Upregulation of ELAM-1 expression on trabecular meshwork cells using IL-1β

Purpose. ELAM-1 (E-selectin) is a cell adhesion molecule which can function as a ligand for Sialyl Lewis X (SLe^x). ELAM-1, undetectable on normal trabecular meshwork (TM) cells, is significantly expressed on glaucomatous TM cells and may have a role in outflow facility. This study attempts to stimulate the expression of ELAM-1 on normal TM cells using IL1β. Methods. TM cells from normal and glaucomatous human cadaver eyes were isolated and cultured on sterile cover slips. Normal TM cells were incubated with varying concentrations of IL1β at specific time intervals. These cells were then stained with anti-ELAM-1 using Avidin-Biotin-Peroxidase Complex. Non-stimulated normal and glaucomatous TM cells were also stained with ELAM-1. Incubations with recombinate human IL1β were performed at 0, 4, 8, 12, and 24 hours. Variable concentrations (0-40ng) were used. All TM cells were then subjected to the exogenous addition of BSA-SLe^x protein and stained using anti-SLe^x. Results. Non-stimulated normal TM cells showed no staining for ELAM-1. Non-stimulated glaucomatous TM cells stained for ELAM-1; this was statistically significant (p=.0037). Normal TM cells incubated with IL1β upregulated ELAM-1 expression in a time and concentration dependent manner. Stimulated and unstimulated normal TM cells did not stain for SLe^x. TM cells incubated with SLe^x-BSA did stain for SLe^x. Conclusions. Glaucomatous TM cells expressed ELAM-1, while normal TM cells did not; however, normal TM cells could be induced to express ELAM-1 with IL1β. This suggests that TM cells are capable of expressing ELAM-1, a ligand to SLe^x. The role of ELAM-1 in physiological regulation of outflow facility is unclear; however, modification of ELAM-1 expression may affect outflow facility.