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

被引:48
作者
Otani, Koji [1 ]
Watanabe, Toshio [1 ]
Tanigawa, Tetsuya [1 ]
Okazaki, Hirotoshi [1 ]
Yarnagami, Hirokazu [1 ]
Watanabe, Kenji [1 ]
Tominaga, Kazunari [1 ]
Fujiwara, Yasuhiro [1 ]
Oshitani, Nobuhide [1 ]
Arakawa, Tetsuo [1 ]
机构
[1] Osaka City Univ, Dept Gastroenterol, Grad Sch Med, Abeno Ku, Osaka 5458585, Japan
关键词
Helicobacter pylori; IL-17A; Mouse; INDUCED COLITIS; MOUSE MODEL; INTERLEUKIN-17; INFLAMMATION; MICE; CELLS; DISTINCT; PATHOGENESIS; INFECTION; LINEAGE;
D O I
10.1016/j.bbrc.2009.02.107
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:252 / 258
页数:7
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