Ozone-induced bronchial epithelial cytokine expression differs between healthy and asthmatic subjects

被引:51
作者
Bosson, J
Stenfors, N
Bucht, A
Helleday, R
Pourazar, J
Holgate, ST
Kelly, FJ
Sandström, T
Wilson, S
Frew, AJ
Blomberg, A [1 ]
机构
[1] Univ Umea Hosp, Dept Resp Med & Allergy, SE-90185 Umea, Sweden
[2] Swedish Def Res Agcy, Umea, Sweden
[3] Univ Southampton, Air Pollut Res Grp, Sch Med, Southampton, Hants, England
[4] Univ London Kings Coll, Environm & Hlth Res Grp, Dept Hlth & Life Sci, London WC2R 2LS, England
关键词
air pollution; asthmatics; bronchial epithelium; cytokines; ozone;
D O I
10.1046/j.1365-2222.2003.01662.x
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:777 / 782
页数:6
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