PURPOSE: To determine the cytokine-mediated pathways of inflammation in the clinical course of proliferative vitreoretinopathy (PVR). METHODS: Cytokines IL-2, IL-6, INF-gamma were measured by enzyme-linked immunosorbent assays. Aspirates of subretinal fluid were obtained from 14 eyes with PVR and six with uncomplicated rhegmatogenous retinal detachments. Aspirates obtained via pars plana from ten cadaver vitreouses of normal eyes were used as controls. RESULTS: Subretinal fluids from eyes with PVR, uncomplicated rhegmatogenous retinal detachment and cadaver vitreous contained low concentrations of IL-2, with inconsequential differences between groups. IL-6 and IFN-gamma were twice as high in the subretinal fluid from eyes with rhetmatogenous retinal detachment as in cadaver vitreous. INF-gamma was elevated up to six times in eyes with PVR compared to controls. Fibronectin was found in a larger proportion of eyes with PVR than with uncomplicated rhegmatogenous retinal detachment and cadaver vitreous from healthy persons. CONCLUSIONS: These are only preliminary investigations and are too few for statistical analysis. The results suggest that cytokine-mediated pathways of inflammation are involved in the pathogenesis of rhegmatogenous retinal detachment and in cellular interactions leading to the development of PVR.
PURPOSE: To determine the cytokine-mediated pathways of inflammation in the clinical course of proliferative vitreoretinopathy (PVR). METHODS: Cytokines IL-2, IL-6, INF-gamma were measured by enzyme-linked immunosorbent assays. Aspirates of subretinal fluid were obtained from 14 eyes with PVR and six with uncomplicated rhegmatogenous retinal detachments. Aspirates obtained via pars plana from ten cadaver vitreouses of normal eyes were used as controls. RESULTS: Subretinal fluids from eyes with PVR, uncomplicated rhegmatogenous retinal detachment and cadaver vitreous contained low concentrations of IL-2, with inconsequential differences between groups. IL-6 and IFN-gamma were twice as high in the subretinal fluid from eyes with rhetmatogenous retinal detachment as in cadaver vitreous. INF-gamma was elevated up to six times in eyes with PVR compared to controls. Fibronectin was found in a larger proportion of eyes with PVR than with uncomplicated rhegmatogenous retinal detachment and cadaver vitreous from healthy persons. CONCLUSIONS: These are only preliminary investigations and are too few for statistical analysis. The results suggest that cytokine-mediated pathways of inflammation are involved in the pathogenesis of rhegmatogenous retinal detachment and in cellular interactions leading to the development of PVR.
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