Abstract
Cyclosporine A ophthalmic solutions have recently emerged as an effective treatment for vernal keratoconjunctivitis (VKC). Cyclosporine A is known to have multiple inhibitory effects on T-cells, and allergic conjunctivitis models have shown that cyclosporine A eye drops can effectively inhibit T-cell-mediated eosinophil and neutrophil migration. Inhibitory effects of cyclosporine A on other inflammatory cells have also been documented. Release of histamine and cytokines from mast cells was shown to be inhibited by cyclosporine A and cyclosporine A eye drops were able to inhibit histamine release and migration of inflammatory cells in allergic conjunctivitis models mediated by mast cells. Cyclosporine A has also been reported to induce eosinophil apoptosis and block the ability of these cells to release eosinophil cationic protein (ECP). In neutrophils, cyclosporine A can inhibit the release of myeloperoxidase (MPO) and reactive oxygen species. In fibroblasts, cyclosporine A has been demonstrated to inhibit proliferation and pro-collagen production. In vitro, cyclosporine A has variable effects on inflammatory cells, underscoring the need for further experimentation to elucidate the full range of its cytologic effects and their relation to therapeutic outcome. The diverse inhibitory effects of cyclosporine A on inflammatory cells clearly underlie the ability of this drug to alleviate the symptoms of VKC.
Keywords: Cyclosporine A, Vernal keratoconjunctivitis, Ophthalmic solution, Inflammatory cells, T cells, Mast cells
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