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

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2009年 / 382卷 / 02期

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

页码：252 / 258

页数：7

共 25 条

[1] Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17 [J].