文献类型：期刊文献

英文题名：The Edwardsiella piscicida thioredoxin-like protein inhibits ASK1-MAPKs signaling cascades to promote pathogenesis during infection

作者：Yang, Dahai[1,2];Liu, Xiaohong[1,2];Xu, Wenting[1];Gu, Zhaoyan[1];Yang, Cuiting[1];Zhang, Lingzhi[1];Tan, Jinchao[1];Zheng, Xin[1];Wang, Zhuang[1];Quan, Shu[1];Zhang, Yuanxing[1,2];Liu, Qin[1,2,3]

机构：[1]East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai, Peoples R China;[2]Shanghai Engn Res Ctr Maricultured Anim Vaccines, Shanghai, Peoples R China;[3]Qingdao Natl Lab Marine Sci & Technol, Lab Marine Biol & Biotechnol, Qingdao, Shandong, Peoples R China

年份：2019

卷号：15

期号：7

外文期刊名：PLOS PATHOGENS

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000478663700019)】；

基金：This work was supported by the National Natural Science Foundation of China No. 31602187 (DY) and 31430090 (YZ). DY was supported by the Young Elite Scientists Sponsorship Program by CAST No. 2016QNRC001 and Shanghai Chenguang Program No. 16CG33. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

语种：英文

摘要：It is important that bacterium can coordinately deliver several effectors into host cells to disturb the cellular progress during infection, however, the precise role of effectors in host cell cytosol remains to be resolved. In this study, we identified a new bacterial virulence effector from pathogenic Edwardsiella piscicida, which presents conserved crystal structure to thioredoxin family members and is defined as a thioredoxin-like protein (Trxlp). Unlike the classical bacterial thioredoxins, Trxlp can be translocated into host cells, mimicking endogenous thioredoxin to abrogate ASK1 homophilic interaction and phosphorylation, then suppressing the phosphorylation of downstream Erk1/2- and p38-MAPK signaling cascades. Moreover, Trxlp-mediated inhibition of ASK1-Erk/p38-MAPK axis promotes the pathogenesis of E. piscicida in zebrafish larvae infection model. Taken together, these data provide insights into the mechanism underlying the bacterial thioredoxin as a virulence effector in downmodulating the innate immune responses during E. piscicida infection.