The DOI matches its Crossref record; 20 of the 20 references it cites were found in a registry or an index.
Dysbiosis-Induced Secondary Bile Acid Deficiency Promotes Intestinal Inflammation
Open accessAbstract
SUMMARY 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 ileal pouches (surgically created resevoirs) in colectomy-treated patients with ulcerative colitis (UC) versus controls (familial adenomatous polyposis, FAP). We show relative to FAP, UC pouches have reduced levels of lithocholic acid and deoxycholic acid (normally the most abundant gut SBAs), genes required to convert PBAs to SBAs, and Ruminococcaceae (one of few taxa known to include SBA-producing bacteria). In three murine colitis models, SBA supplementation reduces intestinal inflammation. This anti-inflammatory effect is in part dependent on the TGR5 bile acid receptor. These data suggest that dysbiosis induces SBA deficiency in inflammatory-prone UC patients, which promotes a pro-inflammatory state within the intestine that may be treated by SBA restoration.
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Metadata
- Authors
- Sinha, S. R., Haileselassie, Y., Nguyen, L. P., Tropini, C., Wang, M., Becker, L. S., Sim, D., Jarr, K., Spear, E. T., Singh, G., Namkoong, H., Bittinger, K., Fischbach, M. A., Sonnenburg, J. L., & Habtezion, A.
- Venue
- Cell Host & Microbe
- Publisher
- Elsevier BV
- Published
- 2020-04
- Volume
- 27
- Issue
- 4
- Pages
- 659-670.e5
- ISSN
- 1931-3128 (ISSN-L)
- OpenAlex
- W3007555042
- Cited by
- 852
- References
- 20
- FWCI
- 7.53
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Sinha, S. R., Haileselassie, Y., Nguyen, L. P., Tropini, C., Wang, M., Becker, L. S., Sim, D., Jarr, K., Spear, E. T., Singh, G., Namkoong, H., Bittinger, K., Fischbach, M. A., Sonnenburg, J. L., & Habtezion, A. (2020). Dysbiosis-Induced Secondary Bile Acid Deficiency Promotes Intestinal Inflammation. Cell Host & Microbe. https://doi.org/10.1016/j.chom.2020.01.021
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