嗜酸粒细胞性伴鼻息肉的慢性鼻-鼻窦炎（Eos CRSwNP）发病机制尚不清楚。Pendrin可通过降低黏液纤毛传输功能参与气道炎症性疾病发病。我们前期研究发现Pendrin在CRSwNP中表达增高，Th2细胞因子刺激可使人鼻黏膜上皮细胞高表达Pendrin。综上我们推测Pendrin通过调控鼻黏膜黏液纤毛传输系统的功能参与Eos CRSwNP发病。我们拟：1.干预Pendrin基因敲除小鼠和野生型小鼠体内Pendrin含量，建立Eos CRSwNP小鼠型观察不同Pendrin表达量对模型形成速度，病理学特征以及黏液纤毛传输功能的影响；2.采用气液交界面人鼻黏膜上皮细胞和组织块培养技术Pendrin对黏液纤毛传输功能的影响以及调控Pendrin表达及功能的具体分子机制。本研究有助于阐明Pendrin参与Eos CRSwNP发病的机制，为EosCRSwNP的治疗提供新途径。

The pathogenesis of Eos CRSwNP remains unclear. Pendrin play a role in process of airway inflammatory diseases by depressing mucocilliary clearence. Our previousstudy showed Pendrin expression is elevated in CRSwNP compared with CRSsNP as well as normal controls and its expression in human nasal epithelial cells increased by stimulation of Th2 cytokines.These findings lead to the hypothesis that Pendrin paticipate in pathogenesis of Eos CRSwNP. This study is designed to:1.Establishing Eos CRSwNP mouse model after interfering Pendrin expression amount in Pendrin knock out mouse and wild mouse and investigating development speed, pathologic character and mucociliary transport of mouse model.2.By means of air liquid interface culture of human nasal epithelial cell and nasal tissue block, observing the influence of Pendrin on mucociliary clearence and exact molecular mechanisms in regulation of Pendrin’s expression and function. Our study is aimed to demostrate the mechanism by which Pendrin contributes to pathogensis and new therapeutic approach of Eos CRSwNP.