Chenodeoxycholic acid administration redirects the bile acid synthetic pathway to limit pro-inflammatory neutrophil infiltration and alleviate colitis - PubMed
5 days ago
- #bile acid
- #inflammatory bowel disease
- #neutrophil infiltration
- Patients with inflammatory bowel disease (IBD) have a dysregulated bile acid pool due to gut microbiota dysfunction.
- Colitis enhances the classical bile acid synthesis pathway while suppressing the alternative pathway.
- Oral administration of chenodeoxycholic acid (CDCA) redirects bile acid synthesis to the alternative pathway and alleviates colitis in mice.
- CDCA reduces pro-inflammatory neutrophil accumulation in the colon by downregulating epithelial-derived CXCL2.
- Lithocholic acid (LCA), a CDCA metabolite, activates colonic epithelial VDR, suppressing CXCL2 via NFκB inhibition.
- A higher cholic acid (CA) to CDCA ratio correlates with increased neutrophil counts and CXCL2 levels in IBD patients.
- CDCA is highlighted as a potential therapeutic candidate for IBD.