Abstract
Purpose:
To test the hypothesis that TLR5 contributes to bacterial recognition and inflammation during Bacillus cereus endophthalmitis. B. cereus possesses flagella which allow the organism to migrate within the eye during endophthalmitis. Flagella is a TLR5 ligand.
Methods:
Experimental endophthalmitis was induced in B6.129S1-Tlr5tm1Flv/J TLR5-/- mice and wild type C57BL/6J mice by intravitreally injecting 100CFU of B. cereus ATCC 14579. At various time points after infection, eyes were analyzed for intraocular bacterial growth, retinal function, and acute intraocular inflammation by published methods. Values represented N≥4 eyes/time point, mean ± SEM.
Results:
The intraocular growth rates of B. cereus in infected eyes were determined following 4, 8 and 12 hours of infection. B. cereus grew rapidly and at similar rates in infected eyes of wild type mice and TLR5-/- mice. A greater loss in retinal function in both groups of mice was observed at 8 and 12 hours following infection. Retinal architecture disruption and acute inflammation (neutrophil infiltration and proinflammatory cytokine concentrations) increased during the course of infection and were significant at 8 and 12 hours postinfection. Acute inflammation was comparable in TLR5-/- and control mice.
Conclusions:
The absence of TLR5 did not have a significant effect on limiting the intraocular growth rates of B. cereus during endophthalmitis.TLR5-/- mice had retinal function loss and retinal architecture disruption similar to wild type mice, suggesting that TLR5 deficiency does not alter vision loss in the endophthalmitis model. Moreover, deficiency of TLR5 did not lead to a significant change in the intraocular inflammatory process to infection. These results suggest that the inflammatory cascade in endophthalmitis is initiated by TLRs other than TLR5 following intraocular recognition of B. cereus.
Keywords: 513 endophthalmitis •
433 bacterial disease •
594 microbial pathogenesis: experimental studies