Evidence map›Paper›PMID 21654154›Full record

ArticleJournal of innate immunity2011

Staphylococcus aureus evades the extracellular antimicrobial activity of mast cells by promoting its own uptake.

Jens Abel, Oliver Goldmann, Christina Ziegler, Claudia Höltje, Mark S Smeltzer, Ambrose L Cheung, Daniela Bruhn, Manfred Rohde, Eva Medina

Open access · bronzeAbstract read
In one paragraph

Article in Journal of innate immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

44 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Impact ofFrontiers in gastroenterology (Lausanne, Switzerland) · 2024
    Review
  5. Review
  6. Review
  7. Antigen specific activation of cytotoxic CD8Frontiers in cellular and infection microbiology · 2023
    Article
  8. Review
  9. Review
  10. Extracellular traps and the role in thrombosis.Frontiers in cardiovascular medicine · 2022
    Review
  11. Review
  12. Review
  13. Investigation of aInternational journal of molecular sciences · 2020
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Frontiers in cellular and infection microbiology · 2019
    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

9 authors at 4 institutions in 3 countries.

Jens AbelInfection Immunology Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Oliver Goldmann
Christina Ziegler
Claudia Höltje
Mark S Smeltzer
Ambrose L Cheung
Daniela Bruhn
Manfred Rohde
Eva Medina
Biology of Infection · FRHelmholtz Centre for Infection Research · DEDartmouth College · USUniversity of Arkansas for Medical Sciences · US

Funding

SAR-MEDIATED REGULATION IN STAPHYLOCOCCUS AUREUSR01AI043356 · NIAID · UNIV OF ARKANSAS FOR MED SCIS · PI SMELTZER, MARK S · 1998 to 2008
$2.0M
Regulation of biofilm formation in clinical isolates of Staphylococcus aureusR01AI074935 · NIAID · UNIV OF ARKANSAS FOR MED SCIS · PI SMELTZER, MARK S · 2007 to 2011
$1.6M
NIAID NIH HHS R01 AI043356NIAID NIH HHS R01 AI074935
6 · The paper itself

Abstract

In this study, we investigated the interactions of Staphylococcus aureus with mast cells, which are multifunctional sentinels lining the surfaces of the body. We found that bone marrow-derived murine mast cells (BMMC) exerted a powerful phagocytosis-independent antimicrobial activity against S. aureus. Both the release of extracellular traps as well as discharge of antimicrobial compounds were the mechanisms used by the BMMC to kill extracellular S. aureus. This was accompanied by the secretion of mediators such as TNF-α involved in the recruitment of effector cells. Interestingly, S. aureus subverted the extracellular antimicrobial activity of the BMMC by internalizing within these cells. S. aureus was also capable to internalize within human mast cells (HMC-1) and within murine skin mast cells during in vivo infection. Bacteria internalization was, at least in part, mediated by the α5β1 integrins expressed on the surface of the mast cell. In the intracellular milieu, the bacterium survived and persisted by increasing the cell wall thickness and by gaining access into the mast cell cytosol. The expression of α-hemolysin was essential for staphylococci intracellular persistence. By hiding within the long-life mast cells, staphylococci not only avoid clearance but also establish an infection reservoir that could contribute to chronic carriage.

Indexed as

AnimalsApoptosisBacterial ToxinsCarrier StateCell LineCytotoxicity, ImmunologicDisease ReservoirsEndocytosisHemolysin ProteinsHost-Pathogen InteractionsHumansImmune EvasionIntegrin alpha5beta1Mast CellsMiceMice, Inbred C57BLBacterial ToxinsHemolysin ProteinsIntegrin alpha5beta1staphylococcal alpha-toxinTumor Necrosis Factor-alpha

Identifiers

PMID21654154
PMCPMC11990236
OpenAlexW2091286928

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.