Antigen-induced airway hyperresponsiveness is associated with infiltration of eosinophils in lung tissue, but not with bronchoalveolar lavage eosinophilia or neutrophilia.

To examine the role of airway inflammation in airway hyperresponsiveness (AHR), we developed an animal model of AHR in guinea pigs and examined the histopathologic changes of these airways. Guinea pigs were actively sensitized with dinitrophenylated Ascaris suum extract and challenged with inhalation of the same extract. Six and 24 h after antigen challenge, airway responsiveness to inhaled acetylcholine (ACh), bronchoalveolar lavage fluid (BALF) and lung histology were studied. Airway responsiveness to inhaled ACh increased 6 h after antigen challenge (p < 0.05), but an increase in airway responsiveness was not observed 24 h after antigen challenge as determined by PC300 (the minimum concentration of ACh at which the respiratory resistance exceeded 300% of baseline value). The number of eosinophils and neutrophils in BALF increased 6 and 24 h after antigen challenge compared to sensitized, nonchallenged guinea pigs, peaking at 24 h after antigen challenge. On the other hand, the numbers of infiltrating eosinophils in bronchial and bronchiolar tissues increased 6 and 24 h after antigen challenge compared to sensitized, nonchallenged guinea pigs, peaking at 6 h after antigen challenge. We therefore conclude that AHR after allergen exposure in sensitized guinea pigs is associated with an increase in infiltrating eosinophils in lung tissue but not with BAL eosinophilia or BAL neutrophilia.