ArticleInfection and immunity2006
Staphylococcus aureus-induced corneal inflammation is dependent on Toll-like receptor 2 and myeloid differentiation factor 88.
Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 86 citations in OpenAlex.
- Impact of innate immune factors on the persistence of Staphylococcus aureus in the ocular environment.Experimental eye research · 2025Article
- Epithelial Heparan Sulfate PromotesProteoglycan research · 2025Article
- Innate Immune System Activation, Inflammation and Corneal Wound Healing.International journal of molecular sciences · 2022Review
- Role of surfactant protein-D in ocular bacterial infection.International ophthalmology · 2022Review
- Bacteria and Dry Eye: A Narrative Review.Journal of clinical medicine · 2022Review
- Review
- Foundational concepts in the biology of bacterial keratitis.Experimental eye research · 2021Review
- The role of Staphylococcus aureus lipoproteins in hematogenous septic arthritis.Scientific reports · 2020Article
- A Pyrrhic Victory: The PMN Response to Ocular Bacterial Infections.Microorganisms · 2019Review
- Staphylococcus aureus alpha-hemolysin impairs corneal epithelial wound healing and promotes intracellular bacterial invasion.Experimental eye research · 2019Article
- Mast Cells Initiate the Recruitment of Neutrophils Following Ocular Surface Injury.Investigative ophthalmology & visual science · 2018Article
- The expression profiles of immune genes in Mus musculus macrophages during Staphylococcus aureus infection.PloS one · 2018Article
- Toll-like receptor 2 has a prominent but nonessential role in innate immunity toPhysiological reports · 2017Article
- Non-invasive objective and contemporary methods for measuring ocular surface inflammation in soft contact lens wearers - A review.Contact lens & anterior eye : the journal of the British Contact Lens Association · 2017Review
- Ex vivo rabbit and human corneas as models for bacterial and fungal keratitis.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2017Article
- MyD88 contribution to ocular surface homeostasis.PloS one · 2017Article
- Pattern recognition receptors in microbial keratitis.Eye (London, England) · 2015Review
- Review
- Inhibition of Corneal Inflammation by the Resolvin E1.Investigative ophthalmology & visual science · 2015Article
- In Vivo Role of TLR2 and MyD88 Signaling in Eliciting Innate Immune Responses in Staphylococcal Endophthalmitis.Investigative ophthalmology & visual science · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Toll-like receptors (TLRs) expressed by the corneal epithelium represent a first line of host defense to microbial keratitis. The current study examined the role of TLR2, TLR4, and TLR9 and the common adaptor molecule myeloid differentiation factor 88 (MyD88) in a Staphylococcus aureus model of corneal inflammation. The corneal epithelia of C57BL/6, TLR2(-/-), TLR4(-/-), TLR9(-/-), and MyD88(-/-) mice were abraded using a trephine and epithelial brush and were exposed to heat- or UV-inactivated S. aureus clinical strain 8325-4 and other clinical isolates. Corneal thickness and haze were measured by in vivo confocal microscopy, neutrophil recruitment to the corneal stroma was quantified by immunohistochemistry, and cytokine production was measured by enzyme-linked immunosorbent assay. The exposure of corneal epithelium to S. aureus induced neutrophil recruitment to the corneal stroma and increased corneal thickness and haze in control C57BL/6 mice but not in TLR2(-/-) or MyD88(-/-) mice. The responses of TLR4(-/-) and TLR9(-/-) mice were similar to those of C57BL/6 mice. S. aureus-induced cytokine production by corneal epithelial cells and neutrophils was also significantly reduced in TLR2(-/-) mice compared with that in C57BL/6 mice. These findings indicate that S. aureus-induced corneal inflammation is mediated by TLR2 and MyD88 in resident epithelial cells and infiltrating neutrophils.
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.