文献类型：期刊文献

英文题名：EvpP inhibits neutrophils recruitment via Jnk-caspy inflammasome signaling in vivo

作者：Tan, Jinchao[1];Yang, Dahai[1,3];Wang, Zhuang[1];Zheng, Xin[1];Zhang, Yuanxing[1,3];Liu, Qin[1,2,3]

机构：[1]East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[2]Qingdao Natl Lab Marine Sci & Technol, Lab Marine Biol & Biotechnol, Qingdao 266071, Shandong, Peoples R China;[3]Shanghai Engn Res Ctr Maricultured Anim Vaccines, Shanghai 200237, Peoples R China

年份：2019

卷号：92

起止页码：851

外文期刊名：FISH & SHELLFISH IMMUNOLOGY

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000483634300092)】；

基金：This work was supported by the National Natural Science Foundation of China No. 31472308, 31622059 (Q.L.) and the Fundamental Research Funds for the Central Universities No. 222201714022 (D.Y.). Dahai Yang was supported by the Young Elite Scientists Sponsorship Program by CAST No. 2016QNRC001, Shanghai Pujiang Program No.16PJD020, Shanghai Chenguang Program No.16CG33, and the Talent Program of the School of Biotechnology of the East China University of Science and Technology, Shanghai, China.

语种：英文

外文关键词：Edwardsiella piscicida; T6SS effector; Jnk-caspy inflammasome pathway; Neutrophils recruitment

摘要：Innate immunity is regulated by phagocytic cells and is critical for host control of bacterial infection. In many bacteria, the type VI secretion system (T6SS) can affect bacterial virulence in certain environments, but little is known about the mechanisms underlying T6SS regulation of innate immune responses during infection in vivo. Here, we developed an infection model by microinjecting bacteria into the tail vein muscle of 3-day-post-fertilized zebrafish larvae, and found that both macrophages and neutrophils are essential for bacterial clearance. Further study revealed that EvpP plays a critical role in promoting the pathogenesis of Edwardsiella piscicida (E. piscicida) via inhibiting the phosphorylation of Ink signaling to reduce the expression of chemokine (CXC motif) ligand 8 (cxcl8a), matrix metallopeptidase 13 (rmip13) and interleukin-1 beta (IL-10) in vivo. Subsequently, by utilizing Tg (mpo:eGFP(+/+)) zebrafish larvae for E. piscicida infection, we found that the EvpP-inhibited Jnk-caspy (caspase-1 homolog) inflammasome signaling axis significantly suppressed the recruitment of neutrophils to infection sites, and the caspy- or /L-1 beta-morpholino (MO) knockdown larvae were more susceptible to infection and failed to restrict bacterial colonization in vivo. taken together, this interaction improves our understanding about the complex and contextual role of a bacterial T6SS effector in modulating the action of neutrophils during infection, and offers new insights into the warfare between bacterial weapons and host immunological surveillance.