Evidence map›Paper›PMID 24481289›Full record

ArticleJournal of innate immunity2014

A Staphylococcus aureus TIR domain protein virulence factor blocks TLR2-mediated NF-κB signaling.

Fatemeh Askarian, Nina M van Sorge, Maria Sangvik, Federico C Beasley, Jørn R Henriksen, Johanna U E Sollid, Jos A G van Strijp, Victor Nizet, Mona Johannessen

Open access · hybridAbstract read
In one paragraph

Article in Journal of innate immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.3field-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

43 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
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  3. Review
  4. Review
  5. Review
  6. Article
  7. Exploring the Accessory Genome of Multidrug-ResistantAntibiotics (Basel, Switzerland) · 2023
    Article
  8. Characterization ofFrontiers in immunology · 2023
    Article
  9. Article
  10. Article
  11. Review
  12. AmBio · 2021
    Article
  13. Regulation of Expression of thePathogens (Basel, Switzerland) · 2021
    Article
  14. Inhibitory Role of anFrontiers in microbiology · 2021
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

9 authors at 4 institutions in 3 countries.

Fatemeh AskarianResearch Group of Host-Microbe Interactions, Department of Medical Biology, Faculty of Health Sciences, UiT The Artic University of Norway, Tromsø, Norway.
Nina M van Sorge
Maria Sangvik
Federico C Beasley
Jørn R Henriksen
Johanna U E Sollid
Jos A G van Strijp
Victor Nizet
Mona Johannessen
University Medical Center Utrecht · NLArcticZymes (Norway) · NOUniversity of California, San Diego · USUniversity of Montana · US

Funding

Vaccines and Therapies Against BotulismU54AI057153 · NIAID · UNIVERSITY OF CHICAGO · PI MISSIAKAS, DOMINIQUE M. · 2003 to 2013
$87.6M
Boosting Innate Immunity Through HIF to Treat Drug-Resistant Bacterial InfectionsR56AI090863 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JOHNSON, RANDALL SCOTT, NIZET, VICTOR · 2010 to 2010
$704k
NIAID NIH HHS AI057153NIAID NIH HHS R56 AI090863NIAID NIH HHS U54 AI057153
6 · The paper itself

Abstract

Signaling through Toll-like receptors (TLRs), crucial molecules in the induction of host defense responses, requires adaptor proteins that contain a Toll/interleukin-1 receptor (TIR) domain. The pathogen Staphylococcus aureus produces several innate immune-evasion molecules that interfere with the host's innate immune response. A database search analysis suggested the presence of a gene encoding a homologue of the human TIR domain in S. aureus MSSA476 which was named staphylococcal TIR domain protein (TirS). Ectopic expression of TirS in human embryonic kidney, macrophage and keratinocyte cell lines interfered with signaling through TLR2, including MyD88 and TIRAP, NF-κB and/or mitogen-activated protein kinase pathways. Moreover, the presence of TirS reduced the levels of cytokines MCP-1 and G-CSF secreted in response to S. aureus. The effects on NF-κB pathway were confirmed using S. aureus MSSA476 wild type, an isogenic mutant MSSA476ΔtirS, and complemented MSSA476ΔtirS +pTirS in a Transwell system where bacteria and host cells were physically separated. Finally, in a systematic mouse infection model, TirS promoted bacterial accumulation in several organs 4 days postinfection. The results of this study reveal a new S. aureus virulence factor that can interfere with PAMP-induced innate immune signaling in vitro and bacterial survival in vivo.

Indexed as

Adaptor Proteins, Vesicular TransportAmino Acid SequenceAnimalsBacterial LoadBacterial ProteinsCell LineChemokine CCL2Disease Models, AnimalFemaleGranulocyte Colony-Stimulating FactorHumansImmune EvasionMembrane GlycoproteinsMiceMice, Inbred C57BLMolecular Sequence DataAdaptor Proteins, Vesicular TransportBacterial ProteinsCCL2 protein, humanChemokine CCL2Granulocyte Colony-Stimulating FactorMembrane GlycoproteinsMyeloid Differentiation Factor 88NF-kappa BReceptors, Interleukin-1TICAM1 protein, humanTIRAP protein, humanTIR domain protein, Staphylococcus aureusToll-Like Receptor 2Virulence Factors

Identifiers

PMID24481289
PMCPMC4198549
OpenAlexW2107139181

What OpenQuestion holds

Textmetadata
LicenceTDM
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.