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V. M. Utz, Y. Sun, S. Platt, R. Ramadan, A. Hise, E. Pearlman; Staphyloccocus Aureus Keratitis Is Mediated by the IL-1R1 and MyD88, but Not TLR2. Invest. Ophthalmol. Vis. Sci. 2009;50(13):1200.
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Staphylococcus aureus keratitis is a major cause of vision loss and disability world-wide and is the most common isolate in ocular surgery-related cases of microbial keratitis. Toll-like receptors (TLRs) and Interleukin-1 Receptors (IL-1R1) expressed on the corneal epithelium represent a first-line defense against microbial invasion. MyD88 is an essential adaptor molecule for TLR and IL-1R1 signaling. This study evaluated the role of TLR2, IL-1R1 and MyD88 in the early stages of the innate immune response to Staphyloccus aureus in the cornea.
The corneal epithelia of C57BL/6, TLR2-/-, IL1R1-/- and MyD88-/- mice were abraded using a trephine and Alger brush and exposed to 1.0 x 106 CFU S. aureus (strain 8325-4) in 5 µL). CFU were quantified by track dilution at 1 and 24 hours after infection, and neutrophil infiltration to the corneal stroma was quantified by immunohistochemistry (number of neutrophils/cornea)
After 24h, there was pronounced neutrophil infiltration in the corneal stroma of C57BL/6 (352 + 21) and TLR2-/- mice (321 + 32) compared with IL1R1-/- mice (46 + 11) and MyD88-/- mice (56 + 20); conversely, CFU recovered from eyes of IL1R1-/- mice and MyD88-/- mice was significantly elevated compared with C57BL/6 and TLR2-/- mice. No significant differences in CFUs or neutrophil recruitment were found between C57BL/6 and TLR2-/- mice at 24h.
These findings demonstrate that S. aureus keratitis is mediated by IL-1R1 / MyD88, whereas TLR2 is not essential for either neutrophil recruitment to the corneal stroma or for bactericidal activity.
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