Evidence map›Paper›PMID 32628772›Full record

ArticleAlcoholism, clinical and experimental research2020

Deficiency of Intestinal α1-2-Fucosylation Exacerbates Ethanol-Induced Liver Disease in Mice.

Rongrong Zhou, Cristina Llorente, Jinling Cao, Bei Gao, Yi Duan, Lu Jiang, Yanhan Wang, Vipin Kumar, Peter Stärkel, Lars Bode and 2 more

Open access · greenAbstract read
In one paragraph

Article in Alcoholism, clinical and experimental research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 19 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 3 countries.

Rongrong ZhouFrom the Department of Infectious Diseases, Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha, China.
Cristina LlorenteDepartment of Medicine, University of California San Diego, La Jolla, California, USA.
Jinling CaoDepartment of Medicine, University of California San Diego, La Jolla, California, USA.
Bei GaoDepartment of Medicine, University of California San Diego, La Jolla, California, USA.
Yi DuanDepartment of Medicine, University of California San Diego, La Jolla, California, USA.
Lu JiangDepartment of Medicine, University of California San Diego, La Jolla, California, USA.
Yanhan WangDepartment of Medicine, University of California San Diego, La Jolla, California, USA.
Vipin KumarDepartment of Medicine, University of California San Diego, La Jolla, California, USA.ORCID 0000-0002-2838-2472
Peter StärkelSt Luc University Hospital, Université Catholique de Louvain, Brussels, Belgium.
Lars BodeDepartment of Pediatrics and Larsson-Rosenquist Foundation Mother-Milk-Infant Center of Research Excellence (MOMI CORE), University of California San Diego, La Jolla, California, USA.
Xuegong FanFrom the Department of Infectious Diseases, Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha, China.
Bernd SchnablDepartment of Medicine, University of California San Diego, La Jolla, California, USA.ORCID 0000-0002-6281-825X
University of California San Diego · USCentral South University · CNShanxi Agricultural University · CNUCLouvain · BE

Funding

The Southernearch Center for ALPD and CirrhosisP50AA011999 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ANNA S. GUKOVSKAYA · 1999 to 2026
$45.8M
San Diego Digestive Diseases Research CenterP30DK120515 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Tatiana Kisseleva · 2019 to 2026
$10.8M
The Role of the Intestinal Mycobiome in Alcoholic Liver DiseaseR01AA024726 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Bernd G. Schnabl · 2018 to 2026
$3.9M
Microbiome and intestinal innate immune response in alcoholic liver diseaseR01AA020703 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SCHNABL, BERND G. · 2011 to 2020
$3.6M
Microbiome and Intestinal Innate Immune Response in Alcoholic Liver DiseaseR37AA020703 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Bernd G. Schnabl · 2021 to 2026
$2.5M
Interplay Among NKT Cell Subsets in Alcoholic Liver DiseaseR01AA020864 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KUMAR, VIPIN · 2012 to 2016
$1.8M
Microbiome as therapeutic target in alcoholic hepatitisU01AA026939 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FOUTS, DERRICK E, SCHNABL, BERND G. · 2018 to 2022
$1.7M
The role of pathobionts in alcoholic liver diseaseI01BX004594 · VA · VA SAN DIEGO HEALTHCARE SYSTEM · PI Bernd G. Schnabl · 2019 to 2026
–
MOLECULAR EPIDEMIOLOGY OF SALMONELLA TYPHI INFECTIONSF05TW004594 · FIC · NEW YORK MEDICAL COLLEGE · PI FICA, ALBERTO E · 1992 to 1992
–
Biomedical Laboratory Research & Development Service of the VA Office of Research and Development BX004594BLRD VA I01 BX004594NIAAA NIH HHS P50 AA011999NIAAA NIH HHS R01 AA020703NIAAA NIH HHS R01 AA020864NIAAA NIH HHS R01 AA024726NIAAA NIH HHS R37 AA020703NIAAA NIH HHS U01 AA026939NIDDK NIH HHS P30 DK120515
6 · The paper itself

Abstract

backgroundFucosyltransferase 2 (Fut2)-mediated intestinal α1-2-fucosylation is important in maintaining a symbiotic host-microbiota relationship and can protect against several pathogens. Intestinal dysbiosis is an important factor for the progression of experimental ethanol (EtOH)-induced liver disease, but the role of Fut2 in modulating the intestinal glycocalyx during alcohol-associated liver disease is unknown. We investigated the role of Fut2-mediated intestinal α1-2-fucosylation for the development of alcohol-associated liver disease.

methodsImmunohistochemistry staining was applied to evaluate α1-2-fucosylation in duodenal biopsies from patients with alcohol use disorder. Wild-type (WT) and Fut2-deficient littermate mice were subjected to Lieber-DeCarli models of chronic EtOH administration and the chronic-binge EtOH diet (NIAAA model).

resultsIntestinal α1-2-fucosylation was down-regulated in patients with alcohol use disorder. Lack of α1-2-fucosylation in Fut2-deficient mice exacerbates chronic EtOH-induced liver injury, steatosis, and inflammation without affecting EtOH metabolism. Dietary supplementation of the α1-2-fucosylated glycan 2'-fucosyllactose (2'-FL) ameliorates EtOH-induced liver disease in Fut2-deficient mice in the NIAAA model. Despite no direct effects on growth of Enterococcus faecalis in vitro, intestinal α1-2-fucosylation reduces colonization of cytolysin-positive E. faecalis in the intestine of EtOH-fed mice.

conclusionsIntestinal α1-2-fucosylation acts as a host-protective mechanism against EtOH-induced liver disease. 2'-FL is an oligosaccharide naturally present in human milk that could be considered as therapeutic agent for alcohol-associated liver disease.

Indexed as

AlcoholismAnimalsCentral Nervous System DepressantsDisease Models, AnimalDysbiosisEthanolFucosyltransferasesGalactoside 2-alpha-L-fucosyltransferaseGastrointestinal MicrobiomeGlycocalyxIntestinal MucosaLiverLiver Diseases, AlcoholicMiceCentral Nervous System DepressantsEthanolFucosyltransferasesGalactoside 2-alpha-L-fucosyltransferaseAlcoholic Liver DiseaseCytolysinFucosyltransferase 2MicrobiomeMicrobiota

Identifiers

PMID32628772
PMCPMC7808344
OpenAlexW3041023675

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.