Evidence map›Paper›PMID 32911590›Full record

ReviewClinical and molecular hepatology2020

From intestinal dysbiosis to alcohol-associated liver disease.

Beatriz Garcia Mendes, Bernd Schnabl

Open access · goldAbstract readReview
In one paragraph

Review in Clinical and molecular hepatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Enhanced Bioactivity ofFood science & nutrition · 2026
    Article
  5. Review
  6. Article
  7. Synergistic toxicity in alcohol-associated liver disease and PFAS exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

2 authors at 1 institution in 2 countries.

Beatriz Garcia MendesDepartment of Clinical Analysis, Federal University of Santa Catarina, Florianopolis, SC, Brazil.
Bernd SchnablDepartment of Medicine, University of California San Diego, La Jolla, CA, USA.
University of California, San Diego · US

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 LARS ECKMANN, Bernd G. Schnabl · 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 as therapeutic target in alcoholic hepatitisU01AA026939 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FOUTS, DERRICK E, SCHNABL, BERND G. · 2018 to 2022
$1.7M
NIAAA NIH HHS P50 AA011999NIAAA NIH HHS R01 AA020703NIAAA NIH HHS R01 AA024726NIAAA NIH HHS U01 AA026939NIDDK NIH HHS P30 DK120515NIH HHS R01 AA020703NIH HHS U01 AA026939
6 · The paper itself

Abstract

Alcohol-associated intestinal dysbiosis and bacterial overgrowth can lead to a dysregulation of tryptophan metabolism and lower production of indoles. Several of these indole derivatives are aryl hydrocarbon receptor ligands that, in turn, are involved in antimicrobial defense via induction of interleukin-22 (IL-22). IL-22 increases the expression of intestinal regenerating islet-derived 3 (Reg3) lectins, which maintain low bacterial colonization of the inner mucus layer and reduce bacterial translocation to the liver. Chronic alcohol consumption is associated with reduced intestinal expression of Reg3β and Reg3γ, increased numbers of mucosa-associated bacteria and bacterial translocation. Translocated microbial products and viable bacteria reach the liver and activate the innate immune system. Release of inflammatory molecules promotes inflammation, contributes to hepatocyte death and results in a fibrotic response. This review summarizes the mechanisms by which chronic alcohol intake changes the gut microbiota and contributes to alcohol-associated liver disease by changing microbial-derived metabolites.

Indexed as

Gastrointestinal MicrobiomeLiver Diseases, AlcoholicBacteriaDysbiosisHumansIntestinal MucosaAlcohol-associated liver diseaseAryl hydrocarbon receptorDysbiosisInterleukin-22Tryptophan

Identifiers

PMID32911590
PMCPMC7641547
OpenAlexW3085593616

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.