文献类型：期刊文献

英文题名：Characterization of the Japanese flounder NLRP3 inflammasome in restricting Edwardsiella piscicida colonization in vivo

作者：Chen, Hao[1];Ding, Shuangfei[1];Tan, Jinchao[1];Yang, Dahai[1,2];Zhang, Yuanxing[1,2];Liu, Qin[1,2]

机构：[1]East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[2]Shanghai Engn Res Ctr Maricultured Anim Vaccines, Shanghai 200237, Peoples R China

年份：2020

卷号：103

起止页码：169

外文期刊名：FISH & SHELLFISH IMMUNOLOGY

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000540375500020)】；

基金：This work was supported by the National Natural Science Foundation of China (31622059 to Q.L.) and the Young Elite Scientists Sponsorship Program by CAST (2016QNRC001 to D.Y.), the Fundamental Research Funds for the Central Universities, and Shanghai Engineering Research Center (19DZ2284400 to Q.L.).

语种：英文

外文关键词：Japanese flounder; NLRP3 inflammasome; Edwardsiella piscicida; Bacterial colonization

摘要：NLRP3 inflammasome is one of the most well-known inflammasomes in mammals, which plays critical roles in innate immunity. However, knowledge about this inflammasome in non-mammalian species, especially in teleost fish, remains rarely known. Herein, we established an Edwardsiella piscicida-head-kidney macrophages (HKMs) infection model in Japanese flounder, and found a robust caspase-1 activation and IL-1 beta maturation. To characterize the upstream receptor, we established a bioinformatic screening analysis, and found an NLRP3 homolog (JfNLRP3) from Japanese flounder, which shares an overall conservative structure architecture to human NLRP3. Moreover, the JfNLRP3 can assemble JfASC through PYD-PYD domain interaction and trigger JfCaspase-1 activation and JfIL-1 beta maturation. Meanwhile, the classical inflammasome activation stimulators, including nigericin, ATP or MSU, can trigger the JfCaspase-1 activation and JfIL-1 beta maturation in Japanese flounder HKMs. During intraperitoneal infection of E. piscicida in Japanese flounder, we found a dynamic upregulated transcription of JfNLRP3 and JfCaspase-1 in vivo. Furthermore, knockdown of either JfNLRP3 or JfCaspase-1 reduces the serum JfIL-1 beta level, and promotes the bacterial colonization in systemic immune organs at 2 day-post infection, while overexpression of JfNLRP3 or JfCaspase-1 hampers the bacterial colonization in these organs of Japanese flounder. Taken together, our results identified the NLRP3 inflammasome paradigm in Japanese flounder, which not only providing new insight into the molecular mechanisms of teleost NLRP3 inflammasome and revealing its role in restricting bacterial infection in vivo, but also shedding light on the evolutionary of NLRP3 inflammasome in teleost.