Intestinal Dysbiosis Amplifies Acetaminophen-Induced Acute Liver Injury.


Journal

Cellular and molecular gastroenterology and hepatology
ISSN: 2352-345X
Titre abrégé: Cell Mol Gastroenterol Hepatol
Pays: United States
ID NLM: 101648302

Informations de publication

Date de publication:
2021
Historique:
received: 02 06 2020
revised: 31 10 2020
accepted: 02 11 2020
pubmed: 16 11 2020
medline: 8 3 2022
entrez: 15 11 2020
Statut: ppublish

Résumé

Acute liver failure (ALF) represents an unmet medical need in Western countries. Although the link between intestinal dysbiosis and chronic liver disease is well-established, there is little evidence for a functional role of gut-liver interaction during ALF. Here we hypothesized that intestinal dysbiosis may affect ALF. To test this hypothesis, we assessed the association of proton pump inhibitor (PPI) or long-term antibiotics (ABx) intake, which have both been linked to intestinal dysbiosis, and occurrence of ALF in the 500,000 participants of the UK BioBank population-based cohort. For functional studies, male Nlrp6 Multivariate Cox regression analyses revealed a significantly increased risk (odds ratio, 2.3-3) for developing ALF in UK BioBank participants with PPI or ABx. Similarly, dysbiotic Nlrp6 Our data show an important yet unknown function of intestinal microbiota during ALF. Intestinal dysbiosis was transferrable to healthy WT mice via FMT and aggravated liver injury. Our study highlights intestinal microbiota as a targetable risk factor for ALF.

Sections du résumé

BACKGROUND & AIMS
Acute liver failure (ALF) represents an unmet medical need in Western countries. Although the link between intestinal dysbiosis and chronic liver disease is well-established, there is little evidence for a functional role of gut-liver interaction during ALF. Here we hypothesized that intestinal dysbiosis may affect ALF.
METHODS
To test this hypothesis, we assessed the association of proton pump inhibitor (PPI) or long-term antibiotics (ABx) intake, which have both been linked to intestinal dysbiosis, and occurrence of ALF in the 500,000 participants of the UK BioBank population-based cohort. For functional studies, male Nlrp6
RESULTS
Multivariate Cox regression analyses revealed a significantly increased risk (odds ratio, 2.3-3) for developing ALF in UK BioBank participants with PPI or ABx. Similarly, dysbiotic Nlrp6
CONCLUSIONS
Our data show an important yet unknown function of intestinal microbiota during ALF. Intestinal dysbiosis was transferrable to healthy WT mice via FMT and aggravated liver injury. Our study highlights intestinal microbiota as a targetable risk factor for ALF.

Identifiants

pubmed: 33189892
pii: S2352-345X(20)30181-8
doi: 10.1016/j.jcmgh.2020.11.002
pmc: PMC7900526
pii:
doi:

Substances chimiques

Analgesics, Non-Narcotic 0
Nod-like receptor pyrin domain-containing protein 6, mouse 0
Receptors, Cell Surface 0
Acetaminophen 362O9ITL9D

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

909-933

Subventions

Organisme : Medical Research Council
ID : MC_PC_17228
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_QA137853
Pays : United Kingdom

Informations de copyright

Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.

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Auteurs

Kai Markus Schneider (KM)

Department of Medicine III, University Hospital RWTH Aachen, Aachen, Germany; Department of Microbiology; Institute for Immunology; and Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.

Carsten Elfers (C)

Department of Medicine III, University Hospital RWTH Aachen, Aachen, Germany.

Ahmed Ghallab (A)

Leibniz Research Centre for Working Environment and Human Factors at the Technical University Dortmund, Dortmund, Germany; Department of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, South Valley University, Qena, Egypt.

Carolin Victoria Schneider (CV)

Department of Medicine III, University Hospital RWTH Aachen, Aachen, Germany.

Eric J C Galvez (EJC)

Helmholtz Centre for Infection Research, Braunschweig, Germany; and Hannover Medical School, Hannover, Germany.

Antje Mohs (A)

Department of Medicine III, University Hospital RWTH Aachen, Aachen, Germany.

Wenfang Gui (W)

Department of Medicine III, University Hospital RWTH Aachen, Aachen, Germany.

Lena Susanna Candels (LS)

Department of Medicine III, University Hospital RWTH Aachen, Aachen, Germany.

Theresa Hildegard Wirtz (TH)

Department of Medicine III, University Hospital RWTH Aachen, Aachen, Germany.

Sebastian Zuehlke (S)

Department of Chemistry and Chemical Biology, Institute of Experimental Research (INFU), TU Dortmund University, Dortmund, Germany.

Michael Spiteller (M)

Department of Chemistry and Chemical Biology, Institute of Experimental Research (INFU), TU Dortmund University, Dortmund, Germany.

Maiju Myllys (M)

Leibniz Research Centre for Working Environment and Human Factors at the Technical University Dortmund, Dortmund, Germany.

Alain Roulet (A)

Vaiomer, Labège, France.

Amirouche Ouzerdine (A)

Vaiomer, Labège, France.

Benjamin Lelouvier (B)

Vaiomer, Labège, France.

Konrad Kilic (K)

Department of Medicine III, University Hospital RWTH Aachen, Aachen, Germany.

Lijun Liao (L)

Department of Medicine III, University Hospital RWTH Aachen, Aachen, Germany; Department of Anesthesiology and Pain Management, Shanghai East Hospital, Tongji University, Shanghai, China.

Anika Nier (A)

Department of Nutritional Sciences, R.F. Molecular Nutritional Science, University of Vienna, Vienna, Austria.

Eicke Latz (E)

Institute for Innate Immunity, University of Bonn, Bonn, Germany.

Ina Bergheim (I)

Department of Nutritional Sciences, R.F. Molecular Nutritional Science, University of Vienna, Vienna, Austria.

Christoph A Thaiss (CA)

Department of Microbiology; Institute for Immunology; and Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.

Jan G Hengstler (JG)

Leibniz Research Centre for Working Environment and Human Factors at the Technical University Dortmund, Dortmund, Germany.

Till Strowig (T)

Helmholtz Centre for Infection Research, Braunschweig, Germany; and Hannover Medical School, Hannover, Germany.

Christian Trautwein (C)

Department of Medicine III, University Hospital RWTH Aachen, Aachen, Germany. Electronic address: ctrautwein@ukaachen.de.

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