TcpA, a novel Yersinia ruckeri TIR-containing virulent protein mediates immune evasion by targeting MyD88 adaptors
文献类型： 外文期刊
作者： Liu, Tao 1 ; Wang, Erlong 1 ; Wei, Wenyan 3 ; Wang, Kaiyu 1 ; Yang, Qian 1 ; Ai, Xiaohui 4 ;
作者机构： 1.Sichuan Agr Univ, Vet Med Coll, Dept Basic Vet, Chengdu, Sichuan, Peoples R China
2.Sichuan Agr Univ, Key Lab Anim Dis & Human Hlth Sichuan Prov, Chengdu, Sichuan, Peoples R China
3.Chengdu Agr & Forestry Acad, Inst Fisheries, Chengdu, Sichuan, Peoples R China
4.Chinese Acad Fishery Sci, Yangtze River Fisheries Res Inst, Wuhan, Hubei, Peoples R China
关键词： Yersinia ruckeri; TIR; TcpA; MyD88; Immune evasion
期刊名称：FISH & SHELLFISH IMMUNOLOGY （ 影响因子：4.581； 五年影响因子：4.851 ）
ISSN： 1050-4648
年卷期： 2019 年 94 卷
页码：
收录情况： SCI
摘要： TIR domain-containing protein is an important member for some bacterial pathogens to subvert host defenses. Here we described a fish virulent Yersinia rucked SC09 strain that interfered directly with Toll-like receptor (TLR) function by a TIR-containing protein. Firstly, the novel TIR-containing protein was identified by bioinformatics analysis and named as TcpA. Secondly, the toxic effects of TcpA in fish was demonstrated in vivo challenge experiments through knockout mutant and complement mutant of tcpA gene. Thirdly, The study in vivo revealed that TcpA could down-regulate the expression and secretion of IL-6, IL-1 beta and TNF-alpha. Finally, we demonstrated that TcpA could inhibit the TLR signaling pathway through interaction with myeloid differentiation factor 88 (MyD88) in experiments such as NF-kappa B dependent luciferase reporter system, co-immunoprecipitation, GST pulldown and yeast two-hybrid. The study revealed that TcpA was essential for virulence and was able to interact with the TIR adaptor protein MyD88 and inhibit the pre-inflammatory signal of immune cells and promote the intracellular survival of pathogenic Yersinia ruckeri SCO9 strain. In conclusion, our results showed that TcpA acted as a new virulence factor in Y. ruckeri could suppress innate immune response and increase virulence by inhibiting TLR and MyD88-mediated specific signaling, highlighting a novel strategy for innate immune evasion in bacteria.
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