Evidence map›Paper›PMID 24810614›Full record

ArticlePloS one2014

Heterogeneity of host TLR2 stimulation by Staphylocoocus aureus isolates.

Dina Hilmi, Marijo Parcina, Daniel Stollewerk, Jenny Ostrop, Michaele Josten, Alina Meilaender, Ulrich Zaehringer, Thomas A Wichelhaus, Gabriele Bierbaum, Klaus Heeg and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Frontiers in microbiology · 2022
    Review
  2. Article
  3. LipoproteinmBio · 2020
    Article
  4. Article
  5. Article
  6. Article
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  11. Review
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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

12 authors at 6 institutions in 1 country.

Dina HilmiDepartment for Infectious Disease, Medical Microbiology and Hygiene, University Hospital Heidelberg, Heidelberg, Germany; Institute for Medical Microbiology, Immunology and Parasitology, University Hospital Bonn, Bonn, Germany.
Marijo ParcinaDepartment for Infectious Disease, Medical Microbiology and Hygiene, University Hospital Heidelberg, Heidelberg, Germany; Institute for Medical Microbiology, Immunology and Parasitology, University Hospital Bonn, Bonn, Germany.
Daniel StollewerkInstitute for Medical Microbiology, Immunology and Parasitology, University Hospital Bonn, Bonn, Germany.
Jenny OstropDepartment for Infectious Disease, Medical Microbiology and Hygiene, University Hospital Heidelberg, Heidelberg, Germany.
Michaele JostenInstitute for Medical Microbiology, Immunology and Parasitology, University Hospital Bonn, Bonn, Germany.
Alina MeilaenderInstitute for Medical Microbiology, Immunology and Parasitology, University Hospital Bonn, Bonn, Germany.
Ulrich ZaehringerLG Immunchemie, Research Center Borstel, Borstel, Germany.
Thomas A WichelhausInstitute of Medical Microbiology and Infection Control, Hospital of Goethe-University, Frankfurt am Main, Germany.
Gabriele BierbaumInstitute for Medical Microbiology, Immunology and Parasitology, University Hospital Bonn, Bonn, Germany.
Klaus HeegDepartment for Infectious Disease, Medical Microbiology and Hygiene, University Hospital Heidelberg, Heidelberg, Germany.
Christiane WolzIMIT-Interfakultäres Institut für Mikrobiologie und Infektionsmedizin, Universitätsklinikum Tuebingen, Tuebingen, Germany.
Isabelle Bekeredjian-DingDepartment for Infectious Disease, Medical Microbiology and Hygiene, University Hospital Heidelberg, Heidelberg, Germany; Institute for Medical Microbiology, Immunology and Parasitology, University Hospital Bonn, Bonn, Germany.
University Hospital Bonn · DEHeidelberg University · DEUniversity Hospital Heidelberg · DEGoethe University Frankfurt · DEResearch Center Borstel - Leibniz Lung Center · DEUniversitätsklinikum Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High lipoprotein expression and potent activation of host Toll-like receptor-2 (TLR2) are characteristic features of the staphylococcal species. Expression of TLR2 in the host is important for clearance of Staphylococcus aureus infection and host survival. Thus, we hypothesized that bacterial regulation of its intrinsic TLR2-stimulatory capacity could represent a means for immune evasion or host adaptation. We, therefore, compared clinical S. aureus isolates in regards to their TLR2 activation potential and assessed the bacterial factors that modulate TLR2-mediated recognition. S. aureus isolates displayed considerable variability in TLR2-activity with low to absent TLR2-activity in 64% of the isolates tested (68/106). Notably, strain-specific TLR2-activity was independent of the strain origin, e.g. no differences were found between strains isolated from respiratory specimen from cystic fibrosis patients or those isolated from invasive disease specimen. TLR2-activity correlated with protein A expression but not with the agr status. Capsule expression and small colony variant formation had a negative impact on TLR2-activity but any disruption of cell wall integrity enhanced TLR2 activation. Altogether, heterogeneity in host TLR2-activity reflects differences in metabolic activity and cell wall synthesis and/or remodeling.

Indexed as

Cell WallHEK293 CellsHumansImmunity, InnateLipoproteinsStaphylococcal InfectionsStaphylococcus aureusToll-Like Receptor 2LipoproteinsToll-Like Receptor 2

Identifiers

PMID24810614
PMCPMC4014498
OpenAlexW1977207224

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Registered trials

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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.