Evidence map›Paper›PMID 26053426›Full record

ArticlePloS one2015

Role of Staphylococcus aureus Virulence Factors in Inducing Inflammation and Vascular Permeability in a Mouse Model of Bacterial Endophthalmitis.

Ajay Kumar, Ashok Kumar

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

37 citing papers in PubMed, 51 citations in OpenAlex.

  1. Infection and immunity · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. The Role of C-X-C Chemokines in Staphylococcus aureus Endophthalmitis.Investigative ophthalmology & visual science · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Journal of dental sciences · 2022
    Article
  13. Article
  14. Damage-Associated Molecular Patterns (DAMPs) in Retinal Disorders.International journal of molecular sciences · 2022
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. [Postoperative endophthalmitis-a review of literature].Der Ophthalmologe : Zeitschrift der Deutschen Ophthalmologischen Gesellschaft · 2021
    Review
  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

2 authors at 1 institution in 1 country.

Ajay KumarDepartment of Ophthalmology, Kresge Eye Institute, Wayne State University, Detroit, Michigan, United States of America.
Ashok KumarDepartment of Ophthalmology, Kresge Eye Institute, Wayne State University, Detroit, Michigan, United States of America; Department of Anatomy and Cell Biology, Wayne State University, Detroit, Michigan, United States of America; Department of Immunology and Microbiology, Wayne State University, Detroit, Michigan, United States of America.
Wayne State University · US

Funding

Toll-like receptors and bacterial endophthalmitisR01EY019888 · NEI · WAYNE STATE UNIVERSITY · PI KUMAR, ASHOK · 2010 to 2014
$1.6M
NEI NIH HHS R01 EY019888NEI NIH HHS R01 EY19888
6 · The paper itself

Abstract

Staphylococcus (S.) aureus is a common causative agent of bacterial endophthalmitis, a vision threatening complication of eye surgeries. The relative contribution of S. aureus virulence factors in the pathogenesis of endophthalmitis remains unclear. Here, we comprehensively analyzed the development of intraocular inflammation, vascular permeability, and the loss of retinal function in C57BL/6 mouse eyes, challenged with live S. aureus, heat-killed S. aureus (HKSA), peptidoglycan (PGN), lipoteichoic acid (LTA), staphylococcal protein A (SPA), α-toxin, and Toxic-shock syndrome toxin 1 (TSST1). Our data showed a dose-dependent (range 0.01 μg/eye to 1.0 μg/eye) increase in the levels of inflammatory mediators by all virulence factors. The cell wall components, particularly PGN and LTA, seem to induce higher levels of TNF-α, IL-6, KC, and MIP2, whereas the toxins induced IL-1β. Similarly, among the virulence factors, PGN induced higher PMN infiltration. The vascular permeability assay revealed significant leakage in eyes challenged with live SA (12-fold) and HKSA (7.3-fold), in comparison to other virulence factors (~2-fold) and controls. These changes coincided with retinal tissue damage, as evidenced by histological analysis. The electroretinogram (ERG) analysis revealed a significant decline in retinal function in eyes inoculated with live SA, followed by HKSA, SPA, and α-toxin. Together, these findings demonstrate the differential innate responses of the retina to S. aureus virulence factors, which contribute to intraocular inflammation and retinal function loss in endophthalmitis.

Indexed as

Capillary PermeabilityAnimalsDisease Models, AnimalEndophthalmitisEye ProteinsFemaleFundus OculiInflammationMice, Inbred C57BLNeutrophil InfiltrationPeptidoglycanRetinaStaphylococcal InfectionsStaphylococcus aureusVirulence FactorsEye ProteinsPeptidoglycanVirulence Factors

Identifiers

PMID26053426
PMCPMC4459968
OpenAlexW1521005370

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.