详细信息

ScRNA-seq reveals trained immunity-engaged Th17 cell activation against Edwardsiella piscicida-induced intestinal inflammation in teleost  ( SCI-EXPANDED收录 EI收录)  

文献类型:期刊文献

英文题名:ScRNA-seq reveals trained immunity-engaged Th17 cell activation against Edwardsiella piscicida-induced intestinal inflammation in teleost

作者:Yang, Jin[1];Cui, Shu[1];Shao, Boning[1];Zhao, Yanbo[1];Wang, Zhuang[1];Liu, Qin[1,2,3,4];Zhang, Yuanxing[1,3,4];Yang, Dahai[1,2,4]

机构:[1]East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Lab Aquat Anim Dis, Shanghai 200237, Peoples R China;[2]Qingdao Marine Sci & Technol Ctr, Lab Marine Biol & Biotechnol, Qingdao, Peoples R China;[3]Southern Marine Sci & Engn Guangdong Lab Zhuhai, Zhuhai, Peoples R China;[4]Shanghai Engn Res Ctr Maricultured Anim Vaccines, Shanghai 200237, Peoples R China

年份:2024

卷号:289

外文期刊名:MICROBIOLOGICAL RESEARCH

收录:;EI(收录号:20243917102165);WOS:【SCI-EXPANDED(收录号:WOS:001325047200001)】;

基金:This work was supported by the National Natural Science Foundation of China (32122090 to D.Y.) , the National Key Research and Develop-ment Program of China (2022YFD2402000 to D.Y., 2022YFC2804300 to D.Y.) and the Fundamental Research Funds for the Central Universities (222201231733) .

语种:英文

外文关键词:Edwardsiella piscicida; beta-Glucan; Th17 cells; Intestinal inflammation; Teleost

摘要:Mucosal immunity typically involves innate and adaptive immune cells, while the cellular mechanism of teleost's intestinal immune cells that engages gut homeostasis against bacterial infection remains largely unknown. Taking advantage of the enteric fish pathogen (Edwardsiella piscicida) infection-induced intestinal inflammation in turbot (Scophthalmus maximus), we find that beta-glucan training could mitigate the bacterial infection-induced intestinal inflammation. Through single-cell transcriptome profiling and cellular function analysis, we identify that E. piscicida infection could tune down the activation of intestinal Th17 cells, while beta-glucan-training could preserve the potential to amplify and restore the function of intestinal Th17 cells. Moreover, through pharmacological inhibitor treatment, we identify that Th17 cells are essential for ameliorating bacterial infectioninduced intestinal inflammation in teleost. Taken together, these results suggest a new concept of trained immunity activation to regulate the intestinal Th17 cells' function, which might contribute to better developing strategies for maintaining gut homeostasis against bacterial infection.

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