Evidence map›Paper›PMID 20542250›Full record

ArticleCell host & microbe2010

Human formyl peptide receptor 2 senses highly pathogenic Staphylococcus aureus.

Dorothee Kretschmer, Anne-Kathrin Gleske, Maren Rautenberg, Rong Wang, Martin Köberle, Erwin Bohn, Torsten Schöneberg, Marie-Joséphe Rabiet, Francois Boulay, Seymour J Klebanoff and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell host & microbe, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers.

0numbers the graph read from it
0cells of the map it votes in
152citing papers in PubMed
8.2field-weighted citation impact, top 2% 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

152 citing papers in PubMed, 277 citations in OpenAlex.

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  6. The Pathogenicity Mechanisms ofInternational journal of molecular sciences · 2025
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  7. bioRxiv : the preprint server for biology · 2025
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  9. Molecular Characteristics and Pathogenicity ofInternational journal of molecular sciences · 2023
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  13. Virulence Mechanisms of Staphylococcal Animal Pathogens.International journal of molecular sciences · 2023
    Review
  14. Review
  15. Microbes and the fate of neutrophils.Immunological reviews · 2023
    Review
  16. Review
  17. Article
  18. Genotypes ofToxins · 2022
    Article
  19. Exploring the Role ofToxins · 2022
    Review
  20. Phenol-soluble modulins PSMα3 and PSMβ2 form nanotubes that are cross-α amyloids.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article

92 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 8 institutions in 4 countries.

Dorothee KretschmerCellular and Molecular Microbiology Division, Interfaculty Institute of Microbiology and Infection Medicine, University of Tübingen, Elfriede-Aulhorn-Strasse 6, 72076 Tübingen, Germany.
Anne-Kathrin Gleske
Maren Rautenberg
Rong Wang
Martin Köberle
Erwin Bohn
Torsten Schöneberg
Marie-Joséphe Rabiet
Francois Boulay
Seymour J Klebanoff
Kok A van Kessel
Jos A van Strijp
Michael Otto
Andreas Peschel
University of Tübingen · DEUniversity Medical Center Utrecht · NLInstitut de Recherches en Technologies et Sciences pour le Vivant · FRLeipzig University · DENational Institute of Allergy and Infectious Diseases · USNational Institutes of Health · USUniversité Joseph Fourier · FRUniversity of Washington · US

Funding

Staphylococcal pathogenesisZIAAI000904 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI OTTO, MICHAEL · 2009 to 2025
$22.6M
Intramural NIH HHS ZIA AI000904
6 · The paper itself

Abstract

Virulence of emerging community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) and other highly pathogenic S. aureus strains depends on their production of phenol-soluble modulin (PSM) peptide toxins, which combine the capacities to attract and lyse neutrophils. The molecular basis of PSM-stimulated neutrophil recruitment has remained unclear. Here, we demonstrate that the human formyl peptide receptor 2 (FPR2/ALX), which has previously been implicated in control of endogenous inflammatory processes, senses PSMs at nanomolar concentrations and initiates proinflammatory neutrophil responses to CA-MRSA. Specific blocking of FPR2/ALX or deletion of PSM genes in CA-MRSA severely diminished neutrophil detection of CA-MRSA. Furthermore, a specific inhibitor of FPR2/ALX and of its functional mouse counterpart blocked PSM-mediated leukocyte infiltration in vivo in a mouse model. Thus, the innate immune system uses a distinct FPR2/ALX-dependent mechanism to specifically sense bacterial peptide toxins and detect highly virulent bacterial pathogens. FPR2/ALX represents an attractive target for new anti-infective or anti-inflammatory strategies.

Indexed as

Host-Pathogen InteractionsAnimalsBacterial ToxinsCommunity-Acquired InfectionsFemaleHumansMethicillin-Resistant Staphylococcus aureusMiceMice, Inbred BALB CModels, BiologicalNeutrophilsProtein BindingReceptors, Formyl PeptideReceptors, LipoxinStaphylococcal InfectionsBacterial Toxinsformyl peptide receptor 2, mouseFPR2 protein, humanReceptors, Formyl PeptideReceptors, Lipoxinstaphylococcal delta toxin

Identifiers

PMID20542250
PMCPMC3417054
OpenAlexW2013424910

What OpenQuestion holds

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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.