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

If pulmonary surfactant develops a dysfunction, its ability to maintain patency of narrow conducting airways diminishes, which is likely to cause an increased airway resistance. We hypothesized that antigen challenge will cause inflammation in the conducting airways and that this will cause a surfactant dysfunction. Twenty atopic patients underwent bronchoalveolar lavage (BAL) 5 min and 48 h after challenge with antigen in one segment and with saline solution in another. BAL fluid (BALF) cell count, differential, and proteins were determined. Surfactant function was studied with a capillary surfactometer (CS), an instrument specifically designed to evaluate surfactant's ability to maintain patency. Eosinophils increased 80-fold 48 h after antigen challenge and total protein increased from 84 to 241 micrograms/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 negatively correlated with percent openness (r = -0.62, p = 0.005). We conclude that 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 exacerbation of asthma.