感觉神经与肺区域免疫反应相互作用可导致或加重呼吸系统疾病。肺C类神经纤维（PCFs）是支配呼吸道的主要感觉传入神经。前期研究表明：肺区域免疫反应与RSV感染后急、慢性炎症密切相关, 有效控制过度Ⅱ类因子产生可能是预防RSV感染后反复喘息的关键；建立去除PCFs小鼠模型，发现KPCFs小鼠感染RSV后病毒滴度与气道炎症显著降低，推测PCFs参与RSV感染早期肺部抗病毒效应，后期介导肺部Ⅱ类免疫反应微环境的形成和维持。本研究拟进一步揭示：PCFs激活是否导致VIP/SP失衡，通过与其受体结合，影响RSV感染早期气道上皮细胞I型干扰素产生，参与抗病毒效应？后期是否影响气道上皮细胞修复和上皮细胞源性细胞因子分泌、释放，参与肺部Ⅱ类免疫反应形成？研究结果将进一步阐明肺区域抗病毒免疫应答及其Ⅱ类免疫反应形成和维持的上游通路，为神经激活控制及激活后神经肽物质用于治疗Ⅱ类免疫反应介导的疾病提供理论基础。

Respiratory syncytial virus (RSV) remains the leading cause of viral bronchiolitis and pneumonia in infants and young children throughout the world. Children with acute RSV infection often develop sequelae of more wheezing episodes. To date, it’s short of safety and effective preventing and therapy strategies for RSV infection. The local immune response in lung plays an important role in the early and later stage post RSV infection in our previous studies. It’s critical to control the excessive production of type 2 associated effectors for preventing repeat wheezing induced by RSV infection. The interaction of sensory nerve and lung immune could cause or accelerate airway diseases. Pulmonary C fibers mainly innervate afferent nerve for respiratory tract. In the present study, we will investigate the effect of PCFs on lung immune antiviral at the early stage of RSV infection, and type 2 response in lung at the later stage, with RSV – infected animal model (BALB/c mice and degenerated – PCFs mice). Moreover, we will uncover that the imbalance of VIP/SP could affect the production of type I interferon producing of airway epithelial cells through VPAC/NK1R to promote antiviral. And then the imbalance of VIP/SP also influences the repair of airway epithelial and the release of epithelial cells – derived cytokines to involve in type 2 response in lung. The results will provide evidence and new intervention strategies for antiviral effects and treatment of airway diseases mediated by type 2 response in lung.