This study aims at identifying prostaglandin D2 (PGD2) involvement in osmotic airway hyperresponsiveness of asthmatics. PGD2 primary plasma metabolite, 11β-PGF2α, was analyzed in exhaled breath condensate (EBC) in response to ultrasonically nebulized distilled water (UNDW) and in serum in asthmatics with different airway response to the hypoosmotic stimulus. The total group of asthmatics (n=27) had a lower basal level of 11β-PGF2α (0.38±0.13 pg/ml, mean±SEM) in EBC compared to a group of healthy subjects (0.86±0.31 pg/ml, n=5), which decreased following the UNDW challenge to 0.30±0.09 and 0.53±0.12, respectively. The group of asthmatics with airway hyperresponsiveness to UNDW (≥10% FEV1 drop from baseline, n=14) had a lower concentration of the metabolite (0.28±0.14 pg/ml) as compared to the group without hyperresponsiveness (0.49±0.31 pg/ml, n=10). The 11β-PGF2α concentration decreased in the both groups after the challenge: 0.20±0.04 and 0.23±0.07 pg/ml in the groups with and without hyperresponsiveness to UNDW, respectively . Serum content of 11β-PGF2α was ranging from 0 to 61 pg/ml in asthmatics (n=17) and from 7.3 to 85.4 pg/ml in healthy subjects (n=8). It was lower in the group with airway hyperresponsiveness to UNDW (8.4±1.7 pg/ml, n=9) than in the group without the hyperresponsiveness (21.0±8.8 pg/ml, n=8). The obtained results do not support the involvement of PGD2 in the pathophysiology of asthma with airway hyperresponsiveness to a hypoosmotic stimulus unless other conversions of the prostaglandin occur in the airway under these conditions with formation of metabolites different from 11β-PGF2α.
Endothelin-1 in exhaled breath condensate of allergic asthma patients with exercise-induced bronchoconstriction
