Evidence map›Paper›PMID 22733574›Full record

ArticleInfection and immunity2012

Host response signature to Staphylococcus aureus alpha-hemolysin implicates pulmonary Th17 response.

Karen M Frank, Tong Zhou, Liliana Moreno-Vinasco, Brian Hollett, Joe G N Garcia, Juliane Bubeck Wardenburg

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. IL-33-mediated Eosinophilia Protects against Acute Lung Injury.American journal of respiratory cell and molecular biology · 2021
    Article
  5. Frontiers in immunology · 2020
    Article
  6. Co-infection ofFrontiers in cellular and infection microbiology · 2020
    Article
  7. Article
  8. Review
  9. Article
  10. The open microbiology journal · 2018
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Where does a Staphylococcus aureus vaccine stand?Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases · 2014
    Review
  18. Review
  19. TGFBR1 is required for mouse myometrial development.Molecular endocrinology (Baltimore, Md.) · 2014
    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

6 authors at 2 institutions in 1 country.

Karen M FrankDepartment of Pathology, University of Chicago, Chicago, Illinois, USA. karen.frank@nih.gov
Tong Zhou
Liliana Moreno-Vinasco
Brian Hollett
Joe G N Garcia
Juliane Bubeck Wardenburg
University of Chicago · USUniversity of Illinois Chicago · US

Funding

Vaccines and Therapies Against BotulismU54AI057153 · NIAID · UNIVERSITY OF CHICAGO · PI MISSIAKAS, DOMINIQUE M. · 2003 to 2013
$87.6M
Role of Staphylococcus aureus alpha-hemolysin in diseaseR01AI097434 · NIAID · WASHINGTON UNIVERSITY · PI BUBECK WARDENBURG, JULIANE · 2012 to 2021
$4.0M
NIAID NIH HHS 2-U54-AI-057153NIAID NIH HHS AI097434NIAID NIH HHS R01 AI097434NIAID NIH HHS U54 AI057153
6 · The paper itself

Abstract

Staphylococcus aureus pneumonia causes significant morbidity and mortality. Alpha-hemolysin (Hla), a pore-forming cytotoxin of S. aureus, has been identified through animal models of pneumonia as a critical virulence factor that induces lung injury. In spite of considerable molecular knowledge of how this cytotoxin injures the host, the precise host response to Hla in the context of infection remains poorly understood. We employed whole-genome expression profiling of infected lungs to define the host response to wild-type S. aureus compared with the response to an Hla-deficient isogenic mutant in experimental pneumonia. These data provide a complete expression profile at 4 and at 24 h postinfection, revealing a unique response to the toxin-expressing strain. Gene ontogeny analysis revealed significant differences in the extracellular matrix and cardiomyopathy pathways, both of which govern cellular interactions in the tissue microenvironment. Evaluation of individual transcript responses to Hla-secreting staphylococci was notable for upregulation of host cytokine and chemokine genes, including the p19 subunit of interleukin-23. Consistent with this observation, the cellular immune response to infection was characterized by a prominent Th17 response to the wild-type pathogen. These findings define specific host mRNA responses to Hla-producing S. aureus, coupling the pulmonary Th17 response to the secretion of this cytotoxin. Expression profiling to define the host response to a single virulence factor proved to be a valuable tool in identifying pathways for further investigation in S. aureus pneumonia. This approach may be broadly applicable to the study of bacterial toxins, defining host pathways that can be targeted to mitigate toxin-induced disease.

Indexed as

Host-Pathogen InteractionsAnimalsBacterial ToxinsDisease Models, AnimalFemaleGene Expression ProfilingHemolysin ProteinsHumansLungMiceMice, Inbred C57BLPneumonia, StaphylococcalStaphylococcus aureusTh17 CellsTime FactorsVirulence FactorsBacterial ToxinsHemolysin Proteinsstaphylococcal alpha-toxinVirulence Factors

Identifiers

PMID22733574
PMCPMC3418743
OpenAlexW2151770040

What OpenQuestion holds

Textmetadata
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.