Premium
Ozone‐induced bronchial epithelial cytokine expression differs between healthy and asthmatic subjects
Author(s) -
Bosson J.,
Stenfors N.,
Bucht A.,
Helleday R.,
Pourazar J.,
Holgate S. T.,
Kelly F. J.,
Sandström T.,
Wilson S.,
Frew A. J.,
Blomberg A.
Publication year - 2003
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1046/j.1365-2222.2003.01662.x
Subject(s) - cytokine , immunology , medicine , asthma , inflammation , interleukin 8 , chemokine , bronchus , respiratory disease , lung
Summary 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 β 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‐α, GRO‐α, 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.