Department of Otolaryngology, Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, China.
Department of Otolaryngology, Case Western Reserve University, Cleveland, OH, 44106, USA.
J Assoc Res Otolaryngol. 2022 Apr;23(2):213-223. doi: 10.1007/s10162-022-00838-2. Epub 2022 Feb 3.
Otitis media (OM) disease is a common cause of hearing loss that is primarily the result of middle ear infection. At present, our understanding of the mechanisms leading to OM is limited due to the lack of animal models of OM with effusion (OME). Here, we report that the mice with genetic otitis media one (gom1) mutants are prone to OM. gom1 Mice were produced by the N-ethyl-N-nitrosourea (ENU) mutagenesis program as an animal model to study OM. These mice demonstrate many common features of OM, such as middle ear effusion and hearing impairment. We revealed that gom1 mice display various signs of middle ear and inner ear dysfunctions, including elevated thresholds of auditory-evoked brainstem response (ABR) and lack of cochlear microphonic responses. Decreased compliance in tympanometry measurements indicates tympanic membrane and ossicular chain malfunction. We confirmed through histological examinations of middle ear structures that 34/34 (100 %) of the mutant mice suffered from severe OME. While individual ears had different levels of effusion and inflammatory cells in the middle ear cavity, all had thickened middle ear mucosa and submucosa compared to control mice (B6). Moreover, the mutant mice displayed cochlear hair cell loss. These observations also suggested the craniofacial abnormalities in the gom1 mouse model. Together, these results indicate that gom1 mice could be valuable for investigating the genetic contribution to the development of middle ear disease.
中耳炎（OM）疾病是听力损失的常见原因，主要是中耳感染的结果。目前，由于缺乏渗出性中耳炎（OME）的动物模型，我们对导致 OM 的机制的了解有限。在这里，我们报告具有遗传中耳炎的小鼠（gom1）突变体易患 OM。gom1 小鼠是通过 N-乙基-N-亚硝脲（ENU）诱变程序产生的，作为研究 OM 的动物模型。这些小鼠表现出许多 OM 的共同特征，例如中耳积液和听力障碍。我们揭示了 gom1 小鼠表现出各种中耳和内耳功能障碍的迹象，包括听觉诱发脑干反应（ABR）阈值升高和耳蜗微音响应缺失。鼓室图测量中的顺应性降低表明鼓膜和听小骨链功能障碍。我们通过对中耳结构的组织学检查证实，34/34（100%）的突变小鼠患有严重的 OME。虽然个别耳朵的中耳腔中有不同程度的积液和炎症细胞，但与对照小鼠（B6）相比，所有耳朵的中耳粘膜和粘膜下层都增厚。此外，突变小鼠还表现出耳蜗毛细胞丧失。这些观察结果还表明 gom1 小鼠模型存在颅面异常。总之，这些结果表明 gom1 小鼠可用于研究中耳疾病发展的遗传贡献。
