Vitronectin: Possible contribution to the closed-eye external host-defense mechanism

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Abstract
Eye closure causes a shift in the preocular tear film, from a reflex tear-rich layer which is in dynamic equilibrium to a secretory IgA-rich layer which is stagnant in nature. This is accompanied by complement conversion and plasminogen activation, followed by polymorphonuclear (PMN) cell recruitment. It is suggested that this shift to a secretory IgA and PMN cell-rich layer serves to protect the ocular surfaces from trapped microorganisms. The mechanisms whereby autologous damage is avoided are uncertain. In other tissues, vitronectin (VN) may be an inhibitor of complement and plasmin induced autolytic damage and a potentiator of microbial phagocytosis. Its presence in the external ocular environment is unknown. To screen for VN, normal human reflex (R), open-eye (O) and closed-eye (C) tear samples were collected, separated by SDS PAGE, and immunoblot probed. Detection was carried out using monoclonal antibodies (MAbs) raised against human VN, coupled to an avidin biotin conjugate-horseradish peroxidase amplification system. Quantitative analysis was carried out using a sandwich ELISA assay. Bovine corneas were sectioned and immunohistochemically stained with MAbs to bovine VN. Results revealed that in going from R to O to C tear fluid there is a marked progressive increase in VN (0.08, 0.75, 3.65 μ/ml). This is accompanied by a shift from the intact 75kDa molecule to the 65kDa breakdown product which is still biologically active, with further degradation occasionally encountered. Immunohistochemical staining of bovine cornea revealed that VN is localized in the corneal epithelium and stromal keratocytes. These findings are compatible with either a local or serological origin for VN, and support the contention that VN may be a component in the external closed-eye host-defense system.
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