Evidence map›Paper›PMID 37267419›Full record

ArticlePLoS pathogens2023

The methylglyoxal pathway is a sink for glutathione in Salmonella experiencing oxidative stress.

Sashi Kant, Lin Liu, Andres Vazquez-Torres

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. A putativeFrontiers in immunology · 2026
    Article
  5. Article
  6. Review
  7. Review
  8. Identification of glyoxalase A in group BInfection and immunity · 2025
    Article
  9. Article
  10. Methylglyoxal Formation-Metabolic Routes and Consequences.Antioxidants (Basel, Switzerland) · 2025
    Review
  11. Identification of Glyoxalase A in Group BbioRxiv : the preprint server for biology · 2024
    Article
  12. 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

3 authors at 2 institutions in 1 country.

Sashi KantUniversity of Colorado School of Medicine, Department of Immunology and Microbiology, Aurora, Colorado, United States of America.
Lin LiuUniversity of Colorado School of Medicine, Department of Immunology and Microbiology, Aurora, Colorado, United States of America.
Andres Vazquez-TorresUniversity of Colorado School of Medicine, Department of Immunology and Microbiology, Aurora, Colorado, United States of America.ORCID 0000-0002-6181-4185
University of Colorado Denver · USVA Eastern Colorado Health Care System · US

Funding

Salmonella evasion of NADPH oxidase-dependent killingR01AI054959 · NIAID · UNIVERSITY OF COLORADO DENVER · PI VAZQUEZ-TORRES, ANDRES · 2003 to 2018
$5.2M
Molecular determinants of oxidative stress in Salmonella pathogenesisR01AI136520 · NIAID · UNIVERSITY OF COLORADO DENVER · PI Andres Vazquez-Torres · 2018 to 2026
$3.7M
Analysis of regulatory networks in Salmonella pathogenesis.R01AI155493 · NIAID · UNIVERSITY OF COLORADO DENVER · PI VAZQUEZ-TORRES, ANDRES · 2020 to 2024
$2.5M
Molecular Analysis of Bacterial Adaptive Response to Host Reactive SpeciesI01BX002073 · VA · VA EASTERN COLORADO HEALTH CARE SYSTEM · PI Andres Vazquez-Torres · 2013 to 2026
–
Development of DksA-targeted Antibiotics for Treatment of Gram-negative InfectionsI01BX005733 · VA · VA EASTERN COLORADO HEALTH CARE SYSTEM · PI Andres Vazquez-Torres · 2023 to 2026
–
BLRD Research Career Scientist Award ApplicationIK6BX005384 · VA · VA EASTERN COLORADO HEALTH CARE SYSTEM · PI VAZQUEZ-TORRES, ANDRES · 2021 to 2025
–
BLRD VA I01 BX002073BLRD VA I01 BX005733BLRD VA IK6 BX005384NIAID NIH HHS R01 AI054959NIAID NIH HHS R01 AI136520NIAID NIH HHS R01 AI155493
6 · The paper itself

Abstract

Salmonella suffer the cytotoxicity of reactive oxygen species generated by the phagocyte NADPH oxidase in the innate host response. Periplasmic superoxide dismutases, catalases and hydroperoxidases detoxify superoxide and hydrogen peroxide (H2O2) synthesized in the respiratory burst of phagocytic cells. Glutathione also helps Salmonella combat the phagocyte NADPH oxidase; however, the molecular mechanisms by which this low-molecular-weight thiol promotes resistance of Salmonella to oxidative stress are currently unknown. We report herein that Salmonella undergoing oxidative stress transcriptionally and functionally activate the methylglyoxal pathway that branches off from glycolysis. Activation of the methylglyoxal pathway consumes a substantial proportion of the glutathione reducing power in Salmonella following exposure to H2O2. The methylglyoxal pathway enables Salmonella to balance glucose utilization with aerobic respiratory outputs. Salmonella take advantage of the metabolic flexibility associated with the glutathione-consuming methylglyoxal pathway to resist reactive oxygen species generated by the enzymatic activity of the phagocyte NADPH oxidase in macrophages and mice. Taken together, glutathione fosters oxidative stress resistance in Salmonella against the antimicrobial actions of the phagocyte NADPH oxidase by promoting the methylglyoxal pathway, an offshoot metabolic adaptation of glycolysis.

Indexed as

PyruvaldehydeSuperoxidesAnimalsGlutathioneHydrogen PeroxideMiceNADPH OxidasesOxidative StressReactive Oxygen SpeciesSalmonella typhimuriumGlutathioneHydrogen PeroxideNADPH OxidasesPyruvaldehydeReactive Oxygen SpeciesSuperoxides

Identifiers

PMID37267419
PMCPMC10266609
OpenAlexW4379184688

What OpenQuestion holds

Textmetadata
LicenceCC0
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.