Tomiyama S, Kinoshita T, Jinnouchi K, Ikezono T, Gotoh Y, Pawanker R, Yagi T
Department of Otolaryngology, Nippon Medical School, Tokyo, Japan.
ORL J Otorhinolaryngol Relat Spec. 1995 May-Jun;57(3):122-8. doi: 10.1159/000276724.
This study has investigated immune injuries to the inner ear auditory system of guinea pigs. Following secondary antigen challenge to the endolymphatic sac, the mean hearing threshold significantly increased in the early phase from day 1 to day 3 and thereafter recovered. In the early phase, hearing threshold significantly increased simultaneously to the elevation of perilymph antibody levels. The size of hydrops was not the only factor that causes an increase in hearing loss as well as in AP/SP ratio. Scale-out hearing loss was seen in 2 animals with severe degeneration of the stria vascularis as well as the organ of Corti associated with the inflammatory cellular infiltration especially in the perilymphatic space, even in the absence of keyhole limpet hemocyanin antigen in the cochlea. On the other hand, control animals did not suffer hearing loss. These results suggest that an immune reaction in the endolymphatic sac is a possible pathogenic etiology of Ménière's disease or sudden deafness.
本研究调查了豚鼠内耳听觉系统的免疫损伤情况。在内淋巴囊受到二次抗原攻击后，平均听力阈值在第1天至第3天的早期显著升高，此后恢复。在早期，听力阈值与外淋巴抗体水平的升高同时显著增加。积水的大小并非导致听力损失以及动作电位/总和电位（AP/SP）比值增加的唯一因素。在2只动物中观察到扩展性听力损失，这些动物存在血管纹以及柯蒂氏器的严重退化，并伴有炎症细胞浸润，尤其是在外淋巴间隙，即使耳蜗中不存在钥孔血蓝蛋白抗原。另一方面，对照动物未出现听力损失。这些结果表明，内淋巴囊中的免疫反应可能是梅尼埃病或突发性聋的致病病因。
