Dysbiosis-Induced Secondary Bile Acid Deficiency Promotes Intestinal Inflammation

• Published in: Cell host & microbe Vol. 27; no. 4; pp. 659 - 670.e5
• Main Authors: Sinha, Sidhartha R., Haileselassie, Yeneneh, Nguyen, Linh P., Tropini, Carolina, Wang, Min, Becker, Laren S., Sim, Davis, Jarr, Karolin, Spear, Estelle T., Singh, Gulshan, Namkoong, Hong, Bittinger, Kyle, Fischbach, Michael A., Sonnenburg, Justin L., Habtezion, Aida
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 08.04.2020
• Subjects: Adenomatous Polyposis Coli - microbiology; Animals; bile acids; Bile Acids and Salts - metabolism; Bile Acids and Salts - pharmacology; colitis; Colitis - etiology; Colitis - microbiology; Colonic Pouches - microbiology; Disease Models, Animal; dysbiosis; Dysbiosis - complications; Feces - microbiology; Humans; Inflammation - drug therapy; Inflammation - etiology; inflammatory bowel disease; Intestines - drug effects; Intestines - pathology; metabolomics; Metagenome; Mice; Microbiota; pouchitis; Receptors, G-Protein-Coupled - drug effects; Receptors, G-Protein-Coupled - metabolism; Ruminococcus - isolation & purification; Transcriptome; ulcerative colitis; colitis; bile acids; metabolomics; pouchitis; ulcerative colitis; inflammatory bowel disease; dysbiosis

Secondary bile acids (SBAs) are derived from primary bile acids (PBAs) in a process reliant on biosynthetic capabilities possessed by few microbes. To evaluate the role of BAs in intestinal inflammation, we performed metabolomic, microbiome, metagenomic, and transcriptomic profiling of stool from il...