Dysbiosis modulates capacity for bile acid modification in the gut microbiomes of patients with inflammatory bowel disease: a mechanism and marker of disease?: Figure 1
Open accessAbstract
The recently published article by Gadaleta and co-workers1 has demonstrated that activation of the bile acid (BA) nuclear receptor, Farnesoid X receptor α (FXR), affords multi-level protection against intestinal inflammation and inflammatory bowel disease (IBD) in mice. Of the numerous avenues of research into IBD diagnosis and treatment that are opened by these findings, the questions posed by Gadaleta and co-workers regarding the contribution of gut bacteria to FXR modulation and aetiology of IBD are of particular significance. Bacteria resident in the human gastrointestinal tract collectively encode a distributed pathway of BA modification, the products of which are the natural ligands for FXR,2 and there is growing appreciation that this may be a key activity through which the gut microbiota integrates factors relating to diet and mucosal inflammation, to initiate or exacerbate disease.3 These modified BAs display altered binding profiles for BA receptors, with several secondary BAs being among the most potent agonists. Moreover, microbial transformation could also influence BA bioavailability for …
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The gut microbiota of patients with IBD is characterized by low BSH activity.
“The gut microbiota of patients with IBD is characterized by low BSH activity”
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 Ogilvie and Jones, 2012
The paper’s discussion of Figure 1 reports reduced total abundance of BSH-like sequences and a significant reduction in Firmicutes-affiliated sequences in the Crohn’s disease group. It measures gene-sequence abundance in silico, not BSH activity directly, and does not establish low activity across all patients with IBD. (LLM, conf=0.86)
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References 6 · Cited by 61
Research works printed but not linked: 4
- [3]O'Keefe SJD Nutrition and colonic health: the critical role of the microbiota. Curr Opin Gastroen 2008; 24: 51– 8 18043233
- [4]Ridlon JM Kang DJ Hylemon PB Bile salt biotransformations by human intestinal bacteria. J Lipid Res 2006; 47: 241– 59 16299351
- [5]Jones BV Begley M Hill C Functional and comparative metagenomic analysis of bile salt hydrolase activity in the human gut microbiome. Proc Natl Acad Sci USA 2008; 105: 13580– 5 18757757 PMC2533232
- [6]Qin J Li R Raes J A human gut microbial gene catalogue established by metagenomic sequencing. Nature 2010; 464: 59– 65 20203603 PMC3779803
- Authors
- Ogilvie, L. A., & Jones, B. V.
- Affiliations
- University of Brighton (GB)
- Corresponding author
- Jones, Brian V
- Venue
- Gut
- Publisher
- BMJ
- Published
- 2012-04-05
- Volume
- 61
- Issue
- 11
- Pages
- 1642-1643
- ISSN
- 0017-5749 (ISSN-L)
- 1468-3288
- PMC
- PMC3463861
- OpenAlex
- W2162174507
- Cited by
- 61
- References
- 6
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 2 · 2023: 7 · 2022: 8 · 2021: 7 · 2020: 5 · 2018: 2 · 2017: 4 · 2016: 6 · 2015: 3 · 2014: 6 · 2013: 4 · 2012: 1
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- Gut (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- University of Brighton Repository (University of Brighton) (submittedVersion, cc-by-nc)
- Funders
- Medical Research Council (G0901553)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Keywords
- inflammatory bowel disease, gut dysbiosis, gut microbiota, farnesoid X receptor, FXR activation, secondary bile acids, intestinal inflammation, disease biomarkers
- MeSH terms
- Animals, Chenodeoxycholic Acid, Humans, Intestinal Absorption, Inflammatory Bowel Diseases, Receptors, Cytoplasmic and Nuclear
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