ArticleInfection and immunity2015
Unexpected Roles for Toll-Like Receptor 4 and TRIF in Intraocular Infection with Gram-Positive Bacteria.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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.
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.
Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Cytometric Evaluation of Cytokine Factors in Serum and Vitreous from Endophthalmitis Patients: Correlated Elevation in Neutrophil Markers.Biomedicines · 2025Article
- Novel Anti-Microbial/Anti-Inflammatory Combination Improves Clinical Outcome of Bacillus cereus Endophthalmitis.Investigative ophthalmology & visual science · 2025Article
- The Role of CCL Chemokines in Experimental Staphylococcus aureus Endophthalmitis.Investigative ophthalmology & visual science · 2024Article
- Therapeutic potential ofmSphere · 2023Article
- The Role of C-X-C Chemokines in Staphylococcus aureus Endophthalmitis.Investigative ophthalmology & visual science · 2023Article
- Roles of CCL2 and CCL3 in intraocular inflammation during Bacillus endophthalmitis.Experimental eye research · 2022Article
- C-X-C Chemokines Influence Intraocular Inflammation During Bacillus Endophthalmitis.Investigative ophthalmology & visual science · 2021Article
- Immune Inhibitor A Metalloproteases Contribute to Virulence inInfection and immunity · 2021Article
- Intravitreal Injection and Quantitation of Infection Parameters in a Mouse Model of Bacterial Endophthalmitis.Journal of visualized experiments : JoVE · 2021Article
- Transcriptomic and Histological Analysis of Exacerbated Immune Response in Multidrug-ResistantFrontiers in immunology · 2021Article
- Innate Immune Interference Attenuates Inflammation In Bacillus Endophthalmitis.Investigative ophthalmology & visual science · 2020Article
- Toll-like receptors in acute post-cataract surgery endophthalmitis.International ophthalmology · 2020Article
- Toll-like receptor 2 (TLR2) engages endoplasmic reticulum stress sensor IRE1α to regulate retinal innate responses in Staphylococcus aureus endophthalmitis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Glycolytic inhibitor 2-deoxyglucose suppresses inflammatory response in innate immune cells and experimental staphylococcal endophthalmitis.Experimental eye research · 2020Article
- The cereus matter of Bacillus endophthalmitis.Experimental eye research · 2020Review
- Article
- A Pyrrhic Victory: The PMN Response to Ocular Bacterial Infections.Microorganisms · 2019Review
- Targets of immunomodulation in bacterial endophthalmitis.Progress in retinal and eye research · 2019Review
- Zebrafish are Resistant toPathogens (Basel, Switzerland) · 2019Article
- S-layer Impacts the Virulence of Bacillus in Endophthalmitis.Investigative ophthalmology & visual science · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Inflammation caused by infection with Gram-positive bacteria is typically initiated by interactions with Toll-like receptor 2 (TLR2). Endophthalmitis, an infection and inflammation of the posterior segment of the eye, can lead to vision loss when initiated by a virulent microbial pathogen. Endophthalmitis caused by Bacillus cereus develops as acute inflammation with infiltrating neutrophils, and vision loss is potentially catastrophic. Residual inflammation observed during B. cereus endophthalmitis in TLR2(-/-) mice led us to investigate additional innate pathways that may trigger intraocular inflammation. We first hypothesized that intraocular inflammation during B. cereus endophthalmitis would be controlled by MyD88- and TRIF-mediated signaling, since MyD88 and TRIF are the major adaptor molecules for all bacterial TLRs. In MyD88(-/-) and TRIF(-/-) mice, we observed significantly less intraocular inflammation than in eyes from infected C57BL/6J mice, suggesting an important role for these TLR adaptors in B. cereus endophthalmitis. These results led to a second hypothesis, that TLR4, the only TLR that signals through both MyD88 and TRIF signaling pathways, contributed to inflammation during B. cereus endophthalmitis. Surprisingly, B. cereus-infected TLR4(-/-) eyes also had significantly less intraocular inflammation than infected C57BL/6J eyes, indicating an important role for TLR4 in B. cereus endophthalmitis. Taken together, our results suggest that TLR4, TRIF, and MyD88 are important components of the intraocular inflammatory response observed in experimental B. cereus endophthalmitis, identifying a novel innate immune interaction for B. cereus and for this disease.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.