Microbial bile acid metabolites modulate gut RORγ+ regulatory T cell homeostasis
Open accessAbstract
The metabolic pathways encoded by the human gut microbiome constantly interact with host gene products through numerous bioactive molecules1. Primary bile acids (BAs) are synthesized within hepatocytes and released into the duodenum to facilitate absorption of lipids or fat-soluble vitamins2. Some BAs (approximately 5%) escape into the colon, where gut commensal bacteria convert them into various intestinal BAs2 that are important hormones that regulate host cholesterol metabolism and energy balance via several nuclear receptors and/or G-protein-coupled receptors3,4. These receptors have pivotal roles in shaping host innate immune responses1,5. However, the effect of this host–microorganism biliary network on the adaptive immune system remains poorly characterized. Here we report that both dietary and microbial factors influence the composition of the gut BA pool and modulate an important population of colonic FOXP3+ regulatory T (Treg) cells expressing the transcription factor RORγ. Genetic abolition of BA metabolic pathways in individual gut symbionts significantly decreases this Treg cell population. Restoration of the intestinal BA pool increases colonic RORγ+ Treg cell counts and ameliorates host susceptibility to inflammatory colitis via BA nuclear receptors. Thus, a pan-genomic biliary network interaction between hosts and their bacterial symbionts can control host immunological homeostasis via the resulting metabolites. Both dietary and microbial factors influence the composition of the gut bile acid pool, which in turn modulates the frequencies and functionalities of RORγ-expressing colonic FOXP3+ regulatory T cells, contributing to protection from inflammatory colitis.
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There is an important bidirectional relationship between intestinal microbiota and bile acids.
“In recent years, it has been found that there is an important bidirectional relationship between intestinal microbiota and bile acids.”
From The role of gut dysbiosis in Parkinson’s disease: mechanistic insights and therapeutic options (2021) · cites this paper as [206]
The Abstract reports that gut bacteria convert primary bile acids into intestinal bile acids and that microbial factors influence the gut bile-acid pool. It does not establish the reverse direction—that bile acids affect the intestinal microbiota—so it supports an interaction but not the claimed bidirectional relationship. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe gut microbiome regulates the activity of RORγ+ Treg cells, and dysregulation of these cells can lead to diseases such as colitis, food allergy, and colon cancer.
“In addition, the gut microbiome regulates the activity of retinoic acid receptor-related orphan receptor gamma-positive (RORγ+) Treg cells, dysregulation of which can lead to diseases such as colitis, food allergy, and colon cancer.622,701–704”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [702]
Microbiota-derived secondary bile acids regulate gut RORγ+ regulatory T cell homeostasis.
“A recent work showed that microbiota-derived secondary bile acids regulate gut RORγ+ regulatory T cell homeostasis.115”
From Interaction between microbiota and immunity in health and disease (2020) · cites this paper as [115]
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- Authors
- Song, X., Sun, X., Oh, S. F., Wu, M., Zhang, Y., Zheng, W., Geva-Zatorsky, N., Jupp, R., Mathis, D., Benoist, C., & Kasper, D. L.
- Affiliations
- Harvard University (US)
- Brigham and Women's Hospital (US)
- UCB Pharma (United Kingdom) (GB)
- Corresponding author
- Kasper, Dennis L.
- ORCID
- Venue
- Nature
- Published
- 2019-12-25
- Volume
- 577
- Issue
- 7790
- Pages
- 410-415
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC7274525
- OpenAlex
- W2997490540
- Semantic Scholar
- d1182c47b88ba7d85c1444019d3f773e56152e74
- Cited by
- 1,024
- References
- 34
- Citations by year
- 2026: 137 · 2025: 188 · 2024: 174 · 2023: 150 · 2022: 150 · 2021: 145 · 2020: 80
- FWCI
- 31.18
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Institutes of Health (5k01dk102771-05)
- National Institute of Allergy and Infectious Diseases (R01AI125603)
- National Institute of Diabetes and Digestive and Kidney Diseases (K01-DK102771)
- National Center for Complementary and Integrative Health (R01AT010268)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Keywords
- bile acids, gut microbiota, Foxp3+ regulatory T cells, bile acid metabolism, host-microbe interactions, inflammatory colitis, dietary bile acids, gut symbionts
- MeSH terms
- Gastrointestinal Microbiome, Animals, Bile Acids and Salts, Homeostasis, Intestines, Mice, Inbred C57BL, T-Lymphocytes, Regulatory, Nuclear Receptor Subfamily 1, Group F, Member 3
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