Abstract
Background: Smoking may modify airway inflammatory pattern. There is some evidence that the elevated levels of PGE2 in the exhaled breath condensate of patients with asthma are mainly related to smoking habit [Kostikas et al ERJ 2003].
Objective: To evaluate the concentrations of PGE2 and cysLTs in sputum supernatants of patients with asthma and to determine whether smoking affects significantly their measurements.
Methods: We studied 98 patients with asthma (47 smokers), under optimal treatment with ICS. We also studied 40 control subjects (20 smokers). All subjects underwent sputum induction, pulmonary function tests, measurement of FeNO and BHR to methacholine expressed as PD15.
Results: Median [IQR] sputum cysLTs concentration was significantly higher in asthmatic smokers compared to non asthmatic smokers and both smoking and non smoking controls [503 (400,731) vs. 345 (210-509) vs. 93 (75-121) vs. 121 (95,175) pg/ml, respectively; p<0.0001]. Similar results were observed for PGE2 concentrations which were significantly higher in smoking asthmatics [754 (654,901) vs 532 (345,654), vs 212 (132,342) vs 164 (102,207) pg/ml, p<0.001]. In patients with smoking asthma, significant positive associations was observed between cysLTs concentration and sputum eosinophils and PGE2 concentration and sputum neutrophils.
Conclusions: The increased concentrations of PGE2 and cysLTS in sputum supernatants of smoking asthma are consistent with the hypothesis that these two mediators are up-regulated in this specific phenotype of asthma. Furthermore, cysLTs are associated with the persistent eosinophilic inflammation observed in smoking asthma, while PGE2 is associated with the neutrophilic one.
- © 2011 ERS
