Antigen-induced airway hyperresponsiveness and pulmonary inflammation in allergic dogs.
We studied whether antigen-induced airway hyperresponsiveness was associated with pulmonary inflammation in 11 anesthetized ragweed-sensitized dogs. Airway responsiveness to acetylcholine aerosol was determined before and at 2, 6, and 24 h after ragweed or sham aerosol challenge. Pulmonary inflammation was assessed by bronchoalveolar lavage (BAL) performed at either 2 or 6 h. Total pulmonary resistance increased 11-fold at 5 min after ragweed. Airway responsiveness was unchanged at 2 h but was increased 6.6-fold at 6 h in 8 of 11 dogs (P less than 0.001); hyperresponsiveness persisted from 4 days to 4 mo. Airway responsiveness was unchanged by aerosols of diluent. Neutrophils in BAL fluid increased approximately sixfold at 2 h (P less than 0.02) and at 6 h (P less than 0.02) after antigen challenge. There were fewer eosinophils in fluid recovered at 6 h after antigen compared with 2 h lavages (P less than 0.05). In three nonresponders, BAL showed no significant changes in neutrophils and eosinophils after antigen. Thus antigen-induced hyperresponsiveness is associated with the presence of pulmonary inflammation, presumably arising from the airways and involving both neutrophils and eosinophils.
D000109:Acetylcholine / Q000276:immunology*; D000818:Animals; D001980:Bronchi / Q000473:pathology; D001985:Bronchial Provocation Tests; D002452:Cell Count; D004285:Dogs; D008170:Lung Compliance; D011014:Pneumonia / Q000139:chemically induced*; D011650:Pulmonary Alveoli / Q000473:pathology; D012130:Respiratory Hypersensitivity / Q000276:immunology* / Q000473:pathology; D007507:Therapeutic Irrigation
D000109:Acetylcholine