Abstract
Purpose: :
To determine the effect of TLR2 deficiency on intraocular inflammation and blood-retinal barrier permeability during experimental Bacillus cereus endophthalmitis.
Methods: :
100 colony forming units (cfu) of vegetative B. cereus were injected into the midvitreous of wild type (WT) C57BL6/J or homozygous TLR2-/- knockout mice. Ocular infections were analyzed by bacterial quantitation, histology, myeloperoxidase (MPO) activity, cytokine/chemokine quantitation, and quantitation of blood-retinal barrier permeability (N≥4 eyes per assay per time point, mean ± SEM).
Results: :
B. cereus
Conclusions: :
The acute intraocular inflammatory response to B. cereus endophthalmitis was altered by the deficiency in TLR2. Impaired blood-retinal barrier permeability due to decreased VEGF levels in TLR2-deficient mice may have delayed this response, preventing the explosive inflammation typically seen during this infection.
Keywords: endophthalmitis • bacterial disease • inflammation