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Raniyah T. Ramadan, Andrea L. Moyer, Michelle C. Callegan; A Role for Tumor Necrosis Factor-α in Experimental Bacillus cereus Endophthalmitis Pathogenesis. Invest. Ophthalmol. Vis. Sci. 2008;49(10):4482-4489. doi: 10.1167/iovs.08-2085.
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purpose. To determine the contribution of tumor necrosis factor-alpha (TNFα) in the pathogenesis of experimental Bacillus cereus endophthalmitis.
methods. Experimental B. cereus endophthalmitis was induced in wild-type control (B6.129F1) and age-matched homozygous TNFα knockout mice (TNFα−/−, B6.129S6-Tnf tm1Gk1 /J). At various times after infection, eyes were analyzed by electroretinography and were harvested for quantitation of bacteria, myeloperoxidase, proinflammatory cytokines and chemokines, and histologic analysis.
results. B. cereus replicated more rapidly in the eyes of TNFα−/− mice than in the eyes of B6.129F1 mice. Retinal function decreased more rapidly in TNFα−/− mice than in B6.129F1 mice. Retinal layers were not as structurally intact at 6 and 12 hours after infection in TNFα−/− eyes as in B6.129F1 eyes. Histologic analysis suggested less polymorphonuclear leukocyte (PMN) infiltration into the vitreous of TNFα−/− mice than of B6.129F1 mice. B6.129F1 eyes also had greater myeloperoxidase concentrations than did eyes of TNFα−/− mice. In general, concentrations of proinflammatory cytokines and chemokines (IL-1β, KC, IL-6, and MIP-1α) were greater in eyes of TNFα−/− mice than of B6.129F1 mice.
conclusions. TNFα is important to intraocular pathogen containment by PMNs during experimental B. cereus endophthalmitis. In the absence of TNFα, fewer PMNs migrated into the eye, facilitating faster bacterial replication and retinal function loss. Although greater concentrations of proinflammatory cytokines were synthesized in the absence of TNFα, the resultant inflammation was diminished, and an equally devastating course of infection occurred.
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