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The G protein-coupled bile acid receptor 1 (TGR5) is a membrane receptor with well-known roles in the regulation of glucose metabolism and energy homeostasis. However, the role and mechanism of TGR5 in the context of inflammation during CHI remains unclear. Wild-type (WT) and TGR5 knockout (TGR5\u2212\/\u2212) mice with CHI induced by bile duct ligation (BDL) were involved in vivo, and WT and TGR5\u2212\/\u2212 bone marrow-derived macrophages (BMDMs) were used in vitro. TGR5 deficiency significantly exacerbated BDL-induced liver injury, inflammatory responses and hepatic fibrosis compared with WT mice in vivo. TGR5\u2212\/\u2212 macrophages were more susceptible to lipopolysaccharide (LPS) stimulation than WT macrophages. TGR5 activation by its ligand suppressed LPS-induced pro-inflammatory responses in WT but not TGR5\u2212\/\u2212 BMDMs. Notably, expression of \u03b2-catenin was effectively inhibited by TGR5 deficiency. Furthermore, TGR5 directly interacted with Gsk3\u03b2 to repress the interaction between Gsk3\u03b2 and \u03b2-catenin, thus disrupting the \u03b2-catenin destruction complex. The pro-inflammatory nature of TGR5-knockout was almost abolished by lentivirus-mediated \u03b2-catenin overexpression in BMDMs. BMDM migration in vitro was accelerated under TGR5-deficient conditions or supernatant from LPS-stimulated TGR5\u2212\/\u2212 BMDMs. From a therapeutic perspective, TGR5\u2212\/\u2212 BMDM administration aggravated BDL-induced CHI, which was effectively rescued by \u03b2-catenin overexpression. Our findings reveal that TGR5 plays a crucial role as a novel regulator of immune-mediated CHI by destabilizing the \u03b2-catenin destruction complex, with therapeutic implications for the management of human CHI.<\/jats:p>","DOI":"10.1093\/intimm\/dxaa002","type":"journal-article","created":{"date-parts":[[2020,1,10]],"date-time":"2020-01-10T12:14:06Z","timestamp":1578658446000},"page":"321-334","source":"Crossref","is-referenced-by-count":29,"title":["Deficiency of TGR5 exacerbates immune-mediated cholestatic hepatic injury by stabilizing the \u03b2-catenin destruction complex"],"prefix":"10.1093","volume":"32","author":[{"given":"Jianhua","family":"Rao","sequence":"first","affiliation":[{"name":"Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China"},{"name":"NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chao","family":"Yang","sequence":"additional","affiliation":[{"name":"Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China"},{"name":"NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shikun","family":"Yang","sequence":"additional","affiliation":[{"name":"Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China"},{"name":"NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hao","family":"Lu","sequence":"additional","affiliation":[{"name":"Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China"},{"name":"NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuanchang","family":"Hu","sequence":"additional","affiliation":[{"name":"Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China"},{"name":"NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ling","family":"Lu","sequence":"additional","affiliation":[{"name":"Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China"},{"name":"NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Feng","family":"Cheng","sequence":"additional","affiliation":[{"name":"Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China"},{"name":"NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuehao","family":"Wang","sequence":"additional","affiliation":[{"name":"Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China"},{"name":"NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2020,1,13]]},"reference":[{"key":"2021121313483337900_CIT0001","doi-asserted-by":"crossref","first-page":"908","DOI":"10.1002\/hep.27085","article-title":"Conjugated bile acids promote cholangiocarcinoma cell invasive growth through activation of sphingosine 1-phosphate receptor 2","volume":"60","author":"Liu","year":"2014","journal-title":"Hepatology"},{"key":"2021121313483337900_CIT0002","doi-asserted-by":"crossref","first-page":"1509","DOI":"10.1194\/jlr.R900007-JLR200","article-title":"Bile acids as regulatory molecules","volume":"50","author":"Hylemon","year":"2009","journal-title":"J. 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