Ozone-induced bronchial epithelial cytokine expression differs between healthy and asthmatic subjects
Ozone-induced bronchial epithelial cytokine expression differs between healthy and asthmatic subjects
复制标题
DOI：
10.1046/j.1365-2222.2003.01662.x
复制
发表时间：
2003-06-01
影响因子：
6.1
通讯作者：
Blomberg, A
中科院分区：
文献类型：
--
作者：
Bosson, J;Stenfors, N;Blomberg, A
臭氧（O-3）是一种常见的空气污染物，对健康有不良影响。目的探讨臭氧暴露对哮喘患者支气管上皮细胞因子表达的影响，方法健康和轻度过敏性哮喘受试者（仅使用吸入的β（2）-激动剂prn）以盲法和随机化顺序暴露于0.2ppm的O-3和过滤空气2小时。暴露后6 h进行支气管镜检查和支气管粘膜活检。用GMA包埋活检组织，用单克隆抗体染色检测IL-4、IL-5、IL-6、IL-8、IL-10、TNF-α、GRO-α、粒细胞-巨噬细胞集落刺激因子（GM-CSF）、Fractalkine和ENA-78的表达。O-3暴露后的上皮细胞的IL-5，GM-CSF，ENA-78和IL-8的表达增加显着哮喘，相比健康subjects.Conclusion本研究证实了轻度特应性哮喘和健康对照之间的上皮细胞因子表达的差异，以及一个差异上皮细胞因子响应O-3。哮喘组中显示的这种O-3诱导的辅助性T细胞2型（Th 2）相关细胞因子和中性粒细胞趋化因子的上调可能导致随后的气道炎症恶化，并有助于解释它们对O-3污染事件的不同敏感性。
Background Ozone (O-3) is a common air pollutant associated with adverse health effects. Asthmatics have been suggested to be a particularly sensitive group.Objective This study evaluated whether bronchial epithelial cytokine expression would differ between healthy and allergic asthmatics after ozone exposure, representing an explanatory model for differences in susceptibility.Methods Healthy and mild allergic asthmatic subjects (using only inhaled beta(2)-agonists prn) were exposed for 2 h in blinded and randomized sequence to 0.2 ppm of O-3 and filtered air. Bronchoscopy with bronchial mucosal biopsies was performed 6 h after exposure. Biopsies were embedded in GMA and stained with mAbs for epithelial expression of IL-4, IL-5, IL-6, IL-8, IL-10, TNF-alpha, GRO-alpha, granulocyte-macrophage colony-stimulating factor (GM-CSF), fractalkine and ENA-78.Results When comparing the two groups at baseline, the asthmatic subjects showed a significantly higher expression of IL-4 and IL-5. After O-3 exposure the epithelial expression of IL-5, GM-CSF, ENA-78 and IL-8 increased significantly in asthmatics, as compared to healthy subjects.Conclusion The present study confirms a difference in epithelial cytokine expression between mild atopic asthmatics and healthy controls, as well as a differential epithelial cytokine response to O-3. This O-3-induced upregulation of T helper type 2 (Th2)-related cytokines and neutrophil chemoattractants shown in the asthmatic group may contribute to a subsequent worsening of the airway inflammation, and help to explain their differential sensitivity to O-3 pollution episodes.