Evidence map›Paper›PMID 34555129›Full record

ArticlePLoS pathogens2021

Salmonella Typhimurium impairs glycolysis-mediated acidification of phagosomes to evade macrophage defense.

Saray Gutiérrez, Julia Fischer, Raja Ganesan, Nina Judith Hos, Gökhan Cildir, Martina Wolke, Alberto Pessia, Peter Frommolt, Vincenzo Desiderio, Vidya Velagapudi and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.7field-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

26 citing papers in PubMed, 35 citations in OpenAlex.

  1. Restricted MHC-II trafficking inbioRxiv : the preprint server for biology · 2026
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  7. Buprenorphine enhancesJournal of oral microbiology · 2026
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  19. BRD4 Regulates Glycolysis-Dependent Nos2 Expression in Macrophages Upon H pylori Infection.Cellular and molecular gastroenterology and hepatology · 2024
    Article
  20. 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

11 authors at 4 institutions in 4 countries.

Saray GutiérrezCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Julia FischerCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.ORCID 0000-0001-6138-7454
Raja GanesanCentre for Cancer Biology, University of South Australia, Adelaide, Australia.ORCID 0000-0002-5408-0478
Nina Judith HosCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Gökhan CildirCentre for Cancer Biology, University of South Australia, Adelaide, Australia.ORCID 0000-0001-7457-9164
Martina WolkeInstitute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany.ORCID 0000-0002-4523-9707
Alberto PessiaMetabolomics Unit, Institute for Molecular Medicine Finland FIMM, Helsinki, Finland.ORCID 0000-0001-8607-9191
Peter FrommoltBioinformatics Facility, CECAD, University of Cologne, Cologne, Germany.
Vincenzo DesiderioDepartment of Precision Medicine, University of Campania "Luigi Vanvitelli", Naples, Italy.ORCID 0000-0003-1819-6083
Vidya VelagapudiMetabolomics Unit, Institute for Molecular Medicine Finland FIMM, Helsinki, Finland.
Nirmal RobinsonCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.ORCID 0000-0002-7361-9491
University of Cologne · DEUniversity of South Australia · AUInstitute for Molecular Medicine Finland · FIUniversity of Campania "Luigi Vanvitelli" · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulation of cellular metabolism is now recognized as a crucial mechanism for the activation of innate and adaptive immune cells upon diverse extracellular stimuli. Macrophages, for instance, increase glycolysis upon stimulation with pathogen-associated molecular patterns (PAMPs). Conceivably, pathogens also counteract these metabolic changes for their own survival in the host. Despite this dynamic interplay in host-pathogen interactions, the role of immunometabolism in the context of intracellular bacterial infections is still unclear. Here, employing unbiased metabolomic and transcriptomic approaches, we investigated the role of metabolic adaptations of macrophages upon Salmonella enterica serovar Typhimurium (S. Typhimurium) infections. Importantly, our results suggest that S. Typhimurium abrogates glycolysis and its modulators such as insulin-signaling to impair macrophage defense. Mechanistically, glycolysis facilitates glycolytic enzyme aldolase A mediated v-ATPase assembly and the acidification of phagosomes which is critical for lysosomal degradation. Thus, impairment in the glycolytic machinery eventually leads to decreased bacterial clearance and antigen presentation in murine macrophages (BMDM). Collectively, our results highlight a vital molecular link between metabolic adaptation and phagosome maturation in macrophages, which is targeted by S. Typhimurium to evade cell-autonomous defense.

Indexed as

AnimalsGene Expression ProfilingGlycolysisHost-Pathogen InteractionsMacrophagesMetabolomicsMicePhagosomesSalmonella Infections, AnimalSalmonella typhimurium

Identifiers

PMID34555129
PMCPMC8491875
OpenAlexW3200625488

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.