Effect of current exposure to Der p 1 on asthma symptoms, airway inflammation, and bronchial hyperresponsiveness in mite-allergic asthmatics

The existence of a dose-response relationship between indoor allergen expos ure and sensitization has been widely described, but the effect of allergen exposure on asthma activity (symptoms, bronchial hyperresponsiveness [BHR] , and inflammation) is not clear. Our aim was to determine the existence of an association among current exposure to mite allergens and symptoms, BHR, and airway inflammation assessed in blood and sputum from asthmatic patien ts sensitized to Dermatophagoides pteronyssinus. We selected 31 mild and re cently diagnosed (12-24 months) asthma patients sensitized to D. pteronyssi nus. Allergenic exposure (Der p 1, Der 2) was assessed by a commercial assa y based on monoclonal antibodies (mAb), carried out on the dust samples col lected from patients' beds in a standardized way. Patients completed an ast hma symptom questionnaire and underwent skin tests, methacholine bronchial challenge, and sputum induction. Sputum cell profile was analyzed and eosin ophil cationic protein (ECP), tryptase, albumin, and interleukin(IL)-5 leve ls were quantified in sputum supernatant. Total eosinophil numbers and ECP levels were measured in blood samples. Most patients were exposed to Der p 1 levels under 2 mu g/g of dust. Der p 1 exposure was higher among the subj ects with positive sputum tryptase detection (P = 0.020). Der p 1 levels sh owed a trend toward correlation with asthma symptoms (P = 0.066, r = 0.36) and correlated with sputum tryptase levels (P = 0.032, r = 0.42). No relati onship between BHR, eosinophilic inflammation, and allergenic exposure was found. Our results suggest that asthma symptoms and lung mast-cell activati on are at least partially dependent on current allergen exposure. The lack of correlation between mite exposure, eosinophilic inflammation, and BHR su pports the role of other factors that enhance the immunologic response init iated by allergen, increasing the activity of asthma.