Evidence map›Paper›PMID 38806059›Full record

ArticleCell host & microbe2024

Salmonella Typhimurium expansion in the inflamed murine gut is dependent on aspartate derived from ROS-mediated microbiota lysis.

Woongjae Yoo, Nicolas G Shealy, Jacob K Zieba, Teresa P Torres, Madi Baltagulov, Julia D Thomas, Catherine D Shelton, Anna G McGovern, Nora J Foegeding, Erin E Olsan and 1 more

Abstract read
In one paragraph

Article in Cell host & microbe, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
–field-weighted citation impact
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

39 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Aspartate aminotransferase is required forInfection and immunity · 2026
    Article
  12. Review
  13. Article
  14. Article
  15. Aspartate aminotransferase is required forbioRxiv : the preprint server for biology · 2026
    Article
  16. Review
  17. Review
  18. Infection strategies ofGut microbes reports · 2026
    Review
  19. Article
  20. Review
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.

Woongjae YooDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA; Department of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang 37673, Republic of Korea.
Nicolas G ShealyDepartment 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.
Teresa P TorresDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Madi BaltagulovDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Julia D ThomasDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Catherine D SheltonDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Anna G McGovernDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Nora J FoegedingDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Erin E OlsanDepartment of Biological Sciences, California State University, Sacramento, CA 95819, USA.
Mariana X ByndlossDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA; Vanderbilt Institute for 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; Howard Hughes Medical Institute, Vanderbilt University Medical Center, Nashville, TN 37232, USA. Electronic address: mariana.x.byndloss@vumc.org.

Funding

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
NIAID NIH HHS F31 AI161882NIAID NIH HHS R01 AI168302NIAID NIH HHS T32 AI112541NIDDK NIH HHS R01 DK131104NIDDK NIH HHS T32 DK007673NIEHS NIH HHS T32 ES007028
6 · The paper itself

Abstract

Inflammation boosts the availability of electron acceptors in the intestinal lumen, creating a favorable niche for pathogenic Enterobacteriaceae. However, the mechanisms linking intestinal inflammation-mediated changes in luminal metabolites and pathogen expansion remain unclear. Here, we show that mucosal inflammation induced by Salmonella enterica serovar Typhimurium (S. Tm) infection increases intestinal levels of the amino acid aspartate. S. Tm used aspartate-ammonia lyase (aspA)-dependent fumarate respiration for growth in the murine gut only during inflammation. AspA-dependent growth advantage was abolished in the gut of germ-free mice and restored in gnotobiotic mice colonized with members of the classes Bacteroidia and Clostridia. Reactive oxygen species (ROS) produced during the host response caused lysis of commensal microbes, resulting in the release of microbiota-derived aspartate that was used by S. Tm, in concert with nitrate-dependent anaerobic respiration, to outcompete commensal Enterobacteriaceae. Our findings demonstrate the role of microbiota-derived amino acids in driving respiration-dependent S. Tm expansion during colitis.

Indexed as

Aspartic AcidGastrointestinal MicrobiomeReactive Oxygen SpeciesSalmonella typhimuriumAnimalsColitisEnterobacteriaceaeGerm-Free LifeInflammationMiceMice, Inbred C57BLSalmonella InfectionsAspartic AcidReactive Oxygen Speciesamino acidscolonization resistanceEnterobacteriaceaeintestinal inflammationmicrobe-microbe interactionsmicrobial metabolismmicrobiomeSalmonella Typhimurium

Identifiers

PMID38806059
PMCPMC11189616

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.