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Mechanism of immuno injury on inner ear autoimmune disease

内耳自身免疫性疾病的免疫损伤机制

基本信息

批准号：
13671806
负责人：
TOMIYAMA Shunichi
金额：
$ 2.11万
依托单位：
Nippon Medical School
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2001
资助国家：
日本
起止时间：
2001 至 2003
项目状态：
已结题

项目摘要

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.

诱导型一氧化氮合酶在内淋巴囊继发性免疫反应后第1天在耳蜗和前庭的多个部位表达。此外，通过ss-DNA、CAD和CPP 32的免疫组化表达，在螺旋韧带和血管纹中观察到凋亡变性。用牛内耳粗抗原反复致敏后，小鼠产生的抗体与牛内耳以及小鼠肾、脑、肺和肝的几种蛋白质反应。为了研究纯化的内耳组分蛋白的抗原性，将粗内耳抗原分离成14个组分，在Mini Whole Gel Eluter上洗脱。55-65 kDa蛋白组分的单一致敏在组分中诱导最高数量的内耳浸润细胞。用全凝胶洗脱器获得大体积的分级分离的内耳蛋白。反复致敏54 ~ 62 kDa的内耳蛋白组分产生的抗体显示单一条带，与牛内耳蛋白的60- 70 kDa的蛋白质，但不与小鼠这些器官的蛋白质反应。IgG和C3补体定位于血管纹的血管中。提示自身免疫性内耳病是由内耳特异性抗原引起的。因此，需要进一步进行听力动力学和病理学的研究，以探讨特异性致病性内耳抗原。此外，对内耳特异性致病蛋白候选物的蛋白质组学分析将是鉴定蛋白质起源的必要条件。