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R. Ramadan, A. L. Moyer, M. C. Callegan; The Contribution of TNF-Alpha to Bacillus cereus Endophthalmitis Pathogenesis. Invest. Ophthalmol. Vis. Sci. 2007;48(13):2663.
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To elucidate the contribution of TNF alpha production to inflammation and retinal function loss during experimental Bacillus endophthalmitis.
Experimental Bacillus endophthalmitis was induced in wild type (B6.129S6) or TNF-alpha knockout mice (B6.129S6-Tnftm1Gk1). At various times postinfection, eyes were analyzed by electroretinography, and harvested for bacterial quantitation, myeloperoxidase and proinflammatory cytokine activities, and histological analysis.
Retinal function decreased less rapidly in the TNF-alpha deficient mice than wild-type control mice. Histological analysis suggested less PMN infiltration in the vitreous in TNF-alpha knockout mice than in wild type control mice, an observation that correlated with decreased myeloperoxidase activities in eyes of TNF-alpha deficient mice. Structural integrity of retinal layers was also less disrupted at 6 and 12 hours postinfection in TNF-alpha deficient mice as compared to wild-type controls. Proinflammatory cytokine levels were greater in TNF-alpha deficient mice than in wild-type controls. IL-1beta, KC (IL-8), IL-6, and MIP1alpha increase significantly up to 12 hours post-infection during Bacillus endophthalmitis.
TNF-alpha appears to contribute significantly to the evolving pathogenesis of experimental Bacillus endophthalmitis. Additional immune mediators may compensate for TNF-alpha in its absence, resulting in a slower course of infection. Future studies are focused on the roles of these mediators in the pathogenesis of Bacillus endophthalmitis.
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