ADHESION MOLECULES IN NORMAL AND PATHOLOGICAL CORNEAS - AN IMMUNOHISTOCHEMICAL STUDY USING MONOCLONAL-ANTIBODIES

Background: Adhesion molecules are cell surface receptors that are pro bably important in various cell-cell and cell-extracellular matrix int eractions of the cornea. Method: In this immunohistochemical light-mic roscopic study we analyzed the expression pattern of adhesion molecule s in normal and pathological human corneas (cases of corneal inflammat ion and degenerative disorders). The analyzed molecules included the b eta 1 integrin or VLA family VLA-1-6, the beta 2 integrins or leukocyt e integrins LFA-1, Mac-1, and p150,95, the immunoglobulins LFA-3, CD2, ICAM-1 and VCAM-1 and the selectins ELAM-1 and GMP-140. Results: Infl amed cornea (in contrast to normal cornea). On corneal epithelium, inc reased expression of the alpha 2 subunit of VLA-2 was detected and ICA M-1 was induced on the basal epithelial cells. On corneal stromal kera tocytes, LFA-3 was induced and expression of the alpha subunits of VLA -1-6 and ICAM-1 was increased. On vascular endothelium, VCAM-1 and ELA M-1 were induced and ICAM-1 and GMP-140 expression was increased. On c orneal endothelium, ELAM-1 was induced and increased levels of the alp ha 1 subunit of VLA-1 and GMP-140 were expressed. Degenerative disorde rs (in contrast to normal cornea). In corneas with degenerative disord ers we found decreased expression of adhesion molecules. Conclusion: I nflammatory cytokines increase the expression of the adhesion molecule s. Increased expression of the VLAs probably promotes cell-extracellul ar matrix and cell-eel interactions. ICAM-1, VCAM-1, LFA-3, ELAM-1 and GMP-140 expression was increased on vascular endothelium in inflamed corneas. Corresponding receptors on leukocytes probably enable a selec tive recruitment of different leukocyte populations in inflammatory co rneal diseases. The decreased expression of adhesion molecules in corn eal degenerative disorders is probably a sign of reduced cell-cell and cell-extracellular matrix interactions.