IgE-mediated allergy and cigarette smoking enhance the generation of leukotrienes B4(LTB4) and C4(LTC4) by leucocytes and bronchial hyperresponsiveness in pations with atopic asthma.

Influences of IgE-mediated allergy and cigarette smoking on pathophysiology, evaluated by bronchial hyperresponsiveness and the generation of LTB4 and LTC4, of asthma were examined in 69 patients with asthma sensitive to inhalant allergens such as house dust mite and Candida albicans. 1 . Bronchial byperresponsiveness was significantly higher in previous and current smokers of asthmatics than in never-smokers. 2 . The generation of leukotrienes 84 (LTB4) and C4 (LTC4) by leucocytes was significantly larger in patients with serum IgE over 350 IU/ml than in those with serum IgE less than 150 IU/ml (LTB4 : pbronchial hyperresponsiveness and LTB4 generation. 4 . Bronchial hyperresponsiveness was not significantly correlated with patient age in thse patients with atopic asthma. The results demonstrate that IgE-mediated allergy significantly enhances the generation of LTB4 and LRC4 by leucocytes, and cigarette smoking significantly enhances bronchial hyperresponsiveness in patients with atopic asthma.