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Gut dysbiosis as a driver in alcohol-induced liver injury

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...

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Detalles Bibliográficos
Autores principales: Fairfield, Bradley, Schnabl, Bernd
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7868813/
https://www.ncbi.nlm.nih.gov/pubmed/33598648
http://dx.doi.org/10.1016/j.jhepr.2020.100220
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author Fairfield, Bradley
Schnabl, Bernd
author_facet Fairfield, Bradley
Schnabl, Bernd
author_sort Fairfield, Bradley
collection PubMed
description 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.
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spelling pubmed-78688132021-02-16 Gut dysbiosis as a driver in alcohol-induced liver injury Fairfield, Bradley Schnabl, Bernd JHEP Rep Review 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. Elsevier 2020-12-10 /pmc/articles/PMC7868813/ /pubmed/33598648 http://dx.doi.org/10.1016/j.jhepr.2020.100220 Text en http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Review
Fairfield, Bradley
Schnabl, Bernd
Gut dysbiosis as a driver in alcohol-induced liver injury
title Gut dysbiosis as a driver in alcohol-induced liver injury
title_full Gut dysbiosis as a driver in alcohol-induced liver injury
title_fullStr Gut dysbiosis as a driver in alcohol-induced liver injury
title_full_unstemmed Gut dysbiosis as a driver in alcohol-induced liver injury
title_short Gut dysbiosis as a driver in alcohol-induced liver injury
title_sort gut dysbiosis as a driver in alcohol-induced liver injury
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7868813/
https://www.ncbi.nlm.nih.gov/pubmed/33598648
http://dx.doi.org/10.1016/j.jhepr.2020.100220
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