EXPRESSION OF INTERCELLULAR-ADHESION MOLECULE-1 DURING INNER-EAR INFLAMMATION

This study was designed to investigate the expression of intercellular adhesion molecule-1 (ICAM-1) on the spiral modiolar vein (SMV) with i ts collecting venules (CVs) and the venules of the endolymphatic sac d uring inner ear inflammation. These data will further elucidate the ro le of adhesion molecules in extravasation of inflammatory cells from b lood vessels during an inner ear immune response. Labyrinthitis was in duced in rats by inoculation of keyhole limpet hemocyanin into the sca la tympani of animals who had been systemically sensitized to it. Expr ession of ICAM-1 was examined with a mouse monoclonal antibody to rat ICAM-1 by immunohistochemistry. ICAM-1 was found weakly on the epithel ium of SMVs and CVs as early as 6 hours postchallenge, reaching a maxi mum by day 2 and then fading away gradually. The maximum influx of imm unocompetent cells into the cochlea was seen between days 3 and 7. Sta ining for ICAM-1 was observed on the epithelium of the endolymphatic s ac and perisaccular region at 12 and 24 hours, respectively, and this was associated with infiltration of cells into these areas 3 days post challenge. By day 28, the inner ear had developed endolymphatic hydrop s, but at this time it showed almost no significant staining with anti -ICAM-1. The molecule was also expressed in the mesothelium of perilym ph, the perineurium of cochlear nerves, the spiral ligament, and the b asal cells of the stria vascularis following immunization. Our data pr ovide evidence that endothelial cells of the SMV and its CVs, as well as other inner ear sites, have the potential to express ICAM-1. This e xpression precedes the influx of immune cells; therefore, it is possib le that this ligand plays a pivotal role in the onset of inflammation in the inner ear. This study also confirmed that the immune response r esults in endolymphatic hydrops as a long-term consequence.