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 hyperresponsivene ss (AHR), we developed an animal model of AHR in guinea pigs and exami ned the histopathologic changes of these airways. Guinea pigs were act ively sensitized with dinitrophenylated Ascaris suum extract and chall enged with inhalation of the same extract. Six and 24 h after antigen challenge, airway responsiveness to inhaled acetylcholine (ACh), bronc hoalveolar 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 concentr ation of ACh at which the respiratory resistance exceeded 300% of base line value). The number of eosinophils and neutrophils in BALF increas ed 6 and 24 h after antigen challenge compared to sensitized, nonchall enged guinea pigs, peaking at 24 h after antigen challenge. On the oth er hand, the numbers of infiltrating eosinophils in bronchial and bron chiolar 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 neutro philia.