慢性咳嗽高敏综合征（CHS）是临床上的常见病症，其发病机制尚不明确，亦无有效的治疗方法。我们假设CHS是由于气道感觉神经末梢瞬时受体电位阳离子通道（TRPV1、TRPA1）异常激活所致。本研究拟在建立TRPV1、TRPA1介导的咳嗽敏感性检测方法的基础上，观察CHS患者TRPV1、TRPA1介导的咳嗽敏感性变化，并比较两者的差异，探讨其与气道黏膜TRPV1、TRPA1表达及气道炎症的关系。通过动物实验模型，观察不同空气污染物(烟草烟雾、汽车尾气提取物)对TRPV1/TRPA1介导的咳嗽敏感性、TRPV1/TRPA1表达、气道炎症的作用及TRPV1/TRPA1阻断剂的作用。最后通过建立TRPV1、TRPA1稳定转染的细胞模型，观察空气污染物相关组分对TRPV1、TRPA1激活的作用。本课题的完成对阐明瞬时受体电位阳离子通道异常激活在CHS发病中的作用及其与环境污染的关系具有重要意义。

Chronic cough hypersensitivity sydrome (CHS) is common in respiratory clinic,while its pathogensis is still uncertain. So far, there is no effective treatment to CHS. We hypothesise that CHS may be caused by overactivated transient receptor potential vanilloid 1(TRPV1）or/and transient receptor potential ankyrin 1(TRPA1).The changes of TRPV1 and TRPA1-mediated cough sensitivity will be investigated and compared in CHS patients, after a method to determined TRPV1/TRPA1- mediated cough sensitivity is established. The relationship of TRPV1/TRPA1-mediated cough sensitivity with TRPV1/TRPA1 expression in bronchus, throat mucosa and airway inflammation. By using animal models ,we observe the influence of different kinds of pollutants (tobacco smoke、vehicle exhaust extract) on TRPV1/TRPA1-mediated cough sensitivityTRPV1/TRPA1 expression,airway inflammation, and TRPV1/TRPA1 inhibitor. Finally, stable TRPV1/TRPA1,transfected cell lines will be set up, and the effect of related components in pollutants on TRPV1/TRPA1 activation will be identified. This study will play an important role on understanding pathogensis of CHS by TRPV1/TRPA1 overactivation and their relationship with environment pollution, which may provide a new direction for drug development of CHS.