{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["15"],"submitter":["Yang X"],"pubmed_abstract":["<h4>Introduction</h4><i>BTBD8</i> has been identified as a susceptible gene for inflammatory bowel diseases (IBD). However, the function of <i>BTBD8</i> in normal development and IBD pathogenesis remains unknown.<h4>Methods</h4>We administered drinking water with 3% dextran sodium sulfate (DSS) to wild-type (WT) and <i>Btbd8</i> knockout (KO) mice for seven consecutive days to induce IBD. Subsequently, we further examined whether <i>Btbd8</i> KO affects intestinal barrier and inflammation.<h4>Results</h4>We demonstrated that <i>Btbd8</i> deficiency partially protects mice from DSS-induced IBD, even though no obvious phenotypes were observed in <i>Btbd8</i> KO mice. <i>Btbd8</i> deletion leads to strengthened tight junctions between intestinal epithelial cells, elevated intestinal stem cell activity, and enhanced mucus layer. All these three mechanisms work together to improve the intestinal barrier integrity in <i>Btbd8</i> KO mice. In addition, <i>Btbd8</i> deficiency mitigates inflammation by reducing the expression of IL-1β and IL-6 by macrophages.<h4>Discussion</h4>Our studies validate the crucial role of <i>Btbd8</i> in IBD pathogenesis, and reveal that <i>Btbd8</i> deficiency may ameliorate DSS-induced IBD through improving the intestinal barrier integrity, as well as suppressing inflammatory response mediated by macrophages. These findings suggest that <i>Btbd8</i> could be a promising therapeutic target for the treatment of IBD."],"journal":["Frontiers in immunology"],"pagination":["1382661"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10978791"],"repository":["biostudies-literature"],"pubmed_title":["<i>Btbd8</i> deficiency reduces susceptibility to colitis by enhancing intestinal barrier function and suppressing inflammation."],"pmcid":["PMC10978791"],"pubmed_authors":["Yang X","Nai S","Zhao N","He Z","Chen L","Du X","Dong Q","Yu J","Duan X"],"additional_accession":[]},"is_claimable":false,"name":"<i>Btbd8</i> deficiency reduces susceptibility to colitis by enhancing intestinal barrier function and suppressing inflammation.","description":"<h4>Introduction</h4><i>BTBD8</i> has been identified as a susceptible gene for inflammatory bowel diseases (IBD). However, the function of <i>BTBD8</i> in normal development and IBD pathogenesis remains unknown.<h4>Methods</h4>We administered drinking water with 3% dextran sodium sulfate (DSS) to wild-type (WT) and <i>Btbd8</i> knockout (KO) mice for seven consecutive days to induce IBD. Subsequently, we further examined whether <i>Btbd8</i> KO affects intestinal barrier and inflammation.<h4>Results</h4>We demonstrated that <i>Btbd8</i> deficiency partially protects mice from DSS-induced IBD, even though no obvious phenotypes were observed in <i>Btbd8</i> KO mice. <i>Btbd8</i> deletion leads to strengthened tight junctions between intestinal epithelial cells, elevated intestinal stem cell activity, and enhanced mucus layer. All these three mechanisms work together to improve the intestinal barrier integrity in <i>Btbd8</i> KO mice. In addition, <i>Btbd8</i> deficiency mitigates inflammation by reducing the expression of IL-1β and IL-6 by macrophages.<h4>Discussion</h4>Our studies validate the crucial role of <i>Btbd8</i> in IBD pathogenesis, and reveal that <i>Btbd8</i> deficiency may ameliorate DSS-induced IBD through improving the intestinal barrier integrity, as well as suppressing inflammatory response mediated by macrophages. These findings suggest that <i>Btbd8</i> could be a promising therapeutic target for the treatment of IBD.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024","modification":"2025-04-19T10:13:20.12Z","creation":"2025-04-19T10:13:20.12Z"},"accession":"S-EPMC10978791","cross_references":{"pubmed":["38558797"],"doi":["10.3389/fimmu.2024.1382661"]}}