Antigen-induced airway inflammation in atopic subjects generates dysfunction of pulmonary surfactant

If pulmonary surfactant develops a dysfunction, its ability to maintain pat ency of narrow conducting airways diminishes, which is likely to cause an i ncreased airway resistance. We hypothesized that antigen challenge will cau se inflammation in the conducting airways and that this will cause a surfac tant dysfunction. Twenty atopic patients underwent bronchoalveolar lavage ( BAL) 5 min and 48 h after challenge with antigen in one segment and with sa line solution in another. BAL fluid (BALF) cell count, differential, and pr oteins were determined. Surfactant function was studied with a capillary su rfactometer (CS), an instrument specifically designed to evaluate surfactan t's ability to maintain patency. Eosinophils increased 80-fold 48 h after a ntigen challenge and total protein increased from 84 to 241 mu g/ml (median values). BALF surfactant lost part of its ability to maintain openness of the capillary, from 68.8% to 14.0% (p < 0.05). Protein concentration negati vely correlated with percent openness (r = -0.62, p = 0.005). We conclude t hat the antigen challenge resulted in an inflammatory reaction that caused pulmonary surfactant to lose some of its ability to maintain airway patency and speculate that surfactant dysfunction is probably an important factor contributing to increased airway obstruction in allergen-induced exacerbati on of asthma.