Uveitis is a potentially blinding and disabling disease that affects otherwise healthy individuals. In a majority of the patients, the cause of uveitis remains obscure even after extensive laboratory investigation. There is no specific treatment of this ocular condition, although it is usually managed by steroids and/or other immuno-suppressive agents. It has been suggested that altered vascular permeability resulting from the initial episode of severe uveitis contributes to the perpetuation of the disease, but the evidence for this hypothesis is contradictory. On the other hand, there are a variety of inflammatory mediators that have been already implicated in prolonging inflammation; only recently potent reactive oxygen metabolites have been included. Study of these metabolites in experimental uveitis, as suggested by our preliminary studies, will provide information concerning perpetuation of ocular inflammation. Furthermore, by neutralizing the toxic effects of these metabolites by antioxidants it seems possible in our studies to modify the severity of the disease and possibly terminate the perpetuation of ocular inflammation. To achieve the above objectives, well-defined animal models of uveitis, such as S-antigen uveitis and lens-induced uveitis, should be studied in relation to production of superoxide anion and neutralization of the oxygen metabolites by superoxide dismutase, catalase, and vitamin E. The proposed studies could provide new direction in the specific management of uveal inflammations. Our laboratory is well-equipped to undertake these studies. The principial investigator has a long-standing interest in ocular inflammatory diseases and has studied the models of experimental uveitis to be tested in these proposed studies. The co-investigator is actively investigating the role of oxygen metabolites in lung diseases and can readily extend his expertise to ocular inflammation.
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