immune responses are skewed toward a T helper (Th) 1 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 IgG2a for 3 days. H. pylori infection markedly increased mRNA for IL-17A. Double immunofluorescence studies showed that IL-17A proteins were expressed on CD4+ T cells, macrophages, and dendritic cells. H. pylori infection elevated mRNAs for IL-12, IFN-γ, and TNF-α 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-γ and TNF-α, 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.
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Authors
Koji Otani, Toshio Watanabe, Tetsuya Tanigawa, Hirotoshi Okazaki, Hirokazu Yamagami, Kenji Watanabe, Kazunari Tominaga, Yasuhiro Fujiwara, Nobuhide Oshitani, Tetsuo Arakawa,