Prednisone blunts airway neutrophilic inflammatory response due to ozone exposure in asthmatic subjects |
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Authors: | Vagaggini Barbara Cianchetti Silvana Bartoli Marialaura Ricci Manrico Bacci Elena Dente Federico L Di Franco Antonella Paggiaro Pierluigi |
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Affiliation: | Pneumology Section, Cardiothoracic Department, University of Pisa, Pisa, Italy. b.vagaggini@ao-pisa.toscana.it |
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Abstract: | BACKGROUND: The effect of corticosteroids on the ozone (O3)-induced airway inflammation is still debated. OBJECTIVE: The aim of the study was to confirm the effect of a short-term treatment with oral glucocorticosteroids on O3-induced airway inflammation, detected by induced sputum analysis, and on functional response in glucocorticosteroid-naive subjects. METHODS: A randomized, placebo-controlled study using oral prednisone (25 mg o.d. for 4 days) was carried out. Nine mild persistent asthmatics were exposed for 2 h, on separatedays, to 0.27 ppm O3 and to air in random order, after 4 days of treatment with prednisone (25 mg o.d.) and after 4 days of placebo.Before and after exposure, pulmonary function test was measured; 6 h afterexposure, sputum induction was done. RESULTS: Oral glucorticosteroids did not prevent pulmonary function decrement due to O3. After placebo, the percentage of neutrophils in induced sputum was significantly higher after O3 than after air [52.1 (15.7-77.3) vs. 17.8 (1.7-58.4), p=0.02, O3 vs. air]. This difference was lost after 4 days of treatment with prednisone [35.2% (10-96.2) vs. 30.9% (6.1-75.6), n.s., O3 vs. air]. Neutrophil elastase in sputum supernatant increased after O3 exposure in the sample obtained after placebo, but not after prednisone treatment. CONCLUSIONS: This study confirms that glucocorticosteroids reduce inflammatory airway response, but do not prevent the airway functional impairment after O3 exposure. |
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