Evidence map›Paper›PMID 25144687›Full record

ArticlePLoS pathogens2014

Production of an attenuated phenol-soluble modulin variant unique to the MRSA clonal complex 30 increases severity of bloodstream infection.

Gordon Y C Cheung, Dorothee Kretschmer, Anthony C Duong, Anthony J Yeh, Trung V Ho, Yan Chen, Hwang-Soo Joo, Barry N Kreiswirth, Andreas Peschel, Michael Otto

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Look Who's Talking: Host and Pathogen Drivers ofInternational journal of molecular sciences · 2022
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  9. Autophagy inFrontiers in cellular and infection microbiology · 2021
    Review
  10. Virulence factors and clonal diversity of Staphylococcus aureus in colonization and wound infection with emphasis on diabetic foot infection.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2020
    Review
  11. Microbial Musings - July 2020.Microbiology (Reading, England) · 2020
    Article
  12. Variable Release of Lipoteichoic Acid FromFrontiers in microbiology · 2020
    Article
  13. Article
  14. Genome Plasticity ofInfection and immunity · 2018
    Article
  15. Fulminant Staphylococcal Infections.Microbiology spectrum · 2018
    Review
  16. Article
  17. Article
  18. Frontiers in immunology · 2018
    Article
  19. Frontiers in cellular and infection microbiology · 2018
    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

10 authors at 4 institutions in 2 countries.

Gordon Y C CheungPathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, The National Institutes of Health, Bethesda, Maryland, United States of America.
Dorothee KretschmerCellular and Molecular Microbiology Division, Interfaculty Institute of Microbiology and Infection Medicine, University of Tübingen, Tübingen, Germany.
Anthony C DuongPathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, The National Institutes of Health, Bethesda, Maryland, United States of America.
Anthony J YehPathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, The National Institutes of Health, Bethesda, Maryland, United States of America.
Trung V HoPathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, The National Institutes of Health, Bethesda, Maryland, United States of America.
Yan ChenPathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, The National Institutes of Health, Bethesda, Maryland, United States of America.
Hwang-Soo JooPathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, The National Institutes of Health, Bethesda, Maryland, United States of America.
Barry N KreiswirthPublic Health Research Institute Tuberculosis Center, New Jersey Medical School, Rutgers University, Newark, New Jersey, United States of America.
Andreas PeschelCellular and Molecular Microbiology Division, Interfaculty Institute of Microbiology and Infection Medicine, University of Tübingen, Tübingen, Germany.
Michael OttoPathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, The National Institutes of Health, Bethesda, Maryland, United States of America.
National Institute of Allergy and Infectious Diseases · USUniversity of Tübingen · DENational Institutes of Health · USRutgers, The State University of New Jersey · US

Funding

Staphylococcal pathogenesisZIAAI000904 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI OTTO, MICHAEL · 2009 to 2025
$22.6M
6 · The paper itself

Abstract

Methicillin-resistant Staphylococcus aureus (MRSA) is a leading cause of morbidity and death. Phenol-soluble modulins (PSMs) are recently-discovered toxins with a key impact on the development of Staphylococcus aureus infections. Allelic variants of PSMs and their potential impact on pathogen success during infection have not yet been described. Here we show that the clonal complex (CC) 30 lineage, a major cause of hospital-associated sepsis and hematogenous complications, expresses an allelic variant of the PSMα3 peptide. We found that this variant, PSMα3N22Y, is characteristic of CC30 strains and has significantly reduced cytolytic and pro-inflammatory potential. Notably, CC30 strains showed reduced cytolytic and chemotactic potential toward human neutrophils, and increased hematogenous seeding in a bacteremia model, compared to strains in which the genome was altered to express non-CC30 PSMα3. Our findings describe a molecular mechanism contributing to attenuated pro-inflammatory potential in a main MRSA lineage. They suggest that reduced pathogen recognition via PSMs allows the bacteria to evade elimination by innate host defenses during bloodstream infections. Furthermore, they underscore the role of point mutations in key S. aureus toxin genes in that adaptation and the pivotal importance PSMs have in defining key S. aureus immune evasion and virulence mechanisms.

Indexed as

AnimalsBacteremiaBacterial ToxinsBlotting, WesternChemotaxis, LeukocyteChromatography, High Pressure LiquidDisease Models, AnimalHumansImmune EvasionImmunity, InnateMethicillin-Resistant Staphylococcus aureusNeutrophil InfiltrationNeutrophilsStaphylococcal InfectionsBacterial Toxinsstaphylococcal delta toxin

Identifiers

PMID25144687
PMCPMC4140855
OpenAlexW1982324424

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.