Abstract:
Corneal epithelial lesions are a characteristic of vernal keratoconjunctivitis. Studies on cultured corneal cells have suggested that corneal fibroblasts may enhance allergic inflammation through the release of chemokines and the expression of adhesion molecules, and that corneal epithelial cells might reduce the extent of such inflammation by separating corneal fibroblasts from cytokines present in tear fluid. The effects of corneal epithelial ablation and consequent exposure of the corneal stroma to tear fluid on conjunctival inflammation were investigated in rats.
Brown Norway rats were sensitized to short ragweed pollen and alum. The corneal epithelium of the right eye was mechanically removed 21 days after sensitization, and the animals were challenged by topical instillation of pollen. Early–phase and late–phase clinical symptoms were scored at 20 min and 24 h after challenge, respectively. Histopathologic changes and the abundance of transcripts for adhesion molecules (ICAM–1, VCAM–1) and chemokines (TARC, IP–10, eotaxin, RANTES, MCP–1) in the conjunctiva were examined 24 h after challenge.
Allergen sensitization and corneal epithelial ablation induced a synergistic increase in the late–phase clinical score (p < 0.05, two–way ANOVA), without affecting that of the early phase, in challenged rats. Corneal epithelial ablation markedly increased eosinophil infiltration as well as the abundance of ICAM–1, TARC, RANTES, and MCP–1 mRNAs in the conjunctiva of sensitized rats.
Corneal epithelial ablation enhances the late phase of conjunctival allergic inflammation by promoting eosinophil infiltration and expression of chemokines and adhesion molecules in the conjunctiva.
Keywords: conjunctivitis • cornea: epithelium