Urinary inflammatory mediators and inhalation of hypertonic saline in children.

The inflammatory mechanisms of hypertonic saline-induced bronchoconstriction are not well understood.,Seventeen asthmatics with (n=11) and without bronchial hyperresponsiveness (BHR) (n=6) and 18 randomly selected nonatopic nonasthmatic controls without BHR were evaluated by urine samples collected before and 1 h after hypertonic saline provocation test. Histamine, 11beta-PGF2alpha, and LTE4 were analysed by enzyme immunoassay (EIA) and eosinophil protein X (EPX) by radioimmunoassay (RIA).,The levels of leukotriene E4 (LTE4) increased significantly after the challenge tests, both in the asthmatics (median: 354 pg/mg pre-challenge vs. 628 pg/mg post-challenge; P=0.05) and in the controls (median: 294 pg/mg pre-challenge vs. 460 pg/mg post-challenge; P <0.01). The levels of histamine also increased significantly in the latter (median: 299 micromol/mg pre-challenge vs. 569 micromol/mg post-challenge; P=0.03). However, the levels of 11beta-PGF2alpha and EPX did not change significantly after the challenge tests either in the asthmatics or in the controls.,The inhalation of hypertonic saline increased urinary excretion of LTE4 both in the asthmatics and in the controls. The slight increase of leukotrienes was enough to induce airway obstruction in some of the asthmatics, because of the hyperresponsiveness in their airways.