Tauroursodeoxycholic Acid Inhibits Clostridioides difficile Toxin-Induced Apoptosis

التفاصيل البيبلوغرافية
العنوان: Tauroursodeoxycholic Acid Inhibits Clostridioides difficile Toxin-Induced Apoptosis
المؤلفون: Colleen M. Pike, John Tam, Roman A. Melnyk, Casey M. Theriot
المصدر: Infection and immunity. 90(8)
سنة النشر: 2022
مصطلحات موضوعية: Inflammation, Clostridioides difficile, Immunology, Ursodeoxycholic Acid, Apoptosis, Microbiology, Antibodies, Bacterial, Anti-Bacterial Agents, Bile Acids and Salts, Taurochenodeoxycholic Acid, Infectious Diseases, Clostridium Infections, Humans, Parasitology, Caco-2 Cells
الوصف: C. difficile infection (CDI) is a highly inflammatory disease mediated by the production of two large toxins that weaken the intestinal epithelium and cause extensive colonic tissue damage. Antibiotic alternative therapies for CDI are urgently needed as current antibiotic regimens prolong the perturbation of the microbiota and lead to high disease recurrence rates. Inflammation is more closely correlated with CDI severity than bacterial burden, thus therapies that target the host response represent a promising yet unexplored strategy for treating CDI. Intestinal bile acids are key regulators of gut physiology that exert cytoprotective roles in cellular stress, inflammation, and barrier integrity, yet the dynamics between bile acids and host cellular processes during CDI have not been investigated. Here we show that several bile acids are protective against apoptosis caused by C. difficile toxins in Caco-2 cells and that protection is dependent on conjugation of bile acids. Out of 20 tested bile acids, taurine conjugated ursodeoxycholic acid (TUDCA) was the most potent inhibitor, yet unconjugated UDCA did not alter toxin-induced apoptosis. TUDCA treatment decreased expression of genes in lysosome associated and cytokine signaling pathways. TUDCA did not affect C. difficile growth or toxin activity
تدمد: 1098-5522
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7b532844f3ea4d34fcadc31c5141b6ffTest
https://pubmed.ncbi.nlm.nih.gov/35862710Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....7b532844f3ea4d34fcadc31c5141b6ff
قاعدة البيانات: OpenAIRE
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