Mechanism of immuno injury on inner ear autoimmune disease

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Expression of iNOS was seen in several sites of the cochlea and vestibule one day following secondary immune reaction in the endolymphatic sac. Furthermore, apoptotic degeneration was seen in the spiral ligament and stria vascularis by immunohistochemical expression of ss-DNA, CAD and CPP32. Following recurrent sensitization with crude inner ear antigens of bovine, mouse produced antibodies that reacted several proteins of bovine inner ear as well as mouse kidney, brain, lung and liver. In order to investigate antigenicity of purified inner ear fractioned proteins, crude inner ear antigens were separated into 14 fractions eluted on Mini Whole Gel Eluter. Single sensitization with 55-65 kDa proteins fraction induced the highest number of inner ear infiltrating cells among the fractions. Large volume of fractioned inner ear proteins was obtained by Whole Gel Eluter. Recurrent sensitization off 54〜62kDa inner ear proteins fraction produced antibody that showed single bands with 60-70kDa of bovine inner ear proteins, but not reacted to proteins of mouse those organs. IgG and C3 complement localized in the vessels of the stria vascularis. These results suggest that autoimmune inner ear disease is caused by inner ear specific antigens. Hearing kinetics as well as pathological study is further necessary to investigate specific pathogenic inner ear antigen. Furthermore, proteome analysis of the candidates of inner ear specific pathogenic protein will be essential to identify protein genesis.