细颗粒物（PM2.5）是慢性鼻-鼻窦炎、变应性鼻炎等慢性鼻病高发的重要原因。鼻腔黏膜上皮细胞纤毛运动功能是维持上呼吸道防御功能的关键因素，但目前PM2.5对鼻腔黏膜上皮细胞纤毛运动功能的作用及机制并不清楚。PM2.5可导致细胞内氧化应激反应，线粒体可能是其效应靶点，最新研究发现线粒体转移在治疗以线粒体损伤为重要发病机制的一些疾病中发挥了良好的治疗效果。本研究拟从人群流行病学、动物试验和人鼻腔黏膜上皮细胞模型三个层面，探讨PM2.5对鼻腔黏膜上皮细胞纤毛运动功能的影响以及线粒体损伤在其中的作用，并结合人骨髓间充质干细胞来源的线粒体共培养干预措施，从干预效果角度进一步探讨线粒体损伤是PM2.5致鼻腔黏膜上皮细胞纤毛运动功能下降的重要机制。本研究有助于解释PM2.5致慢性鼻病高发的机制，对阐明PM2.5的健康危害效应有重要的意义，通过探索新的治疗靶点，对制定PM2.5危害防治措施起到了积极作用。

Fine particulate matter (PM2.5) is an important reason for chronic rhino-sinusitis, allergic rhinitis and other chronic nasal diseases. Ciliary movement of nasal epithelial cells plays an extremely important role in maintaining the stability of defense system in the upper respiratory tract. But the effect of PM2.5 on ciliary movement of nasal epithelial cells and its mechanism is not clear. PM2.5 can cause cellular oxidative stress, which suggested mitochondria might be the target of the toxicity. Recently, some studies have found that transfer of mitochondria can reduce the pathogenesis of some diseases in which mitochondrial damage plays an important role. Thus, we plan to explore the role of mitochondrial injury in PM2.5 induced damage of ciliary movement on nasal epithelial cells and its mechanism. In this study, epidemiological study combined with in vivo animal study and in vitro nasal epithelial cells model study were used. To confirm the mitochondria dysfunction caused by PM2.5 in the nasal mucosal epithelial cells, we plan to measure the interventions of mitochondria derived from human bone marrow mesenchymal stem cells co-cultured with the PM2.5 exposured nasal epithelial cells. This study helps to explain the effect of PM2.5 in the pathogenesis of chronic nasal diseases, also to explore new therapeutic targets of diseases caused by PM2.5 exposure, which provide theoretical basis and technical support for health care of population exposured particulate matter.