Evidence map›Paper›PMID 19381294›Full record

ArticlePloS one2009

Phagocytosis of Staphylococcus aureus by macrophages exerts cytoprotective effects manifested by the upregulation of antiapoptotic factors.

Joanna Koziel, Agnieszka Maciag-Gudowska, Tomasz Mikolajczyk, Malgorzata Bzowska, Daniel E Sturdevant, Adeline R Whitney, Lindsey N Shaw, Frank R DeLeo, Jan Potempa

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

89 citing papers in PubMed, 1 synthesis or guideline pooled it, 151 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Review
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  15. Intracellular Habitation ofBiomedicines · 2022
    Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

29 more citing papers are in PubMed but not listed here.

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 2 countries.

Joanna KozielDepartment of Microbiology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland. kaniajoanna@gmail.com
Agnieszka Maciag-Gudowska
Tomasz Mikolajczyk
Malgorzata Bzowska
Daniel E Sturdevant
Adeline R Whitney
Lindsey N Shaw
Frank R DeLeo
Jan Potempa
Jagiellonian University · PLNational Institute of Allergy and Infectious Diseases · USNational Institutes of Health · USUniversity of South Florida · US

Funding

Mechanisms of Staphylococcus aureus virulenceZIAAI001079 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DELEO, FRANK · 2009 to 2025
$11.8M
Interaction of pathogenic bacteria with human phagocytic leukocytesZIAAI000900 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DELEO, FRANK · 2009 to 2023
$3.6M
Interaction Of Pathogenic Bacteria With LeukocytesZ01AI000900 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI DELEO, FRANK R · 2001 to 2008
$2.8M
Mechanisms of community MRSA virulenceZ01AI001079 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DELEO, FRANK · 2008 to 2008
$806k
Intramural NIH HHS
6 · The paper itself

Abstract

It is becoming increasingly apparent that Staphylococcus aureus are able to survive engulfment by macrophages, and that the intracellular environment of these host cells, which is essential to innate host defenses against invading microorganisms, may in fact provide a refuge for staphylococcal survival and dissemination. Based on this, we postulated that S. aureus might induce cytoprotective mechanisms by changing gene expression profiles inside macrophages similar to obligate intracellular pathogens, such as Mycobacterium tuberculosis. To validate our hypothesis we first ascertained whether S. aureus infection could affect programmed cell death in human (hMDMs) and mouse (RAW 264.7) macrophages and, specifically, protect these cells against apoptosis. Our findings indicate that S. aureus-infected macrophages are more resistant to staurosporine-induced cell death than control cells, an effect partly mediated via the inhibition of cytochrome c release from mitochondria. Furthermore, transcriptome analysis of human monocyte-derived macrophages during S. aureus infection revealed a significant increase in the expression of antiapoptotic genes. This was confirmed by quantitative RT-PCR analysis of selected genes involved in mitochondria-dependent cell death, clearly showing overexpression of BCL2 and MCL1. Cumulatively, the results of our experiments argue that S. aureus is able to induce a cytoprotective effect in macrophages derived from different mammal species, which can prevent host cell elimination, and thus allow intracellular bacterial survival. Ultimately, it is our contention that this process may contribute to the systemic dissemination of S. aureus infection.

Indexed as

PhagocytosisUp-RegulationAnimalsApoptosisBase SequenceBlotting, WesternCells, CulturedDNA PrimersFlow CytometryGene ExpressionHumansMacrophagesMiceMicroscopy, FluorescencePolymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionDNA Primers

Identifiers

PMID19381294
PMCPMC2668171
OpenAlexW1981793562

What OpenQuestion holds

Textmetadata
LicenceCC0
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.