Evidence map›Paper›PMID 34496241›Full record

ArticleCell reports2021

Clostridioides difficile infection induces a rapid influx of bile acids into the gut during colonization of the host.

Aaron G Wexler, Emma R Guiberson, William N Beavers, John A Shupe, M Kay Washington, D Borden Lacy, Richard M Caprioli, Jeffrey M Spraggins, Eric P Skaar

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2021. 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
1.4field-weighted citation impact, top 15% 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, 30 citations in OpenAlex.

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  12. bioRxiv : the preprint server for biology · 2023
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  17. Total glycosides contribute to the anti-diarrheal effects of Qiwei Baizhu PowderFrontiers in cellular and infection microbiology · 2022
    Article
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  19. 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

9 authors at 2 institutions in 1 country.

Aaron G WexlerDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA; Vanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University Medical Center, Nashville, TN, USA.
Emma R GuibersonMass Spectrometry Research Center, Vanderbilt University, Nashville, TN, USA; Department of Chemistry, Vanderbilt University, Nashville, TN, USA.
William N BeaversDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA; Vanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University Medical Center, Nashville, TN, USA.
John A ShupeDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA.
M Kay WashingtonDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA.
D Borden LacyDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA; The Veterans Affairs Tennessee Valley Healthcare System, Nashville, TN, USA.
Richard M CaprioliMass Spectrometry Research Center, Vanderbilt University, Nashville, TN, USA; Department of Chemistry, Vanderbilt University, Nashville, TN, USA; Department of Biochemistry, Vanderbilt University, Nashville, TN, USA; Department of Medicine, Vanderbilt University, Nashville, TN, USA; Department of Pharmacology, Vanderbilt University, Nashville, TN, USA.
Jeffrey M SpragginsMass Spectrometry Research Center, Vanderbilt University, Nashville, TN, USA; Department of Chemistry, Vanderbilt University, Nashville, TN, USA; Department of Biochemistry, Vanderbilt University, Nashville, TN, USA; Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN, USA. Electronic address: jeff.spraggins@vanderbilt.edu.
Eric P SkaarDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA; Vanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University Medical Center, Nashville, TN, USA. Electronic address: eric.skaar@vumc.org.
Vanderbilt University Medical Center · USVanderbilt University · US

Funding

Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Postdoctoral Training in Biomedical MRI and MRST32EB001628 · NIBIB · VANDERBILT UNIVERSITY MEDICAL CENTER · PI John C Gore · 2003 to 2026
$7.0M
Pathobiology of heme inducible transporters in Gram positive pathogensR01AI073843 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI SKAAR, ERIC P · 2009 to 2025
$5.9M
Molecular mapping of microbial communities at the host-pathogen interface by multi-modal 3-dimensional imaging mass spectrometryR01AI138581 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Eric P Skaar, Jeffrey M Spraggins · 2018 to 2026
$5.2M
Chemical Biology of Infectious Diseases (CBID) Training ProgramT32AI112541 · NIAID · VANDERBILT UNIVERSITY · PI Eric P Skaar · 2015 to 2026
$4.0M
Defining the impact of host factors on the molecular architecture and bacterial physiology of Staphylococcus aureus abscessesR01AI145992 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI CASSAT, JAMES E, SKAAR, ERIC P · 2020 to 2024
$3.8M
Structural Mechanisms of Clostridioides difficile pathogenesisR37AI095755 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Dana Borden Lacy · 2021 to 2026
$3.2M
15 Tesla Bruker SolariX FT-ICR mass spectrometerS10OD012359 · OD · VANDERBILT UNIVERSITY · PI CAPRIOLI, RICHARD M · 2012 to 2012
$1.6M
BLRD VA I01 BX002943NIAID NIH HHS R01 AI073843NIAID NIH HHS R01 AI138581NIAID NIH HHS R01 AI145992NIAID NIH HHS R37 AI095755NIAID NIH HHS T32 AI112541NIBIB NIH HHS T32 EB001628NIDDK NIH HHS P30 DK058404NIH HHS S10 OD012359
6 · The paper itself

Abstract

Clostridioides difficile is the leading cause of nosocomial intestinal infections in the United States. Ingested C. difficile spores encounter host bile acids and other cues that are necessary for germinating into toxin-producing vegetative cells. While gut microbiota disruption (often by antibiotics) is a prerequisite for C. difficile infection (CDI), the mechanisms C. difficile employs for colonization remain unclear. Here, we pioneered the application of imaging mass spectrometry to study how enteric infection changes gut metabolites. We find that CDI induces an influx of bile acids into the gut within 24 h of the host ingesting spores. In response, the host reduces bile acid biosynthesis gene expression. These bile acids drive C. difficile outgrowth, as mice receiving the bile acid sequestrant cholestyramine display delayed colonization and reduced germination. Our findings indicate that C. difficile may facilitate germination upon infection and suggest that altering flux through bile acid pathways can modulate C. difficile outgrowth in CDI-prone patients.

Indexed as

AnimalsAnti-Bacterial AgentsBile Acids and SaltsClostridioides difficileClostridium InfectionsGastrointestinal MicrobiomeIntestine, SmallMaleMiceMice, Inbred C57BLAnti-Bacterial AgentsBile Acids and Saltsbile acidsCDIClostridioides difficileenteric infectionMALDI IMSmicrobiotataurocholate

Identifiers

PMID34496241
PMCPMC8445666
OpenAlexW3196771103

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.