基于神经科学领域抑郁等神经精神疾病发生的免疫炎症事件及项目组前期研究结果，抑郁诱导的前炎性单核/巨噬细胞活化，可能在启动神经心理哮喘（neuropsychological asthma, NPA）免疫炎症机制中发挥着核心作用。本项目结合临床流行病学方法，以伴随抑郁症状的NPA为研究对象，采用诱导痰、流式细胞分析、细胞培养、荧光定量PCR、Luminex多重分析技术、免疫荧光等生物学方法，从体内外、多层面，观察NPA前炎性单核/巨噬细胞表型和功能，及其所致低度全身性炎症反应和TH1细胞分化，探讨和分析与此相关的气道炎症细胞表型、β2肾上腺素受体去敏感和糖皮质激素抵抗机制，初步揭示抑郁症状恶化哮喘控制的免疫炎症机制。

Based on immune inflammation of depression in neuroscience and our previous results, we hypothesize that depression-driving activation of pro-inflammatory monocyte/macrophage play a key role in pathogenesis of neuropsychological asthma (NPA) characterized by comorbid psychological symptoms. This proposed project will apply methods of clinical epidemiology, recruit NPA subjects with depression symptoms only, use induced sputum technique, flow cytometry, cell culture, qPCR, Luminex xMAP (Multi-Analyte Profiling) technology, immunofluorescence, etc, to investigate pro-inflammatory monocyte/macrophage-related low-grade systemic inflammation, T cell polarization, and to explore airway cellular inflammation, β2 adrenergic receptor desensitization, glucocorticoid resistance, which would provide with scientific evidence in immune-inflammation for pathogenesis of depression-worsening asthma control.