ArticlePhysiological reports2020
The secondary bile acids, ursodeoxycholic acid and lithocholic acid, protect against intestinal inflammation by inhibition of epithelial apoptosis.
Article in Physiological reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 139 citations in OpenAlex.
- Dysregulated bile acid metabolism impairs intestinal barrier integrity via defective GPBAR1 signaling in low-birth-weight suckling piglet.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Article
- Metabolic shifts driven by host-microbial interactions.The FEBS journal · 2026Review
- L-arabinose: a strategic modulator of pathogen virulence for food system safety.Archives of microbiology · 2026Review
- Targeting the Gut-Heart Axis in Atherosclerosis: Microbial Metabolites, Molecular Mechanisms, and Precision Therapeutics.Probiotics and antimicrobial proteins · 2026Review
- Chenodeoxycholic acid redirects the bile acid synthetic pathway to limit pro-inflammatory neutrophil infiltration and alleviate colitis.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Role of gut microbiota metabolites in maintaining intestinal health and preventing weaning-associated diarrhea in piglets.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Review
- Odoribacter laneus protects intestinal barrier by bile acid-FXR axis in acute pancreatitis.AMB Express · 2026Article
- Effects of Long-term Weightless Stimulating by Tail Suspension on the Gut Microbiota as well as the Gut-liver Axis Homeostasis in Rat.BMC microbiology · 2026Article
- The functions of gut microbiota-mediated bile acid metabolism in intestinal immunity.Journal of advanced research · 2026Review
- Multi-Omics and Molecular Docking Reveal That Oats and Oat Bran Alleviate Chronic Colitis Via IL-17 Pathway Modulation.Nutrients · 2026Article
- Lithocholic Acid Restores Gut Microbiota and Bile Acid Homeostasis to Improve Type 2 Diabetes.Nutrients · 2026Article
- Polysaccharide fromFoods (Basel, Switzerland) · 2026Article
- Toward a gut-AMPK axis: the microbiome and AMPK signaling in nutrition and healthy aging.Frontiers in physiology · 2026Review
- Secondary bile acid lithocholic acid ameliorates colitis-like inflammation in a human intestine-on-chip system.Frontiers in immunology · 2026Article
- Gut microbiota metabolites in inflammatory bowel disease: advances in mechanistic insights.Frontiers in immunology · 2026Review
- CommensalGut · 2025Article
- From gut to liver: Exploring the relationship between inflammatory bowel disease and metabolic dysfunction-associated steatotic liver disease.World journal of hepatology · 2025Review
- Host-pathobiont interactions in Crohn's disease.Nature reviews. Gastroenterology & hepatology · 2025Review
- Gut Microbiota in Heart Failure-The Role of Inflammation.Biomedicines · 2025Review
- The metabolites of gut microbiota: their role in ferroptosis in inflammatory bowel disease.European journal of medical research · 2025Review
20 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Increased epithelial permeability is a key feature of IBD pathogenesis and it has been proposed that agents which promote barrier function may be of therapeutic benefit. We have previously reported the secondary bile acid, ursodeoxycholic acid (UDCA), to be protective in a mouse model of colonic inflammation and that its bacterial metabolism is required for its beneficial effects. The current study aimed to compare the effects of UDCA, LCA, and a non-metabolizable analog of UDCA, 6-methyl-UDCA (6-MUDCA), on colonic barrier function and mucosal inflammation in a mouse model of colonic inflammation. Bile acids were administered daily to C57Bl6 mice by intraperitoneal injection. Colonic inflammation, induced by addition of DSS (2.5%) to the drinking water, was measured as disease activity index (DAI) and histological score. Epithelial permeability and apoptosis were assessed by measuring FITC-dextran uptake and caspase-3 cleavage, respectively. Cecal bile acids were measured by HPLC-MS/MS. UDCA and LCA, but not 6-MUDCA, were protective against DSS-induced increases in epithelial permeability and colonic inflammation. Furthermore, UDCA and LCA inhibited colonic epithelial caspase-3 cleavage both in DSS-treated mice and in an in vitro model of cytokine-induced epithelial injury. HPLC-MS/MS analysis revealed UDCA administration to increase colonic LCA levels, whereas LCA administration did not alter UDCA levels. UDCA, and its primary metabolite, LCA, protect against intestinal inflammation in vivo, at least in part, by inhibition of epithelial apoptosis and promotion of barrier function. These data suggest that clinical trials of UDCA in IBD patients are warranted.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.