Immune Response Of Inner Ear Research Articles

Cell proliferation in the endolymphatic sac in situ during the immune response of inner ear

BackgroundNormally, few immunocompetent cell are present in the endolymphatic sac (ES). During an active immune response in the inner ear, large amount of inflammatory cells, including immunocompetent cells, are seen in the ES. The current study aimed at assessing cellular proliferation within the ES during induced immune response in the inner ear. MethodsFifteen healthy, female SD rats were sensitized systemically with keyhole limpet hemocyanin (KLH), followed by local inoculation in the cochlea through basal turn fenestration with the same antigen. On Days 3, 7 and 14 following inoculation, the animal was sacrificed after intraperitoneal administration of 5-bromo-2’-deoxyuridine (BrdUrd), and the temporal bone harvested. Following decalcification, infiltration by BrdUrd- and IgG-positive cells in the ES was studied on frozen sections with H & E and immunohistochemical staining. ResultsDuring the secondary immune response in the inner ear against T-dependent antigens, there is increased cellular proliferation in the ES. The proliferated cells may differentiate into immunocompetent cells at the same location. ConclusionsThese findings indicate that the ES plays an important role in immune response of inner ear.

Expression of intercellular adhesion molecule-1 in immune response of inner ear.

To understand the role of intercellular adhesion molecule-1 (ICAM-1) in immune response of the inner ear, inner ear immune response was induced in rats by inoculation of keyhole limpet hemocyanine (KLH) into the scala tympani of the animals who had been systemically sensitized. The expression of ICAM-1 in the inner ear was immunohistochemically examined. ICAM-1 was found in the epithelium of the spiral modiolar vein (SMV) with its collecting venules (CVs) as early as 6 h after challenge. Expression of ICAM-1 was observed on the epithelium of the endolymphatic sac (ES) and perisaccular region at 12 h. The intensity of ICAM-1 staining reached its peak within 24-48 h in these sites of the inner ear. By day 28, most specimens were devoid of appreciable staining for ICAM-1. Our study demonstrates that adhesion molecules play an important role in extravasation of inflammatory cells from the systemic circulation in the process of inner ear immune response. It also shows that cytokines that control expression of adhesion molecules may be released by cells outside ES, besides those cells in the ES.