Enterohepatic Axis Reprogramming via S1PR2 Inhibition Activates Compensatory Microbiota-Bile Acid Crosstalk to Ameliorate Colitis
Inflammatory bowel disease (IBD) is a significant global health issue characterized by chronic intestinal inflammation. Studies have found that gut microbiota dysbiosis and bile acid metabolism play important roles in the pathogenesis of IBD, and the gut microbiota can interact with bile acid metabolism. S1PR2, a G protein-coupled receptor, has been shown to exert pro-inflammatory effects in various diseases. We have found that the S1PR2 inhibitor JTE-013 can ameliorate intestinal inflammation in DSS-induced colitis mice, though the underlying mechanism remains unclear. Therefore, this study aims to investigate whether JTE-013 alleviates murine colitis by modulating gut microbiota and/or bile acid metabolism.