Prostaglandin E2 in the expired breath condensate of patients with asthma

Inhaled prostaglandin (PG)E-2 has been found to cause bronchodilation in asthmatics, although it does not have bronchodilative effects in normal subjects. The aim of this study was to investigate the levels of PGE(2) in the expired breath condensate of patients with asthma, the possible contribution of smoking habit to its levels and the possible relationship between PGE(2) and the degree of bronchial hyperresponsiveness, as assessed by the provocation dose of histamine causing a 20%,, fall in forced expiratory volume in one second (FEN1) (PD20). A total of 30 mild asthmatics (15 smokers, all steroid-naive, FEV1 88+/-6 (%+/-SD)) and 20 healthy control subjects (10 smokers) were studied. Histamine challenge testing was performed in all subjects and the PD20 was determined. The results showed that asthmatic smokers had significantly higher values of PGE(2) compared to asthmatic nonsmokers and control subjects (40+/-21 versus 14.5+/-4.5 versus 11.7+/-3 pg.mL(-1), respectively). Further analysis showed that PGE(2) levels were significantly 11.7+/-3 g.mL higher in asthmatic smokers compared to smoker and nonsmoker controls (40+/-21 versus 11.6+/-2 versus 11.7+/-4 pg.mL(-1), respectively). No significant difference was observed between asthmatic nonsmokers and both control smokers and control nonsmokers. No significant correlation was found between PGE(2) levels and PD20 in all groups of asthmatics, irrespective of smoking habit. In conclusion, the elevation of prostaglandin E-2 in the expired breath condensate of patients with asthma is mainly attributed to smoking habit and prostaglandin E-2 levels do not predict the degree of bronchial hyperresponsiveness.