Evidence map›Paper›PMID 19845797›Full record

ArticleImmunology2010

Auxiliary role for D-alanylated wall teichoic acid in Toll-like receptor 2-mediated survival of Staphylococcus aureus in macrophages.

Akiko Shiratsuchi, Kaori Shimizu, Ikuko Watanabe, Yumi Hashimoto, Kenji Kurokawa, Iony M Razanajatovo, Keun H Park, Hae K Park, Bok L Lee, Kazuhisa Sekimizu and 1 more

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Teichoic acid biosynthesis as an antibiotic target.Current opinion in microbiology · 2013
    Review
  8. Article
  9. A Streptococcus pneumoniae infection model in larvae of the wax moth Galleria mellonella.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2012
    Article
  10. Article
  11. 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

11 authors at 4 institutions in 3 countries.

Akiko ShiratsuchiGraduate School of Medical Science, Kanazawa University, Kanazawa, Japan. shira@kenroku.kanazawa-u.ac.jp
Kaori Shimizu
Ikuko Watanabe
Yumi Hashimoto
Kenji Kurokawa
Iony M Razanajatovo
Keun H Park
Hae K Park
Bok L Lee
Kazuhisa Sekimizu
Yoshinobu Nakanishi
Graduate School USA · USPusan National University · KRThe University of Tokyo · JPKanazawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously reported that Staphylococcus aureus avoids killing within macrophages by exploiting the action of Toll-like receptor 2 (TLR2), which leads to the c-Jun N-terminal kinase (JNK)-mediated inhibition of superoxide production. To search for bacterial components responsible for this event, a series of S. aureus mutants, in which the synthesis of the cell wall was interrupted, were screened for the level of JNK activation in macrophages. In addition to a mutant lacking the lipoproteins that have been suggested to act as a TLR2 ligand, two mutant strains were found to activate the phosphorylation of JNK to a lesser extent than the parental strain, and this defect was recovered by acquisition of the corresponding wild-type genes. Macrophages that had phagocytosed the mutant strains produced more superoxide than those engulfing the parental strain, and the mutant bacteria were more efficiently killed in macrophages than the parent. The genes mutated, dltA and tagO, encoded proteins involved in the synthesis of D-alanylated wall teichoic acid. Unlike a cell wall fraction rich in lipoproteins, D-alanine-bound wall teichoic acid purified from the parent strain by itself did not activate JNK phosphorylation in macrophages. These results suggest that the d-alanylated wall teichoic acid of S. aureus modulates the cell wall milieu for lipoproteins so that they effectively serve as a ligand for TLR2.

Indexed as

AnimalsBacterial ProteinsBacteriolysisCarrier ProteinsCell LineCell WallEnzyme ActivationGenetic Complementation TestLipopolysaccharidesMacrophagesMAP Kinase Kinase 4MiceMutagenesis, Site-DirectedMutationPhagocytosisStaphylococcal InfectionsBacterial ProteinsCarrier ProteinsD-alanyl carrier protein, bacteriaLipopolysaccharideslipoteichoic acidMAP Kinase Kinase 4SuperoxidesTeichoic AcidsToll-Like Receptor 2

Identifiers

PMID19845797
PMCPMC2814468
OpenAlexW2052471284

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.