期刊
FISH & SHELLFISH IMMUNOLOGY
卷 94, 期 -, 页码 58-65出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fsi.2019.08.069
关键词
Yersinia ruckeri; TIR; TcpA; MyD88; Immune evasion
资金
- Program for Changjiang Scholars and Innovative Research Team in University [IRT0848]
- Science and Technology Support Program by Science and Technology Department of Sichuan Province [2014NZ0003]
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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