ADHESION MOLECULES AND RELATIONSHIP TO LEUKOCYTE LEVELS IN ALLERGIC EYE DISEASE

PURPOSE. To evaluate the conjunctival expression of leukocyte cell adh esion molecules (CAMs) and their relationship to leukocyte patterns on the microvasculature in the different clinical subtypes of allergic e ye disease. METHODS. Immunohistochemical analysis, using appropriate m onoclonal antibodies, was applied to glycolmethacrylate-embedded biops ies of bulbar and tarsal conjunctival tissue. The proportion of total blood vessels expressing a particular CAM was derived and related to i ndividual cell types identified by cell-specific markers, such as mast cells, eosinophils, neutrophils, T cells, and macrophages. Statistica l analysis was used to correlate adhesion molecule expression and, ult imately, cell type. RESULTS. There was a basal expression of intercell ular adhesion molecule-1 (ICAM-1) (21% bulbar, 18% tarsal), E-selectin (15% bulbar, 21% tarsal), and vascular cell adhesion molecule-1 (VCAM -1) (13% bulbar and tarsal) in normal controls. In seasonal and perenn ial (bulbar rind tarsal conjunctival) allergic tissue, ICAM-1 and E-se lectin were expressed in 40% to 78% of vessels: in chronic disease, th ey were expressed in 45% to 80% of vessels, and in vernal giant papill ae, they were expressed in as many as 90% of vessels. There was also i ncreased expression of endothelial VCAM-1 in all forms of allergic eye disease; the greatest values were found in vernal giant papillae (64% ). Biopsies taken in winter from seasonal sufferers demonstrated a mar ked reduction in levels of all three CAMs compared with those taken in the pollen season. This is almost consistent with values found in nor mal conjunctiva. Positive correlations mere found between the levels o f ICAM-1 and E-selectin expression and the degree of granulocyte and l ymphocyte infiltration, although VCAM-1 expression correlated most clo sely with eosinophil numbers. CONCLUSIONS. Increased levels of cell ad hesion molecules on the microvasculature and the factors that regulate them are likely to be responsible for the infiltration of cells beari ng their ligands and may perpetuate inflammation in the chronic forms of allergic eye disease.