人类鼻腔黏膜上皮结构及功能异常可导致慢性鼻-鼻窦炎（CRS）的发生，我们前期研究发现鼻腔上皮干细胞（hNESPCs）与鼻腔上皮的异常重塑密切相关。研究表明脑源性神经营养因子（BDNF）在气道上皮细胞中的表达与气道功能及疾病发生相关，PI3K/Akt是其发挥作用主要信号通路。我们的前期研究亦证实在鼻腔组织样本中，BDNF/PI3K/Akt通路与鼻上皮干细胞的表型有相关性。但在CRS中该通路对hNESPCs调节的作用尚不明确。因此，我们拟检测不同类型CRS临床样本以明确该通路的活化情况；在体外实验中通过调控信号通路的活化状态，观察其对hNESPCs表型的影响及它们之间的相关性；构建动物模型进一步验证经BDNF/PI3K/Akt调控的hNESPCs细胞对黏膜局部炎症反应的影响。本研究将明确BDNF/PI3K/Akt信号通路调控鼻上皮干细胞参与CRS发病的机制，为寻求新治疗方法提供理论依据

The abnormal structure and function of human nasal mucosa may lead to Chronic rhinosinusitis (CRS). In our recent study, human nasal epithelial stem/progenitor cells (hNESPCs) were closely associated with the remodeling of nasal epithelium. Recent study reported that the expression of Brain Derived Neurotrophic Factor (BDNF) in the airway epithelium was correlated with function and disease of the airway. PI3K/Akt was one of the main signaling pathways of BDNF. In our study, BDNF/PI3K/Akt pathway was involved in the phenotype of nasal stem cells in nasal tissue sample. However, the modulation of BDNF/PI3K/Akt signaling pathway on hNESPCs in CRS patients is still unclearly. Therefore, in this study, we investigate the activation of BDNF/PI3K/Akt pathway from different types of CRS samples. In the vitro research, the hNESPCs phenotype is reported through regulating the activation of BDNF/PI3K/Akt pathway. In the animal model research, we investigate whether the local inflammatory response and inflammatory cells infiltration are affected by the hNESPCs activated by BDNF/PI3K/Akt pathway. The aim of this study is to determine the regulation of BDNF/PI3K/Akt pathway on hNESPCs in pathogenesis of CRS and provide the theory basis for the new treatment.