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Cited by 32Liver Diseases and ImmunityGut microbiota and healthDrug Transport and Resistance Mechanisms

Bacterial and metabolic phenotypes associated with inadequate response to ursodeoxycholic acid treatment in primary biliary cholangitis

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Martinez-Gili, Laura, Pechlivanis, Alexandros, McDonald, Julie A.K., Begum, Sofina, Badrock, Jonathan, Dyson, Jessica K., Jones, Rebecca, Hirschfield, Gideon +10 more·2023·Gut Microbes
DOI 10.1080/19490976.2023.2208501PMC PMC10190197
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Abstract

Primary biliary cholangitis (PBC) is a chronic cholestatic liver disease with ursodeoxycholic acid (UDCA) as first-line treatment. Poor response to UDCA is associated with a higher risk of progressing to cirrhosis, but the underlying mechanisms are unclear. UDCA modulates the composition of primary and bacterial-derived bile acids (BAs). We characterized the phenotypic response to UDCA based on BA and bacterial profiles of PBC patients treated with UDCA. Patients from the UK-PBC cohort (n = 419) treated with UDCA for a minimum of 12-months were assessed using the Barcelona dynamic response criteria. BAs from serum, urine, and feces were analyzed using Ultra-High-Performance Liquid Chromatography-Mass Spectrometry and fecal bacterial composition measured using 16S rRNA gene sequencing. We identified 191 non-responders, 212 responders, and a subgroup of responders with persistently elevated liver biomarkers (n = 16). Responders had higher fecal secondary and tertiary BAs than non-responders and lower urinary bile acid abundances, with the exception of 12-dehydrocholic acid, which was higher in responders. The sub-group of responders with poor liver function showed lower alpha-diversity evenness, lower abundance of fecal secondary and tertiary BAs than the other groups and lower levels of phyla with BA-deconjugation capacity (Actinobacteriota/Actinomycetota, Desulfobacterota, Verrucomicrobiota) compared to responders. UDCA dynamic response was associated with an increased capacity to generate oxo-/epimerized secondary BAs. 12-dehydrocholic acid is a potential biomarker of treatment response. Lower alpha-diversity and lower abundance of bacteria with BA deconjugation capacity might be associated with an incomplete response to treatment in some patients.

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  • In primary biliary cholangitis, the gut microbiota alter both serum and faecal bile acid profiles with a decreased conversion of primary to secondary bile acids.

    “In primary biliary cholangitis, the gut microbiota alter both serum and faecal bile acid profiles with a decreased conversion of primary to secondary bile acids.36,37”

    From Primary biliary cholangitis. (2024) · cites this paper as [37]

    The Discussion (page not provided) reports lower faecal secondary bile acids in a subgroup of UDCA-treated patients with PBC and suggests they might have reduced bacterial bile-acid conversion capacity. It does not establish a general decrease in primary-to-secondary conversion in PBC or show that microbiota alter both serum and faecal profiles; the Discussion says serum bile acids were not associated with treatment response. (LLM, conf=0.87)

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Authors
Martinez-Gili, L., Pechlivanis, A., McDonald, J. A. K., Begum, S., Badrock, J., Dyson, J. K., Jones, R., Hirschfield, G., Ryder, S. D., Sandford, R., Rushbrook, S., Thorburn, D., Taylor-Robinson, S. D., Crossey, M. M. E., Marchesi, J. R., Mells, G., Holmes, E., & Jones, D.
Affiliations
  • Division of Systems Medicine, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK
  • Imperial College London (GB)
  • University of Cambridge (GB)
  • Newcastle upon Tyne Hospitals NHS Foundation Trust (GB)
  • St James's University Hospital (GB)
  • National Institute for Health and Care Research (GB)
  • Nottingham University Hospitals NHS Trust (GB)
  • Norfolk and Norwich University Hospital (GB)
  • The Royal Free Hospital (GB)
  • Murdoch University (AU)
Corresponding author
Jones, David
ORCID
Venue
Gut Microbes
Publisher
Informa UK Limited
Published
2023-05-16
Volume
15
Issue
1
Pages
2208501-2208501
ISSN
  • 1949-0976 (ISSN-L)
  • 1949-0984
DOI
10.1080/19490976.2023.2208501
PMC
PMC10190197
OpenAlex
W4376641583
Cited by
32
References
6
Citations by year
2026: 12 · 2025: 7 · 2024: 11 · 2023: 2
FWCI
5.41
Type
journal article
Language
en
Open access
Licence
Locations
  • Gut Microbes (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • UEA Digital Repository (University of East Anglia) (acceptedVersion)
  • UCL Discovery (University College London) (submittedVersion, cc-by)
  • Spiral (Imperial College London) (submittedVersion, cc-by)
  • Apollo (University of Cambridge) (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Newcastle University ePrints (Newcastle Univesity) (cc-by)
Funders
Medical Research Council (MR/L001489/1)
Topics
  • Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
  • Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
Keywords
primary biliary cirrhosis, ursodeoxycholic acid, treatment response, bile acids, fecal microbiota, bacterial diversity, bile acid deconjugation, secondary bile acids, urinary bile acids, treatment response biomarkers, cholestatic liver disease
MeSH terms
Gastrointestinal Microbiome, Bacteria, Bile Acids and Salts, Cholagogues and Choleretics, Dehydrocholic Acid, Humans, Liver Cirrhosis, Biliary, Phenotype, RNA, Ribosomal, 16S, Ursodeoxycholic Acid, Biomarkers

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