Evidence map›Paper›PMID 30498100›Full record

ReviewScience (New York, N.Y.)2018

Colonocyte metabolism shapes the gut microbiota.

Yael Litvak, Mariana X Byndloss, Andreas J Bäumler

Open access · greenAbstract readReview
In one paragraph

Review in Science (New York, N.Y.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 446 papers.

0numbers the graph read from it
0cells of the map it votes in
446citing papers in PubMed
19.7field-weighted citation impact, top 1% 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

446 citing papers in PubMed, 703 citations in OpenAlex.

  1. Trial
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  11. Colonic metabolomic and transcriptomic alterations in a mouse model of metabolic syndrome.American journal of physiology. Gastrointestinal and liver physiology · 2026
    Article
  12. Review
  13. Article
  14. Microbiota-derived indole limitsScience advances · 2026
    Article
  15. Review
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  18. Review
  19. Article
  20. Article

386 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Yael LitvakDepartment of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, CA 95616, USA.ORCID http://orcid.org/0000-0002-0183-2816
Mariana X ByndlossDepartment of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, CA 95616, USA.
Andreas J BäumlerDepartment of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, CA 95616, USA. ajbaumler@ucdavis.edu.ORCID http://orcid.org/0000-0001-9152-7809
University of California, Davis · US

Funding

Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Virulence Factors of SalmonellaR01AI044170 · NIAID · UNIVERSITY OF CALIFORNIA DAVIS · PI BAUMLER, ANDREAS J · 1999 to 2022
$8.5M
Exacerbation of colitis by the microbiotaR01AI112445 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Andreas J Baumler · 2015 to 2026
$6.2M
Microbiota Outgrowth by SalmonellaR01AI096528 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BAUMLER, ANDREAS J · 2011 to 2025
$6.1M
Mechanism of Colonization ResistanceR01AI112949 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Andreas J Baumler · 2016 to 2026
$5.2M
Salmonella Host interactionsR37AI044170 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Andreas J Baumler, Renee M Tsolis · 2025 to 2026
$1.2M
Mechanism of E. coli colonization resistanceR56AI112949 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BAUMLER, ANDREAS J · 2014 to 2014
$382k
NIAID NIH HHS R01 AI044170NIAID NIH HHS R01 AI096528NIAID NIH HHS R01 AI112445NIAID NIH HHS R01 AI112949NIAID NIH HHS R37 AI044170NIAID NIH HHS R56 AI112949NIDDK NIH HHS P30 DK058404
6 · The paper itself

Abstract

An imbalance in the colonic microbiota might underlie many human diseases, but the mechanisms that maintain homeostasis remain elusive. Recent insights suggest that colonocyte metabolism functions as a control switch, mediating a shift between homeostatic and dysbiotic communities. During homeostasis, colonocyte metabolism is directed toward oxidative phosphorylation, resulting in high epithelial oxygen consumption. The consequent epithelial hypoxia helps to maintain a microbial community dominated by obligate anaerobic bacteria, which provide benefit by converting fiber into fermentation products absorbed by the host. Conditions that alter the metabolism of the colonic epithelium increase epithelial oxygenation, thereby driving an expansion of facultative anaerobic bacteria, a hallmark of dysbiosis in the colon. Enteric pathogens subvert colonocyte metabolism to escape niche protection conferred by the gut microbiota. The reverse strategy, a metabolic reprogramming to restore colonocyte hypoxia, represents a promising new therapeutic approach for rebalancing the colonic microbiota in a broad spectrum of human diseases.

Indexed as

Gastrointestinal MicrobiomeCell PolarityColitis, UlcerativeColonDysbiosisHost-Pathogen InteractionsHumansIntestinal MucosaOxygen Consumption

Identifiers

PMID30498100
PMCPMC6296223
OpenAlexW2902250851

What OpenQuestion holds

Textmetadata
LicenceTDM
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.