Evidence map›Paper›PMID 21777408›Full record

ArticleCellular microbiology2011

In vitro endothelial cell damage is positively correlated with enhanced virulence and poor vancomycin responsiveness in experimental endocarditis due to methicillin-resistant Staphylococcus aureus.

Kati Seidl, Arnold S Bayer, James A McKinnell, Steven Ellison, Scott G Filler, Yan Q Xiong

Open access · bronzeAbstract read
In one paragraph

Article in Cellular microbiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

26 citing papers in PubMed, 32 citations in OpenAlex.

  1. Trial
  2. Staphylococcus aureus-vascular endothelium interactions: Mechanisms and therapeutic opportunities.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026
    Review
  3. Antithrombotic therapy in infective endocarditis: Long-term clinical outcomes of a retrospective cohort study.Clinical research in cardiology : official journal of the German Cardiac Society · 2026
    Article
  4. Article
  5. Neutrophils Protect AgainstArteriosclerosis, thrombosis, and vascular biology · 2023
    Article
  6. Article
  7. Article
  8. Identification of Methicillin-ResistantAntibiotics (Basel, Switzerland) · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. ClinicalToxins · 2019
    Article
  14. Linezolid and Rifampicin Combination to CombatFrontiers in microbiology · 2019
    Article
  15. Article
  16. The ArlRS two-component system is a regulator of Staphylococcus aureus-induced endothelial cell damage.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2018
    Article
  17. Pathogen-related factors affecting outcome of catheter-related bacteremia due to methicillin-susceptible Staphylococcus aureus in a Spanish multicenter study.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2017
    Observational
  18. Article
  19. 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

6 authors at 3 institutions in 1 country.

Kati SeidlLos Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA, USA. katiseidl@gmail.com
Arnold S Bayer
James A McKinnell
Steven Ellison
Scott G Filler
Yan Q Xiong
The Lundquist Institute · USHarbor–UCLA Medical Center · USUCLA Medical Center · US

Funding

ZONA-FREE HAMSTER OVA ASSAY AS AN INDICATOR OF MALE FERTILITYM01RR000425 · NCRR · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI ANDERSON, GAIL V · 1985 to 2011
$74.2M
Staphylococcal Adaptations to Platelet Microbicidal ProteinR01AI039108 · NIAID · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI BAYER, ARNOLD S · 1997 to 2016
$5.1M
Candida Invasion of Endothelium and VirulenceR01AI054928 · NIAID · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI FILLER, SCOTT G · 2004 to 2013
$2.9M
Transcriptional regulation of A. fumigatus virulenceR01AI073829 · NIAID · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI FILLER, SCOTT G · 2007 to 2015
$2.8M
NCRR NIH HHS M01 RR000425NCRR NIH HHS M01-RR00425NIAID NIH HHS R01 AI039108NIAID NIH HHS R01 AI054928NIAID NIH HHS R01AI054928NIAID NIH HHS R01 AI073829NIAID NIH HHS R01AI073829NIAID NIH HHS R01AI-39108
6 · The paper itself

Abstract

The pathogenesis of Staphylococcus aureus infective endocarditis (IE) is postulated to involve invasion and damage of endothelial cells (ECs). However, the precise relationships between S. aureus-EC interactions in vitro and IE virulence and treatment outcomes in vivo are poorly defined. Ten methicillin-resistant S. aureus (MRSA) clinical isolates previously tested for their virulence and vancomycin responsiveness in an experimental IE model were assessed in vitro for their haemolytic activity, protease production, and capacity to invade and damage ECs. There was a significant positive correlation between the in vitro EC damage caused by these MRSA strains and their virulence during experimental IE (in terms of bacterial densities in target tissues; P < 0.02). Importantly, higher EC damage was also significantly correlated with poor microbiological response to vancomycin in the IE model (P < 0.001). Interestingly, the extent of EC damage was unrelated to a strain's ability to invade ECs, haemolytic activity and protease production, or β-toxin gene transcription. Inactivation of the agr locus in two MRSA strains caused ∼20% less damage as compared with the corresponding parental strains, indicating that a functional agr is required for maximal EC damage induction. Thus, MRSA-induced EC damage in vitro is a unique virulence phenotype that is independent of many other prototypical MRSA virulence factors, and may be a key biomarker for predicting MRSA virulence potential and antibiotic outcomes during endovascular infections.

Indexed as

Host-Pathogen InteractionsVancomycin ResistanceAnti-Bacterial AgentsEndocarditisEndothelial CellsGene Expression ProfilingHemolysin ProteinsHumansMethicillin-Resistant Staphylococcus aureusModels, TheoreticalPeptide HydrolasesStaphylococcal InfectionsTranscription, GeneticVancomycinVirulenceAnti-Bacterial AgentsHemolysin ProteinsPeptide HydrolasesVancomycin

Identifiers

PMID21777408
PMCPMC3173605
OpenAlexW1546970515

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.