Gloddek B, Rogowski M, Reiss G, Arnold W
Hals-Nasen-Ohrenklinik und Poliklinik, Technische Universität, München, Germany.
Clin Exp Immunol. 1994 Jul;97(1):133-7. doi: 10.1111/j.1365-2249.1994.tb06591.x.
Sensorineural hearing loss is a common problem in the otolaryngologist's practice, with autoimmune disease of the inner ear being one possible cause. The restoration of auditory function in some patients following immunosuppressive therapy has created a desire to define and understand this disease better. Because of the lack of a well defined detection method to identify this entity clinically, this study was undertaken in order to provide an animal model for autoimmune disease of the inner ear. Previous studies with guinea pigs have demonstrated that sensitized lymphocytes from the systemic circulation migrate to the labyrinth during an immune response in the inner ear. The aim of this study was to prove the capacity of sensitized lymphocytes to transfer autoimmune inner ear disease, and to describe the resulting morphological and physiological changes. Therefore two groups of sensitized lymphocytes partially labelled with a radioactive marker from inbred guinea pigs with an immune response within the inner ear were injected into the bloodstream of naive recipient animals. Most of the labelled cells were observed in the apical turn of the experimental cochlea, while only few cells were detectable in the control cochleas. In addition, the absence of otoacoustic emissions and the loss of outer hair cells observed by electron microscopy were interpreted as a sign of damage caused by the provoked immunopathologic mechanism. The results are discussed as a possible model for a sympathetic cochleolabyrinthitis.
感音神经性听力损失是耳鼻喉科医生临床工作中常见的问题，内耳自身免疫性疾病是其可能病因之一。一些患者在接受免疫抑制治疗后听觉功能得以恢复，这促使人们更想明确并深入了解这种疾病。由于缺乏一种在临床上明确识别该病症的检测方法，开展此项研究是为了建立一种内耳自身免疫性疾病的动物模型。先前对豚鼠的研究表明，在免疫反应期间，来自全身循环的致敏淋巴细胞会迁移至内耳迷路。本研究的目的是证实致敏淋巴细胞引发自身免疫性内耳疾病的能力，并描述由此产生的形态学和生理学变化。因此，将两组来自内耳有免疫反应的近交豚鼠、部分用放射性标记物标记的致敏淋巴细胞注入未致敏受体动物的血液中。在实验性耳蜗的顶转观察到大多数标记细胞，而在对照耳蜗中仅检测到少数细胞。此外，耳声发射缺失以及电子显微镜观察到的外毛细胞损失被解释为由诱发的免疫病理机制造成损伤的迹象。这些结果被作为交感神经性耳蜗迷路炎的一种可能模型进行讨论。
