A platelet-activating factor antagonist reduces corneal allograft inflammation and neovascularization.

We assessed the role of platelet-activating factor (PAF) in corneal allograft rejection and evaluated the effects of a PAF antagonist on corneal inflammation, cellular infiltration, vascularization, and edema. Rabbits with vascularized corneas served as recipients of allogeneic cornea grafts. Rabbits with normal corneas underwent autografts as controls. All of the allografts developed the progression of signs characteristic of rejection. Nevertheless, treatment with the PAF antagonist BN52021 significantly inhibited corneal allograft vascularization for up to 10 days after transplantation and reduced the number of eosinophils in the allografts at 28 days after transplantation. In contrast, saline-treated allografts exhibited florid vascularization and intense inflammatory infiltrates. Control autografts survived without developing significant inflammation or vascularization. The retardation of allograft eosinophilia and graft vascularization by the PAF antagonist was most likely the result of suppression of PAF-mediated reactions in the cornea. These results indicate that PAF may play a role in corneal inflammation and vascularization after corneal transplantation, and that PAF antagonists may be clinically useful in delaying some of the pathophysiologic consequences of corneal graft rejection.