Anti-inflammatory effects of IL-17A on Helicobacter pylori-induced gastritis
Anti-inflammatory effects of IL-17A on Helicobacter pylori-induced gastritis
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DOI：
10.1016/j.bbrc.2009.02.107
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发表时间：
2009-05-01
影响因子：
3.1
通讯作者：
Arakawa, Tetsuo
中科院分区：
文献类型：
--
作者：
Otani, Koji;Watanabe, Toshio;Arakawa, Tetsuo
幽门螺杆菌诱导的免疫应答倾向于T辅助细胞（Th）I表型。最近发现了产生IL-17的Th 17细胞，我们研究了IL-17 A在H.幽门引起的胃炎接种H. pylori感染后，腹腔注射重组IL-17 A、抗IL-17 A抗体或无关IgG（2a）3天。H. pylon感染显著增加IL-17 A的mRNA。免疫荧光双标显示IL-17 A蛋白在CD（4+）T细胞、巨噬细胞和树突状细胞上表达。H.幽门螺杆菌感染使IL-12、IFN-γ和TNF-α的mRNA水平升高，髓过氧化物酶活性增加，而对IL-4和IL-5的mRNA水平无影响。IL-17 A的中和作用提高了IFN-γ和TNF-α的mRNA以及髓过氧化物酶活性，而重组IL-17 A有降低这些参数的趋势。总之，IL-17 A对H.幽门螺杆菌诱导的胃炎通过抑制Th 1分化。(C)2009 Elsevier Inc. All rights reserved.
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.