The DOI matches its Crossref record; 173 of the 174 references it cites were found in a registry or an index.
Interactions between gut bacteria and bile in health and disease
Abstract
Bile acids are synthesized from cholesterol in the liver and released into the intestine to aid the digestion of dietary lipids. The host enzymes that contribute to bile acid synthesis in the liver and the regulatory pathways that influence the composition of the total bile acid pool in the host have been well established. In addition, the gut microbiota provides unique contributions to the diversity of bile acids in the bile acid pool. Gut microbial enzymes contribute significantly to bile acid metabolism through deconjugation and dehydroxylation reactions to generate unconjugated bile acids and secondary bile acids. These microbial enzymes (which include bile salt hydrolase (BSH) and bile acid-inducible (BAI) enzymes) are essential for bile acid homeostasis in the host and represent a vital contribution of the gut microbiome to host health. Perturbation of the gut microbiota in disease states may therefore significantly influence bile acid signatures in the host, especially in the context of gastrointestinal or systemic disease. Given that bile acids are ligands for host cell receptors (including the FXR, TGR5 and Vitamin D Receptor) alterations to microbial enzymes and associated changes to bile acid signatures have significant consequences for the host. In this review we examine the contribution of microbial enzymes to the process of bile acid metabolism in the host and discuss the implications for microbe-host signalling in the context of C. difficile infection, inflammatory bowel disease and other disease states.
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In the citing paper
“BA transformation by BSH-competent bacteria determines the magnitude of BA-induced nuclear FXR activation in the gut (Long et al., 2017; Sun et al., 2018).”
From Bacteroides dorei BDX-01 alleviates DSS-induced experimental colitis in mice by regulating intestinal bile salt hydrolase activity and the FXR-NLRP3 signaling pathway (2023) · cites this paper as Long et al., 2017
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“these enzymes have an important role in the enterohepatic cycling of endogenous substances such as bile acids (Long et al., 2017).”
From Gut reactions: Breaking down xenobiotic–microbiome interactions (2019) · cites this paper as Long et al., 2017
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Metadata
- Authors
- Long, S. L., Gahan, C. G. M., & Joyce, S. A.
- Affiliations
- University College Cork (IE)
- Corresponding author
- Gahan, Cormac G.M.
- Venue
- Molecular Aspects of Medicine
- Publisher
- Elsevier BV
- Published
- 2017-08
- Volume
- 56
- Pages
- 54-65
- ISSN
- 0098-2997 (ISSN-L)
- OpenAlex
- W2626300127
- Cited by
- 495
- References
- 174
- Citations by year
- 2026: 42 · 2025: 52 · 2024: 67 · 2023: 56 · 2022: 82 · 2021: 69 · 2020: 47 · 2019: 38 · 2018: 31 · 2017: 10
- FWCI
- 3.23
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular Aspects of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- APC Microbiome Institute (SFI/12/RC/2273)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Keywords
- gut microbiota, bile acids, bile acid metabolism, bile salt hydrolase, deconjugation, dehydroxylation, secondary bile acids, bile acid homeostasis, farnesoid X receptor, TGR5, vitamin D receptor, Clostridium difficile infection, inflammatory bowel disease, gut-liver axis
- MeSH terms
- Gastrointestinal Microbiome, Receptor, Farnesoid X-Activated, Amidohydrolases, Animals, Bacterial Proteins, Bile Acids and Salts, Biotransformation, Enterocolitis, Pseudomembranous, Gene Expression Regulation, Homeostasis, Humans, Intestinal Mucosa, Intestines, Liver, NADH, NADPH Oxidoreductases, Clostridioides difficile, Receptors, Cytoplasmic and Nuclear, Receptors, Calcitriol, Receptors, G-Protein-Coupled, Host-Pathogen Interactions
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