Inoue Y, Kanzaki J, Ogawa K, Hashiguchi K, Masuda M
Department of Otolaryngology, School of Medicine, Keio University, Tokyo, Japan.
Eur Arch Otorhinolaryngol. 1998;255(5):240-3. doi: 10.1007/s004050050050.
In order to clarify the possible mechanism of hearing loss in immune-mediated sensorineural hearing loss, basic research needed includes animal model studies. In the present investigation, we examined hearing thresholds and cochlear histologies of the MRL/lpr mouse which is now well-known as a model for pathology consistent with systemic lupus erythematosis (SLE). Present findings demonstrated that there were no statistically significant differences in auditory brainstem response (ABR) thresholds between 4- to 6-week-old "young" and 20- to 25-week-old "old" MRL mice. These differences were not sex-dependent. Under light microscopy, there were no abnormal morphological findings in the cochleas of either young or old MRL mice. With immunohistochemistry, mouse IgG was detected around the capillary walls in the stria vascularis in both young and old MRL mice. Serum IgG level of the MRL mice significantly decreased after predonisolone (PSL) administration. However, expression of mouse IgG in the stria vascularis was not observed in the MRL mice after PSL administration. From these results, we speculate that the hearing of the MRL mouse does not always deteriorate, and the deposition of mouse IgG on the capillary wall in the stria vascularis is not a sufficient factor to induce hearing loss. At this point, we conclude that the MRL mouse should not be considered a useful model for immune-mediated sensorineural hearing loss.
为了阐明免疫介导的感音神经性听力损失中听力损失的可能机制,所需的基础研究包括动物模型研究。在本研究中,我们检测了MRL/lpr小鼠的听力阈值和耳蜗组织学,该小鼠现在是一种与系统性红斑狼疮(SLE)病理一致的模型。目前的研究结果表明,4至6周龄的“年轻”MRL小鼠和20至25周龄的“老年”MRL小鼠之间的听觉脑干反应(ABR)阈值没有统计学上的显著差异。这些差异与性别无关。在光学显微镜下,年轻或老年MRL小鼠的耳蜗均未发现异常形态学表现。通过免疫组织化学,在年轻和老年MRL小鼠的血管纹毛细血管壁周围均检测到小鼠IgG。给予泼尼松龙(PSL)后,MRL小鼠的血清IgG水平显著降低。然而,给予PSL后,在MRL小鼠的血管纹中未观察到小鼠IgG的表达。从这些结果来看,我们推测MRL小鼠的听力并不总是恶化,并且小鼠IgG在血管纹毛细血管壁上的沉积不是导致听力损失的充分因素。就此,我们得出结论,MRL小鼠不应被视为免疫介导的感音神经性听力损失的有用模型。