内耳免疫現象の基礎的研究内リンパ嚢局所抗原刺激における内耳初期免疫動態

抄録

The pathogenesis of immune-mediated inner ear diseases are not yet clarified. We previously demonstrated that secondary KLH antigen challenge into the endolymphatic sac of guinea pigs resulted in a rapid formation of endolymphatic hydrops associated with attacks of vertigo and fluctuating hearing loss. In order to elucidate the mechanism involved in immune injury to the inner ear, the present study investigated the afferent site of immunocompetent cells into the inner ear and its relation to the distribution of KLH antigen, time kinetics of perilymph CHSO and anti-KLH antibody levels, as well as the expression of intracellular adhesion molecule-1 (ICAM-1) in the inner ear. KLH antigen was only identified in the lumen of the endolymphatic sac, but not in the vestibule or cochlea. A marked cellular migration occurred in the endolymphatic sac, but minor cellular migration was seen in the perilymphatic space in the cochlea and vestibule. The time kinetics of perilymph anti-KLH levels and CHSO levels, as well as the expression of ICAM-1 in the inner ear demonstrated peak at 10 hours-24 hours in good correlation with our previous study of the cellular infiltration in the endolymphatic sac. Strong ICAM-1 expression occurred in the endothelium of the whole inner ear venules, especially in the endolymphatic sac, the spiral modiolar and collecting venules, the suprastrial and inferior part of the spiral ligament, and the spiral limbus. Altogether, these results suggest that chemical mediators as well as cytokines produced within the endolymphatic sac may spread in all the compartments of the inner ear and lead to immune-defense as well as immune-injury of the inner ear.