Characterization of grass carp (Ctenopharyngodon idella) IL-17D: Molecular cloning, functional implication and signal transduction

被引:48
|
作者
Du, Linyong [1 ]
Qin, Lei [1 ]
Wang, Xinyan [1 ]
Zhang, Anying [1 ]
Wei, He [1 ]
Zhou, Hong [1 ]
机构
[1] Univ Elect Sci & Technol China, Sch Life Sci & Technol, Chengdu 610054, Peoples R China
来源
基金
中国国家自然科学基金;
关键词
IL-17D; Expression analysis; Bioactivity; Signal transduction; Grass carp; INTERLEUKIN-17; FAMILY-MEMBERS; EXPRESSION ANALYSIS; IMMUNE-RESPONSE; TNF-ALPHA; CYTOKINE; GENE; IDENTIFICATION; INVOLVEMENT; ACTIVATION; ZEBRAFISH;
D O I
10.1016/j.dci.2013.09.015
中图分类号
S9 [水产、渔业];
学科分类号
0908 ;
摘要
Although the roles of IL-17 family members during inflammation have been extensively studied in mammals, their knowledge in lower vertebrates is limited. In particular, the biological activities of fish IL-17 and their functional roles are largely unknown. In this study, we cloned grass carp IL-17D (gcIL-17D) and found that its putative protein possessed the conserved features of IL-17 family members. Tissue distribution analysis showed that gcIL-17D was preferentially expressed in the mucosal tissues, including skin, gill and intestine. Subsequently, the involvement of gclL-17D in inflammatory response was demonstrated by examining the expression profiles of gcIL-17D in head kidney and head kidney leukocytes following in vivo bacterial infection and in vitro LPS treatment, respectively. Furthermore, recombinant gcIL-17D (rgcIL-17D) was prepared in grass carp kidney cells and was able to promote the gene expression of some pro-inflammatory cytokines (IL-1 beta TNF-alpha and CXCL-8) in grass carp primary head kidney cells, revealing gcIL-17D can function as a pro-inflammatory cytokine. Moreover, rgclL-17D appeared to activate NF-kappa B signaling by modulating the phosphorylation of I kappa B alpha and up-regulated CXCL-8 mRNA expression possibly through NF-kappa B pathway. Our data shed new light on the functional role of teleost IL-17D in inflammatory response. (C) 2013 Elsevier Ltd. All rights reserved.
引用
收藏
页码:220 / 228
页数:9
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