Jin Yang , Shu Cui , Boning Shao , Yanbo Zhao , Zhuang Wang , Qin Liu , Yuanxing Zhang , Dahai Yang
{"title":"ScRNA-seq揭示了训练有素的免疫激活Th17细胞对鱼腥藻诱发的肠道炎症的抑制作用","authors":"Jin Yang , Shu Cui , Boning Shao , Yanbo Zhao , Zhuang Wang , Qin Liu , Yuanxing Zhang , Dahai Yang","doi":"10.1016/j.micres.2024.127912","DOIUrl":null,"url":null,"abstract":"<div><div>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 (<em>Edwardsiella piscicida</em>) infection-induced intestinal inflammation in turbot (<em>Scophthalmus maximus</em>), we find that β-glucan training could mitigate the bacterial infection-induced intestinal inflammation. Through single-cell transcriptome profiling and cellular function analysis, we identify that <em>E. piscicida</em> infection could tune down the activation of intestinal Th17 cells, while β-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 infection-induced 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.</div></div>","PeriodicalId":18564,"journal":{"name":"Microbiological research","volume":"289 ","pages":"Article 127912"},"PeriodicalIF":6.1000,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"ScRNA-seq reveals trained immunity-engaged Th17 cell activation against Edwardsiella piscicida-induced intestinal inflammation in teleost\",\"authors\":\"Jin Yang , Shu Cui , Boning Shao , Yanbo Zhao , Zhuang Wang , Qin Liu , Yuanxing Zhang , Dahai Yang\",\"doi\":\"10.1016/j.micres.2024.127912\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>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 (<em>Edwardsiella piscicida</em>) infection-induced intestinal inflammation in turbot (<em>Scophthalmus maximus</em>), we find that β-glucan training could mitigate the bacterial infection-induced intestinal inflammation. Through single-cell transcriptome profiling and cellular function analysis, we identify that <em>E. piscicida</em> infection could tune down the activation of intestinal Th17 cells, while β-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 infection-induced 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.</div></div>\",\"PeriodicalId\":18564,\"journal\":{\"name\":\"Microbiological research\",\"volume\":\"289 \",\"pages\":\"Article 127912\"},\"PeriodicalIF\":6.1000,\"publicationDate\":\"2024-09-21\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Microbiological research\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0944501324003136\",\"RegionNum\":1,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"MICROBIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Microbiological research","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0944501324003136","RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"MICROBIOLOGY","Score":null,"Total":0}
ScRNA-seq reveals trained immunity-engaged Th17 cell activation against Edwardsiella piscicida-induced intestinal inflammation in teleost
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 β-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 β-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 infection-induced 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.
期刊介绍:
Microbiological Research is devoted to publishing reports on prokaryotic and eukaryotic microorganisms such as yeasts, fungi, bacteria, archaea, and protozoa. Research on interactions between pathogenic microorganisms and their environment or hosts are also covered.