Evidence map›Paper›PMID 25498344›Full record

ArticleCell host & microbe2014

Gut microbiota-produced succinate promotes C. difficile infection after antibiotic treatment or motility disturbance.

Jessica A Ferreyra, Katherine J Wu, Andrew J Hryckowian, Donna M Bouley, Bart C Weimer, Justin L Sonnenburg

Open access · bronzeAbstract read
In one paragraph

Article in Cell host & microbe, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 244 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
244citing papers in PubMed, 1 pooled it
10.8field-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

244 citing papers in PubMed, 1 synthesis or guideline pooled it, 376 citations in OpenAlex.

  1. Pooled it
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  4. Frontiers in immunology · 2019
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  7. Gut microbes · 2026
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184 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Jessica A FerreyraDepartment of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Katherine J WuDepartment of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Andrew J HryckowianDepartment of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Donna M BouleyDepartment of Comparative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.
Bart C WeimerDepartment of Population Health and Reproduction, University of California, Davis, Davis, CA 95616, USA.
Justin L SonnenburgDepartment of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: jsonnenburg@stanford.edu.
Stanford University · USUniversity of California, Davis · US

Funding

MOLECULAR BASIS OF HOST-PARASITE INTERACTIONT32AI007328 · NIAID · STANFORD UNIVERSITY · PI JUSTIN L SONNENBURG · 1987 to 2026
$11.9M
Impact of Diet on Intestinal Microbiota-Host DynamicsR01DK085025 · NIDDK · STANFORD UNIVERSITY · PI JUSTIN L SONNENBURG · 2010 to 2026
$6.4M
NIDDK NIH HHS R01 DK085025NIDDK NIH HHS R01-DK085025
6 · The paper itself

Abstract

Clostridium difficile is a leading cause of antibiotic-associated diarrhea. The mechanisms underlying C. difficile expansion after microbiota disturbance are just emerging. We assessed the gene expression profile of C. difficile within the intestine of gnotobiotic mice to identify genes regulated in response to either dietary or microbiota compositional changes. In the presence of the gut symbiont Bacteroides thetaiotaomicron, C. difficile induces a pathway that metabolizes the microbiota fermentation end-product succinate to butyrate. The low concentration of succinate present in the microbiota of conventional mice is transiently elevated upon antibiotic treatment or chemically induced intestinal motility disturbance, and C. difficile exploits this succinate spike to expand in the perturbed intestine. A C. difficile mutant compromised in succinate utilization is at a competitive disadvantage during these perturbations. Understanding the metabolic mechanisms involved in microbiota-C. difficile interactions may help to identify approaches for the treatment and prevention of C. difficile-associated diseases.

Indexed as

MicrobiotaAnimalsAnti-Bacterial AgentsBacteroidesClostridioides difficileClostridium InfectionsFemaleGastrointestinal TractHost-Pathogen InteractionsHumansMaleMiceSuccinic AcidAnti-Bacterial AgentsSuccinic Acid

Identifiers

PMID25498344
PMCPMC4859344
OpenAlexW2075702858

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.