Eimeria tenella: Interleukin 17 contributes to host immunopathology in the gut during experimental infection

文献类型： 外文期刊

第一作者： Liu, Renqiang

作者： Liu, Renqiang;Song, Meng;Hu, Yanxin;Pan, Baoliang;Wang, Ming;Zhang, Lei;Wang, Ming;Cai, Jianping;Cai, Jianping

作者机构：

关键词： Eimeria tenella;IL-17;Realtime PCR;Antibody neutralization;Chicken

期刊名称：EXPERIMENTAL PARASITOLOGY （ 影响因子：2.011； 五年影响因子：2.132 ）

ISSN： 0014-4894

年卷期： 2013 年 133 卷 2 期

页码：

收录情况： SCI

摘要： Although IL-17 is a key factor in Th17 lineage host responses and plays critical roles in immunological control of a variety of infectious diseases, the contribution of IL-17 to immune function during Eimeria tenella infection is unknown. In the present study, we used an experimental E. tenella infection model to clarify the role of Th17-associated response in the resulting immune response by quantitative real-time PCR assays. We observed robust production of STAT-3 (the transcription factors), IL-1 beta, IL-6 and IL-17 in cecal intraepithelial lymphocytes during the early infection, peaking at 6 h p.i. and declining thereafter. The expression of TGF-beta was moderately upregulated and had 2 peaks at 6 and 72 h p.i. during the early infection. To further investigate the role of chIL-17 during the infection, we treated the infected chickens with IL-17 and its neutralized antibody. As a result, the reduced fecal oocyst shedding and cecal lesion scores, but enhanced body weight gains were observed in IL-17 neutralized chickens. The results of histopathology showed that the neutrophils recruitment diminished and the parasite burden in IL-17 neutralized chickens decreased. These results may be due to the significant decrease in the production of IL-17, IL-6 and TGF-beta, but enhanced IL-12 and IFN-gamma expression in IL-17 neutralized chickens. The converse results were shown in IL-17 treated infected-chickens in which chickens showed increased fecal oocyst shedding, exacerbated lesion scores, and reduced body weight gains. These results suggested that chicken IL-17 might mediate E. tenella - induced immunopathology during the infection. (C) 2012 Elsevier Inc. All rights reserved.

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