Evidence map›Paper›PMID 34986344›Full record

ArticleCell reports2022

Salmonella enterica serovar Typhimurium uses anaerobic respiration to overcome propionate-mediated colonization resistance.

Catherine D Shelton, Woongjae Yoo, Nicolas G Shealy, Teresa P Torres, Jacob K Zieba, M Wade Calcutt, Nora J Foegeding, Dajeong Kim, Jinshil Kim, Sangryeol Ryu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 69 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

11 authors at 4 institutions in 2 countries.

Catherine D SheltonDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Woongjae YooDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Nicolas G ShealyDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Teresa P TorresDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Jacob K ZiebaDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
M Wade CalcuttMass Spectrometry Research Center and Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
Nora J FoegedingDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Dajeong KimInfectious Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), 125 Gwahak-ro Yuseong-gu, Daejeon 34141, Republic of Korea.
Jinshil KimDepartment of Food and Animal Biotechnology, Department of Agricultural Biotechnology, Research Institute for Agriculture and Life Sciences, Seoul National University, Seoul 08826, Republic of Korea; Center for Food Bioconvergence, Seoul National University, Seoul 08826, Republic of Korea.
Sangryeol RyuDepartment of Food and Animal Biotechnology, Department of Agricultural Biotechnology, Research Institute for Agriculture and Life Sciences, Seoul National University, Seoul 08826, Republic of Korea; Center for Food Bioconvergence, Seoul National University, Seoul 08826, Republic of Korea.
Mariana X ByndlossDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA; Vanderbilt Institute of Infection, Immunology, and Inflammation, Vanderbilt University Medical Center, Nashville, TN 37232, USA; Vanderbilt Digestive Disease Center, Vanderbilt University Medical Center, Nashville, TN 37232, USA; Vanderbilt Microbiome Innovation Center, Vanderbilt University, Nashville, TN 37235, USA. Electronic address: mariana.x.byndloss@vumc.org.
Vanderbilt University Medical Center · USSeoul National University · KRVanderbilt University · USKorea Research Institute of Bioscience and Biotechnology · KR

Funding

Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Vanderbilt-Ingram Cancer Center SPORE in Gastrointestinal CancerP50CA236733 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI STEPHEN W. FESIK · 2019 to 2026
$19.6M
TRAINING PROGRAM IN ENVIRONMENTAL TOXICOLOGYT32ES007028 · NIEHS · VANDERBILT UNIVERSITY · PI F PETER Guengerich, Fiona Edith Harrison · 1985 to 2026
$15.7M
TRAINING IN GASTROENTEROLOGYT32DK007673 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 1992 to 2026
$8.4M
Chemical Biology of Infectious Diseases (CBID) Training ProgramT32AI112541 · NIAID · VANDERBILT UNIVERSITY · PI Eric P Skaar · 2015 to 2026
$4.0M
Mechanisms of Salmonella-mediated disruption of colonization resistance in the inflamed gutR01AI168302 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Mariana Xavier Byndloss · 2022 to 2026
$2.4M
Obesogenic diet-induced intestinal epithelium repair responses link dysbiosis and cardiovascular diseaseR01DK131104 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Mariana Xavier Byndloss · 2022 to 2026
$2.4M
Mechanism of Salmonella-dependent disruption of propionate-mediated colonization resistanceF31AI161882 · NIAID · VANDERBILT UNIVERSITY · PI SHELTON, CATHERINE · 2022 to 2024
$99k
Howard Hughes Medical InstituteNCI NIH HHS P50 CA236733NIAID NIH HHS F31 AI161882NIAID NIH HHS R01 AI168302NIAID NIH HHS T32 AI112541NIDDK NIH HHS P30 DK058404NIDDK NIH HHS R01 DK131104NIDDK NIH HHS T32 DK007673NIEHS NIH HHS T32 ES007028
6 · The paper itself

Abstract

The gut microbiota benefits the host by limiting enteric pathogen expansion (colonization resistance), partially via the production of inhibitory metabolites. Propionate, a short-chain fatty acid produced by microbiota members, is proposed to mediate colonization resistance against Salmonella enterica serovar Typhimurium (S. Tm). Here, we show that S. Tm overcomes the inhibitory effects of propionate by using it as a carbon source for anaerobic respiration. We determine that propionate metabolism provides an inflammation-dependent colonization advantage to S. Tm during infection. Such benefit is abolished in the intestinal lumen of Salmonella-infected germ-free mice. Interestingly, S. Tm propionate-mediated intestinal expansion is restored when germ-free mice are monocolonized with Bacteroides thetaiotaomicron (B. theta), a prominent propionate producer in the gut, but not when mice are monocolonized with a propionate-production-deficient B. theta strain. Taken together, our results reveal a strategy used by S. Tm to mitigate colonization resistance by metabolizing microbiota-derived propionate.

Indexed as

AnaerobiosisAnimalsAntibiosisBacteroides thetaiotaomicronFemaleGastrointestinal MicrobiomeGerm-Free LifeIntestinesMaleMiceMice, Inbred C57BLMice, Inbred CBAMice, KnockoutNitratesPropionatesSalmonella Infections, AnimalNitratesPropionatescolonization resistancegut microbiotaintestinal inflammationmicrobial metabolismpropionateSalmonella

Identifiers

PMID34986344
PMCPMC8800556
OpenAlexW4205542225

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.