中耳炎的危害较大，长期反复发作会引起颅内的并发症和听力损失，中耳炎精确的分子机制尚不明确。Toll样受体2（TLR2）信号在中耳炎感染起着关键调控作用。前期研究中，我们选用Tlr2-/-小鼠通过鼓膜穿刺的方法向中耳注射链球菌肽聚糖多糖（PGPS），构建了类似人类急性化脓性中耳炎的模型，有可能是由于TLR2的缺失，致下游因子失活，造成中耳感染和上皮细胞出现氧化应激、凋亡。近年来有研究报道，TLR2参与多种炎症反应，其机制可能与细胞自噬相关。前期结果表明，Tlr2-/-中耳炎小鼠的自噬起始信号蛋白LC3升高，但自噬底物p62蛋白表达也升高，这表明自噬降解功能有可能损伤。自噬诱导剂雷帕霉素治疗后小鼠听力功能明显改善。本研究我们将验证假设：中耳上皮细胞的自噬功能损伤有可能参与中耳炎产生的机制，修复自噬降解功能或许是治疗中耳炎的有效靶点之一，为今后寻找和研发更多新的中耳炎药物提供依据。

The effect of otitis media is great. The long-term recurrent attacks can cause the intracranial complications and hearing loss. The precise molecular mechanism of otitis media is still not clear. Toll like receptor 2 (TLR2) signal plays a key role in the infection of otitis media. In previous studies, Tlr2-/- mice were inoculated with streptococcal peptidoglycan-polysaccharide (PGPS) into their middle ears of by tympanic membrane puncture. We successfully established a mice model similar to human otitis media. It was suggested that due to the deficiency of TLR2, PGPS cannot active the downstream factors through the TLR2 pathway, causing oxidative stress and apoptosis in the middle ear infection and epithelial cells. Recently, it was reported that TLR2 is involved in a variety of inflammatory responses, and its mechanism may be associated with autophagy. The previous results showed that in Tlr2-/- mice, the autophagy initiating signal protein LC3 increased, but the expression of autophagy substrate protein p62 increased. This indicates that autophagy degradation function may be damaged. The hearing function of mice was obviously improved after the treatment of rapamycin，an autophagy inducer. In this study, we will verify this hypothesis that the impaired function of autophagy in middle ear epithelial cell may be involved in the otitis media. Repair the autophagy degradation function may be one of the effective targets for the therapy of otitis media. These studies will provide new targets to explore protective therapies for otitis media.