Gut dysbiosis as a driver in alcohol-induced liver injury.
AH, alcoholic hepatitis
ALD, Alcohol-related liver disease
AUD, alcohol use disorder
Alcohol
Bile acids
CDR, cirrhosis dysbiosis ratio
Cirrhosis
FGF19, fibroblast growth factor 19
FXR, farnesoid X receptor
Hepatitis
LPS, lipopolysaccharide
MELD, model for end-stage liver disease
Microbiome
Mycobiome
PAMPs, pathogen-associated molecular patterns
PPI, proton pump inhibitor
SCFA, short-chain fatty acid
Virome
Journal
JHEP reports : innovation in hepatology
ISSN: 2589-5559
Titre abrégé: JHEP Rep
Pays: Netherlands
ID NLM: 101761237
Informations de publication
Date de publication:
Apr 2021
Apr 2021
Historique:
received:
09
10
2020
revised:
20
11
2020
accepted:
01
12
2020
entrez:
18
2
2021
pubmed:
19
2
2021
medline:
19
2
2021
Statut:
epublish
Résumé
Alcohol-related liver disease characterises a broad spectrum of hepatic diseases that result from heavy alcohol use, and include alcohol-related steatosis, steatohepatitis, fibrosis, cirrhosis, and alcoholic hepatitis. Amongst heavy drinkers, progression to more severe forms of alcohol-related liver disease is not universal, with only 20% developing cirrhosis and up to one-third developing alcoholic hepatitis. Non-alcohol-related triggers for severe disease are not well understood, but the intestinal microbiome is thought to be a contributing factor. This review examines the role of the microbiome in mild alcohol-related liver disease, cirrhosis, and alcoholic hepatitis. While most of the literature discusses bacterial dysbiosis, we also discuss the available evidence on fungal (mycobiome) and virome alterations in patients with alcohol-related liver disease. Additionally, we explore the mechanisms by which the microbiome contributes to the pathogenesis of alcohol-related liver disease, including effects on intestinal permeability, bile acid dysregulation, and production of hepatotoxic virulence factors.
Identifiants
pubmed: 33598648
doi: 10.1016/j.jhepr.2020.100220
pii: S2589-5559(20)30154-3
pmc: PMC7868813
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
100220Subventions
Organisme : NIDDK NIH HHS
ID : P30 DK120515
Pays : United States
Organisme : NIAAA NIH HHS
ID : R01 AA024726
Pays : United States
Organisme : NIAAA NIH HHS
ID : R37 AA020703
Pays : United States
Organisme : NIAAA NIH HHS
ID : P50 AA011999
Pays : United States
Organisme : NIAAA NIH HHS
ID : U01 AA026939
Pays : United States
Déclaration de conflit d'intérêts
B.S. has been consulting for Ferring Research Institute, Intercept Pharmaceuticals, HOST Therabiomics, Mabwell Therapeutics, Patara Pharmaceuticals and Takeda. B.S.’s institution UC San Diego has received grant support from BiomX, NGM Biopharmaceuticals, CymaBay Therapeutics, Synlogic Operating Company and Axial Biotherapeutics. Please refer to the accompanying ICMJE disclosure forms for further details.
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