Evidence map›Paper›PMID 19633710›Full record

ArticlePloS one2009

Staphylococcus aureus Panton-Valentine leukocidin contributes to inflammation and muscle tissue injury.

Ching Wen Tseng, Pierre Kyme, Jennifer Low, Miguel A Rocha, Randa Alsabeh, Loren G Miller, Michael Otto, Moshe Arditi, Binh An Diep, Victor Nizet and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
9.2field-weighted citation impact, top 1% 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

57 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. In Vivo Pathogenicity of Methicillin-SusceptibleLife (Basel, Switzerland) · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. The bicomponent pore-forming leucocidins of Staphylococcus aureus.Microbiology and molecular biology reviews : MMBR · 2014
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Role of pore-forming toxins in bacterial infectious diseases.Microbiology and molecular biology reviews : MMBR · 2013
    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

13 authors at 6 institutions in 1 country.

Ching Wen TsengDivision of Pediatric Infectious Diseases and the Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Pierre Kyme
Jennifer Low
Miguel A Rocha
Randa Alsabeh
Loren G Miller
Michael Otto
Moshe Arditi
Binh An Diep
Victor Nizet
Terence M Doherty
David O Beenhouwer
George Y Liu
University of California, Los Angeles · USCedars-Sinai Medical Center · USNational Institute of Allergy and Infectious Diseases · USUniversity of California, San Francisco · USUniversity of Montana · USVA Greater Los Angeles Healthcare System · US

Funding

Staphylococcal pathogenesisZIAAI000904 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI OTTO, MICHAEL · 2009 to 2025
$22.6M
Antioxidant-based mechanisms used by staphyloccocus aureus to evade host defensesR01AI074832 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI LIU, GEORGE Y · 2007 to 2010
$1.6M
NIAID NIH HHS AI074832NIAID NIH HHS R01 AI074832Wellcome Trust
6 · The paper itself

Abstract

Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) threatens public health worldwide, and epidemiologic data suggest that the Panton-Valentine Leukocidin (PVL) expressed by most CA-MRSA strains could contribute to severe human infections, particularly in young and immunocompetent hosts. PVL is proposed to induce cytolysis or apoptosis of phagocytes. However, recent comparisons of isogenic CA-MRSA strains with or without PVL have revealed no differences in human PMN cytolytic activity. Furthermore, many of the mouse studies performed to date have failed to demonstrate a virulence role for PVL, thereby provoking the question: does PVL have a mechanistic role in human infection? In this report, we evaluated the contribution of PVL to severe skin and soft tissue infection. We generated PVL mutants in CA-MRSA strains isolated from patients with necrotizing fasciitis and used these tools to evaluate the pathogenic role of PVL in vivo. In a model of necrotizing soft tissue infection, we found PVL caused significant damage of muscle but not the skin. Muscle injury was linked to induction of pro-inflammatory chemokines KC, MIP-2, and RANTES, and recruitment of neutrophils. Tissue damage was most prominent in young mice and in those strains of mice that more effectively cleared S. aureus, and was not significant in older mice and mouse strains that had a more limited immune response to the pathogen. PVL mediated injury could be blocked by pretreatment with anti-PVL antibodies. Our data provide new insights into CA-MRSA pathogenesis, epidemiology and therapeutics. PVL could contribute to the increased incidence of myositis in CA-MRSA infection, and the toxin could mediate tissue injury by mechanisms other than direct killing of phagocytes.

Indexed as

AnimalsBacterial ToxinsBase SequenceDNA PrimersEnzyme-Linked Immunosorbent AssayExotoxinsFluorescent Antibody TechniqueLeukocidinsMiceMice, Inbred StrainsMusclesMutagenesis, Site-DirectedStaphylococcus aureusVirulenceBacterial ToxinsDNA PrimersExotoxinsLeukocidinsPanton-Valentine leukocidin

Identifiers

PMID19633710
PMCPMC2711303
OpenAlexW2164772047

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.