In this grant the alkali injured eye is used as a model of inflammation which can be manipulated to examine the cellular responses to chemical injury. Expansion of our studies on the favorable effect of citrate on the alkali injured eye will focus on the additive effect of ascorbate when both are used as topical treatment. In vivo studies of citrate and calcium levels in different layers of the alkali injured cornea will be performed to corroborate our in vitro findings that calcium chelation, inhibiting PMN activity, is the mechanism of action involved. A visual assay system has been developed to study the inflammatory mediators thought to be present in alkali injured corneas and their modulation by citrate. Injection of the crude extract from alkali treated collagen or refined fractions obtained from sucrose gradient or HPLC fractions will facilitate study of these mediators, as well as their inhibition by citrate, within the corneal stroma. Expansion of our studies on the respiratory stimulant released from alkali treated corneal collagen will include its optimization and characterization. Application of similar techniques will be applied to identify and characterize the stimulant of PMN locomotion also released from alkali injured corneal collagen. Additional studies of albumin levels in the cornea may furnish data which support our contention that albumin in the corneal periphery enhances locomotion while diminished levels in the central cornea promotes respiratory burst and hydrolytic enzyme release from PMN lysis, leading to ulceration. The long term objective of this study is to understand the mechanisms of inflammatory mediation and their inhibition and thereby influence the process of corneal ulceration.
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