AIRWAY EOSINOPHILIC INFLAMMATION AND BRONCHIAL HYPERRESPONSIVENESS AFTER ALLERGEN INHALATION CHALLENGE IN ASTHMA

Allergen exposure in atopic asthmatic patients is associated with recr uitment and activation of eosinophils in the airways. Once activated, eosinophils release toxic products, including the eosinophil cationic protein (ECP), able to damage bronchial structures and to increase bro nchial hyperresponsiveness. With this background, the present study wa s designed to evaluate whether ECP levels in bronchoalveolar lavage (B AL) fluid could reflect, better than BAL eosinophil counts, the cellul ar activation that follows allergen exposure in atopic asthmatics. Twe nty-two atopic patients attended the laboratory on two separate days. On the Ist day, they underwent methacholine (MCh) inhalation challenge to detect the degree of nonspecific bronchial hyperresponsiveness. On the 2nd day, they underwent fiberoptic bronchoscopy and BAL, at basel ine or 4-6 h after allergen inhalation challenge. In this latter patie nt group, MCh challenge was repeated 3-5 h after allergen challenge, 1 h before fiberoptic bronchoscopy. The analysis of the mean baseline F EV, values and the degree of bronchial reactivity to MCh (MCh Pd-20) o n the Ist study day did not demonstrate differences between the two pa tient groups (p > 0.1, each comparison). In addition, in the allergen- challenged group, MCh Pd-20 was decreased significantly after allergen challenge (151.4 mu g/ml and 67.6 mu g/ml, respectively, before and a fter challenge; p < 0.05). Evaluation of the different BAL cell types demonstrated that the proportions of eosinophils and epithelial cells were increased significantly in the allergen-challenged group compared with the group evaluated at baseline (p < 0.01 and p < 0.05, respecti vely). Moreover, ECP levels, corrected by the correspondent albumin le vels (ECP/Alb), were higher in the allergen-challenged group compared with the group evaluated at baseline (p < 0.05). In addition, although a positive correlation was demonstrated between BAL eosinophil percen tages and ECP/Alb values (r = 0.72, p < 0.05) in the group evaluated a t baseline, no links were found between these parameters in the allerg en-challenged group (p > 0.1). However, in this latter group, a weak p ositive correlation was demonstrated between eosinophil percentages an d Delta Mch, i.e., the increased nonspecific bronchial reactivity, whi ch is observed after allergen challenge (r = 0.55; p < 0.05). Thus, in stable asthmatic patients an ongoing activation of eosinophils parall els their migration, but this eosinophilic inflammation is not strictl y related to bronchial reactivity to Mch. By contrast, after allergen inhalation challenge, eosinophil recruitment and activation seem to fo llow different temporal kinetics, and eosinophilic inflammation may be partially associated with the degree of airway hyperresponsiveness.