{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["12"],"submitter":["Zhang B"],"pubmed_abstract":["Clonorchiasis caused by <i>Clonorchis sinensis</i> is a mainly foodborne parasitic disease. It can lead to hepatobiliary duct inflammation, fibrosis, obstructive jaundice, liver cirrhosis, and even cholangiocarcinoma. Interleukin (IL)-10 is an immune-regulatory cytokine which plays an immunosuppressive role during infection. Our previous study found that IL-10 was increased in mice with <i>C. sinensis</i> infection. However, the role and mechanism of IL-10 playing in hepatobiliary injury induced by <i>C. sinensis</i> infection remain unknown. Herein, <i>Il10<sup>+/+</sup></i> mice and <i>Il10<sup>+/-</sup></i> C57BL/6J mice were infected with <i>C. sinensis</i>. It was found that IL-10 deficiency aggravated biliary hyperplasia and exacerbated periductal fibrosis induced by <i>C. sinensis</i> infection. Moreover, IL-10 deficiency increased CD4<sup>+</sup>T cells and CD8<sup>+</sup>T cells but not macrophages in the liver of mice with infection. There were no apparent differences in Th1 and Treg cells between <i>Il10<sup>+/+</sup></i> and <i>Il10<sup>+/-</sup></i> mice infected with <i>C. sinensis</i>. However, the proportion of Th17 cells in CD4<sup>+</sup>T cells in <i>Il10<sup>+/-</sup></i> infected mice was significantly higher than that in <i>Il10<sup>+/+</sup></i> infected mice. IL-10 deficiency also enhanced the increase of Th17 cells induced by ESPs stimulation <i>in vitro</i>. Taken together, our results suggest that IL-10 plays a protective role in hepatobiliary injury in C57BL/6J mice induced by <i>C. sinensis</i> infection <i>via</i> inhibiting Th17 cells, which could deepen our understanding of the immunopathology of clonorchiasis."],"journal":["Frontiers in cellular and infection microbiology"],"pagination":["994838"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9606589"],"repository":["biostudies-literature"],"pubmed_title":["IL-10 regulates Th17 response to inhibit hepatobiliary injury caused by <i>Clonorchis sinensis</i> infection in C57BL/6J mice."],"pmcid":["PMC9606589"],"pubmed_authors":["Li J","Liu M","Yu Q","Yu G","Wang J","Xu J","Hua H","Jiang Z","Koda S","Zhao Q","Zheng KY","Yan C","Zhang B","Xu YH"],"additional_accession":[]},"is_claimable":false,"name":"IL-10 regulates Th17 response to inhibit hepatobiliary injury caused by <i>Clonorchis sinensis</i> infection in C57BL/6J mice.","description":"Clonorchiasis caused by <i>Clonorchis sinensis</i> is a mainly foodborne parasitic disease. It can lead to hepatobiliary duct inflammation, fibrosis, obstructive jaundice, liver cirrhosis, and even cholangiocarcinoma. Interleukin (IL)-10 is an immune-regulatory cytokine which plays an immunosuppressive role during infection. Our previous study found that IL-10 was increased in mice with <i>C. sinensis</i> infection. However, the role and mechanism of IL-10 playing in hepatobiliary injury induced by <i>C. sinensis</i> infection remain unknown. Herein, <i>Il10<sup>+/+</sup></i> mice and <i>Il10<sup>+/-</sup></i> C57BL/6J mice were infected with <i>C. sinensis</i>. It was found that IL-10 deficiency aggravated biliary hyperplasia and exacerbated periductal fibrosis induced by <i>C. sinensis</i> infection. Moreover, IL-10 deficiency increased CD4<sup>+</sup>T cells and CD8<sup>+</sup>T cells but not macrophages in the liver of mice with infection. There were no apparent differences in Th1 and Treg cells between <i>Il10<sup>+/+</sup></i> and <i>Il10<sup>+/-</sup></i> mice infected with <i>C. sinensis</i>. However, the proportion of Th17 cells in CD4<sup>+</sup>T cells in <i>Il10<sup>+/-</sup></i> infected mice was significantly higher than that in <i>Il10<sup>+/+</sup></i> infected mice. IL-10 deficiency also enhanced the increase of Th17 cells induced by ESPs stimulation <i>in vitro</i>. Taken together, our results suggest that IL-10 plays a protective role in hepatobiliary injury in C57BL/6J mice induced by <i>C. sinensis</i> infection <i>via</i> inhibiting Th17 cells, which could deepen our understanding of the immunopathology of clonorchiasis.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022","modification":"2025-04-04T09:41:48.963Z","creation":"2025-04-04T09:41:48.963Z"},"accession":"S-EPMC9606589","cross_references":{"pubmed":["36310865"],"doi":["10.3389/fcimb.2022.994838"]}}