Evidence map›Paper›PMID 21603642›Full record

ArticlePloS one2011

The SaeR/S gene regulatory system induces a pro-inflammatory cytokine response during Staphylococcus aureus infection.

Robert L Watkins, Kyler B Pallister, Jovanka M Voyich

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Effects ofFoods (Basel, Switzerland) · 2023
    Article
  4. Review
  5. Review
  6. Infection and drug resistance · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Epic Immune Battles of History: Neutrophils vs.Frontiers in cellular and infection microbiology · 2017
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Differential regulation of staphylococcal virulence by the sensor kinase SaeS in response to neutrophil-derived stimuli.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  18. Article
  19. 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

3 authors at 1 institution in 1 country.

Robert L WatkinsDepartment of Immunology/Infectious Diseases, Montana State University-Bozeman, Bozeman, Montana, United States of America.
Kyler B Pallister
Jovanka M Voyich
Montana State University · US

Funding

VIRUSES: FROM PARTICLES TO PROTEOMICSP20RR020185 · NCRR · MONTANA STATE UNIVERSITY - BOZEMAN · PI QUINN, MARK T · 2004 to 2011
$17.0M
Role of the Staphylococcus aureus SaeR/S Regulatory System in Neutrophil EvasionR01AI090046 · NIAID · MONTANA STATE UNIVERSITY - BOZEMAN · PI VOYICH, JOVANKA M · 2011 to 2015
$1.7M
NCRR NIH HHS P20 RR020185NCRR NIH HHS RR020185NIAID NIH HHS R01 AI090046PHS HHS PAR98-072
6 · The paper itself

Abstract

Community-associated methicillin-resistant Staphylococcus aureus accounts for a large portion of the increased staphylococcal disease incidence and can cause illness ranging from mild skin infections to rapidly fatal sepsis syndromes. Currently, we have limited understanding of S. aureus-derived mechanisms contributing to bacterial pathogenesis and host inflammation during staphylococcal disease. Herein, we characterize an influential role for the saeR/S two-component gene regulatory system in mediating cytokine induction using mouse models of S. aureus pathogenesis. Invasive S. aureus infection induced the production of localized and systemic pro-inflammatory cytokines, including tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), interleukin (IL)-6 and IL-2. In contrast, mice infected with an isogenic saeR/S deletion mutant demonstrated significantly reduced pro-inflammatory cytokine levels. Additionally, secreted factors influenced by saeR/S elicited pro-inflammatory cytokines in human blood ex vivo. Our study further demonstrated robust saeR/S-mediated IFN-γ production during both invasive and subcutaneous skin infections. Results also indicated a critical role for saeR/S in promoting bacterial survival and enhancing host mortality during S. aureus peritonitis. Taken together, this study provides insight into specific mechanisms used by S. aureus during staphylococcal disease and characterizes a relationship between a bacterial global regulator of virulence and the production of pro-inflammatory mediators.

Indexed as

AnimalsBacterial ProteinsCytokinesHumansInflammation MediatorsMicePeritonitisStaphylococcal InfectionsStaphylococcus aureusBacterial ProteinsCytokinesInflammation Mediators

Identifiers

PMID21603642
PMCPMC3094403
OpenAlexW2050792737

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.