Evidence map›Paper›PMID 25678692›Full record

ArticleInvestigative ophthalmology & visual science2015

In Vivo Role of TLR2 and MyD88 Signaling in Eliciting Innate Immune Responses in Staphylococcal Endophthalmitis.

Deepa Talreja, Pawan Kumar Singh, Ashok Kumar

Open access · hybridAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 54 citations in OpenAlex.

  1. Infection and immunity · 2026
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  10. Immune Fingerprint in Diabetes: Ocular Surface and Retinal Inflammation.International journal of molecular sciences · 2023
    Review
  11. The Role of C-X-C Chemokines in Staphylococcus aureus Endophthalmitis.Investigative ophthalmology & visual science · 2023
    Article
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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

3 authors at 2 institutions in 1 country.

Deepa TalrejaDepartment of Ophthalmology/Kresge Eye Institute, Wayne State University, Detroit, Michigan, United States Department of Biological Sciences, Oakland University, Rochester, Michigan, United States.
Pawan Kumar SinghDepartment of Ophthalmology/Kresge Eye Institute, Wayne State University, Detroit, Michigan, United States Department of Anatomy and Cell Biology, Wayne State University, Detroit, Michigan, United States.
Ashok KumarDepartment of Ophthalmology/Kresge Eye Institute, Wayne State University, Detroit, Michigan, United States.
Wayne State University · USMichigan United · US

Funding

VISION RESEARCH--COREP30EY004068 · NEI · WAYNE STATE UNIVERSITY · PI LINDA D HAZLETT · 1985 to 2026
$13.2M
Toll-like receptors and bacterial endophthalmitisR01EY019888 · NEI · WAYNE STATE UNIVERSITY · PI KUMAR, ASHOK · 2010 to 2014
$1.6M
NEI NIH HHS EY19888NEI NIH HHS P30 EY004068NEI NIH HHS P30EY004068NEI NIH HHS R01 EY019888
6 · The paper itself

Abstract

purposeThe purpose of this study was to investigate the protective mechanisms evoked by TLR2 and MyD88 signaling in bacterial endophthalmitis in vivo.

methodsEndophthalmitis was induced in wild-type (WT), TLR2(-/-), MyD88(-/-), and Cnlp(-/-) mice by intravitreal injections of a laboratory strain (RN6390) and two endophthalmitis isolates of Staphylococcus aureus. Disease progression was monitored by assessing corneal and vitreous haze, bacterial burden, and retinal tissue damage. Levels of inflammatory cytokines/chemokines were determined using quantitative RT-PCR (qRT-PCR) and ELISA. Flow cytometry was used to assess neutrophil infiltration. Cathelicidin-related antimicrobial peptide (CRAMP) expression was determined by immunostaining and dot blot.

resultsEyes infected with either laboratory or clinical isolates exhibited higher levels of inflammatory mediators at the early stages of infection (≤24 hours) in WT mice than in TLR2(-/-) or MyD88(-/-) mice. However, their levels surpassed that of WT mice at the later stages of infection (>48 hours), coinciding with increased bacterial burden and retinal damage. Both TLR2(-/-) and MyD88(-/-) retinas produced reduced levels of CRAMP, and its deficiency (Cnlp(-/-)) rendered the mice susceptible to increased bacterial burden and retinal tissue damage as early as 1 day post infection. Analyses of inflammatory mediators and neutrophil levels in WT versus Cnlp(-/-) mice showed a trend similar to that observed in TLR2 and MyD88 KO mice. Furthermore, we observed that even a 10-fold lower infective dose of S. aureus was sufficient to cause endophthalmitis in TLR2(-/-) and MyD88(-/-) mice.

conclusionsTLR2 and MyD88 signaling plays an important role in protecting the retina from staphylococcal endophthalmitis by production of the antimicrobial peptide CRAMP.

Indexed as

AnimalsAntimicrobial Cationic PeptidesCathelicidinsChemokinesCytokinesEndophthalmitisImmunity, InnateMiceMice, Inbred C57BLMice, KnockoutMyeloid Differentiation Factor 88RetinaSignal TransductionStaphylococcal InfectionsToll-Like Receptor 2Antimicrobial Cationic PeptidesCathelicidinsChemokinesCytokinesMyd88 protein, mouseMyeloid Differentiation Factor 88Tlr2 protein, mouseToll-Like Receptor 2CRAMPendophthalmitisinflammationMyD88retinal damageStaphylococcus aureusTLR2

Identifiers

PMID25678692
PMCPMC4356198
OpenAlexW2031396061

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.