Lectin binding in normal, scarred, and keratoconus corneas.
Słowa kluczowe
Abstrakcyjny
OBJECTIVE
Keratoconus is characterized by central thinning and an increased curvature of cornea. Scarring of cornea accompanies the disease as it proceeds, and the ultimate treatment is keratoplasty. The pathogenesis of keratoconus is still unknown, and therefore we studied normal, keratoconus, and scarred corneas by a panel of lectin conjugates.
METHODS
The following lectin conjugates were used: concanavalin A (Con A), Dolichos biflorus agglutinin (DBA), peanut agglutinin (PNA), Ulex europaeus agglutinin (UEA-I), wheat-germ agglutinin (WGA), Helix aspersa agglutinin (HAA), Psophocarpus tetragonolobus agglutinin (PTA), soybean agglutinin (SBA), Griffonia simplicifolia agglutinin-I-B4 (GSA-I-B4), Ricinus communis agglutinin (RCA-I), and Lotus tetragonolobus agglutin (LTA) conjugates, differently recognizing saccharide residues in glycoconjugates.
RESULTS
One of the keratoconus corneas was badly scarred, whereas no scars were seen on histopathologic examination in other keratoconus corneas. In all keratoconus corneas, discontinuities or breaks (defects) were seen in the Bowman's layer. DBA and HAA conjugates, both blood group A reactive, reacted with corneal and conjunctival epithelium, blood vessels, and endothelium in blood groups A and AB. The blood group B-reactive GSA-I-B4 conjugate reacted with corneal and conjunctival epithelium, blood vessels, and endothelium only in specimens with blood group B. The blood group O-reactive UEA-I conjugate revealed the apical epithelial cells and blood vessels in all blood groups, whereas LTA conjugate, also blood group O reactive, reacted with all structures in cornea and conjunctiva despite blood groups. HAA and DBA conjugates reacted with defects in keratoconus corneas, SBA and RCA-I conjugates with defect area in keratoconus and scar region in scarred corneas, and PNA and WGA conjugates with the scar region of scarred keratoconus and scarred corneas. No other differences in the binding of lectins between normal, scarred, and keratoconus corneas were seen.
CONCLUSIONS
The results indicate that the blood group status influences lectin binding in cornea. Furthermore, the difference in lectin binding to defects in keratoconus corneas (HAA and DBA conjugates) and to scar regions in scarred corneas (PNA and WGA conjugates) suggests that the defects in keratoconus are not solely the results of scarring.
