过敏性气道疾病（AADs）是一类以Th2型免疫反应介导的慢性气道炎症和异常修复疾病，包括过敏性哮喘、过敏性鼻炎和慢性鼻窦炎。目前认为上皮-间质异常通讯是过敏性气道疾病的核心发病机制，但参与其中的关键分子事件尚未明确。IL-25/IL-33/TSLP是上皮来源的促Th2型免疫反应的细胞因子，而循环纤维细胞是一种可介导组织重塑的重要间质细胞，我们前期研究发现IL-25-循环纤维细胞轴在哮喘患者中表达明显上调，且和哮喘严重程度、损伤修复相关。鉴于细胞因子生物学作用的冗余性和“同一气道“理论，我们认为IL-25/IL-33/TSLP-纤维细胞轴可能参与过敏性气道疾病上皮-间质异常通讯。为此，我们拟利用AADs患者生物标本库，制作相应小鼠模型，构建细胞培养/共培养体系，明确IL-25/IL-33/TSLP-循环纤维细胞轴是否是调控AADs的共有关键分子事件，从而为该类疾病患者的共同治疗提供潜在靶点。

Allergic airway diseases are a group of heterogeneous diseases mediated by T helper type 2(Th2) immune response and characterized with airway inflammation and remodeling, includiing allergic asthma, allergic rhinitis and chronic sinusitis. Recently, abnormal epithelial-mesenchymal crosstalk is considered to be the core pathogenesis of allergic airway disease, however, the key regulatory factors and molecular events involved still remain unclear. Epithelium-derived cytokines, including IL-25, IL-33 and TSLP, are shown to promote the Th2 immune response. Also, circulating fibrocyte is an important mesenchymal cell that can mediate tissue remodeling. We previously found that IL-25 - circulating fibrocyte axis was significantly up-regulated in patients with asthma, which greatly contributed to asthmatic airway inflammation and remodeling. Considering the redundancy of cytokines and 'one united airway' theory, we hypothesize that IL-25/IL-33/TSLP-fibrocyte axis may play a vital role in the abnormal epithelial-mesenchymal crosstalk in allergic airway diseases. On the basis of previous work, we aim to further explore whether the IL-25 /IL-33/TSLP-circulating fibrocytel axis is a common key molecular event in allergic airway disease by using the biological sample of patients with asthma, rhinitis, sinusitis with/without nasal polyps, by establishing asthma and rhinitis/sinusitis mice model, and by building the cell culture/co-culture system. This will provide potential targets for the common treatment of patients with allergic airway diseases.