咳嗽高敏综合征（CHS）是常由上呼吸道病毒感染启动的特发性慢性咳嗽。干扰素-γ(IFN-γ)是病毒感染诱导的Th1与CD8阳性T淋巴细胞分泌的核心细胞因子。我们前期发现IFN-γ能增加咳嗽敏感性；CHS患者肺部Th1与CD8阳性T淋巴细胞数量明显增多。在病毒早已清除的情况下，释放IFN-γ的T淋巴细胞为何持续聚集于CHS病人肺部呢？预实验发现IFN-γ滴鼻能增加小鼠肺组织中一种CXC趋化因子（IP-10）表达量与淋巴细胞数量。因而，我们假设IFN-γ通过肺组织的IFNGR—JAK/STAT1—IRF-1信号通路过量表达与分泌CXC趋化因子，然后通过淋巴细胞的CXCR3—ERK—钙离子内流—F-actin聚合过程募集T淋巴细胞（包括分泌IFN-γ的Th1与CD8阳性T淋巴细胞），从而形成炎症正反馈，导致CHS。本项目计划在临床、动物与细胞水平研究上述作用及机制，有望为CHS的防治提供依据。

Cough hypersensitivity syndrome (CHS), which is a chronic idiopathic cough, is most frequently initially triggered by the viral upper respiratory tract infection. The major effector cells induced by the virus infection are cluster of differentiation 4+ (CD4+) T helper type 1 lymphocytes (Th1 lymphocytes) and CD8+ T lymphocytes, which are heavily reliant on interferon-γ (IFN-γ). Our previous studies found that IFN-γ could enhance cough sensitivity. And the lung of patients with CHS had obviously increased number of Th1 lymphocytes and CD8+ T lymphocytes. Why do IFN-γ-released T lymphocytes continue to accumulate in the lung of patients with CHS when the virus has been cleared? Our preliminary experiments showed that the intranasal instillation of IFN-γ could increase the expression of a CXC chemokine (IP-10) and the number of lymphocytes in the lung of mice. Therefore, we hypothesized that IFN-γ might stimulate the excessive local expression and secretion of CXC chemokines through the IFNGR—JAK/STAT1—IRF-1 signaling pathway in lung tissues. These CXC chemokines might recruit T lymphocytes (including IFN-γ-released Th1 lymphocytes and CD8+ T lymphocytes) through the CXCR3—ERK—Ca2+ influx—F-actin polymerization signaling pathway in T lymphocytes. These signaling pathways might form an inflammatory positive feedback loop, which might result in CHS. This study plans to explore the above-mentioned effects and mechanisms by the way of doing experiments in clinic, in vivo and in vitro. And this study is hopeful for laying a solid foundation for the prevention and treatment of patients with CHS.