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Ashok Kumar, Travis J. Kochan; Susceptibility Of Tlr2 And Myd88 Knockout Mice To S. Aureus Endophthalmitis. Invest. Ophthalmol. Vis. Sci. 2011;52(14):2957.
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Our previous studies revealed that TLR2 activation provides retinal innate defense against S. aureus infection. This study is aimed to test the susceptibility of TLR2 and MyD88 deficient mice towards staphylococcal endophthalmitis
Endophthalmitis was induced by intravitreal injection S. aureus (RN 6390 strain). Susceptibility of WT and TLR2-/- and MyD88-/- mice was assessed by determining the number of bacteria required to cause infection and by the severity of the diseases. At various days post infection (dpi) eyes were subjected to clinical scoring, bacterial load determination, cytokine ELISA, histological analysis and myeloperoxidase (MPO) assay to assess neutrophil infiltration.
Compare to WT, the TLR2-/- and MyD88-/- mice showed increased susceptibility to SA, as 10 fold fewer bacteria were able to cause infection in knockout mice, but not in wild type mice. At 1 dpi bacterial burden was 2.5 and 7 fold higher in TLR2-/- and MyD88-/- than the controls, respectively. The cytokine and MPO levels were slightly reduced in TLR2-/- and significantly more in MyD88-/- mice. At 3 dpi, both knockout mice had higher bacterial load, cytokines and PMN infiltration compared to WT. At the histological levels, the retinal tissue destruction was more in knockout mice compare to WT even at early stage of infection.
These findings demonstrate that TLR2 and MyD88-deficient mice had increased susceptibility to staphylococcal endophthalmitis and TLR2 seems to plays a role in controlling bacterial growth at least at early stage of infection.
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