An Animal Model of Hypersensitivity Pneumonitis: Evaluation of the Effects of Immunization and Pulmonary Inflammation on Antigen Uptake Through the Lung

The inhalation of certain organic dusts causes hypersensitivity pneumonitis, which is characterized histologically by an interstitial, alveolar, and sometimes bronchiolargranulomatous inflammation of the lung (1). So far as is known, the disease is localized in the lung with patients suffering from the systemic symptoms of chills, fever, dyspnea and malaise during the acute stages. The disease may 1 ad to coughing, weight loss, airway restriction and fibrosis in the more severe chronic cases (1,2). Clinical symptoms occur 4 to 12 hours after exposure to the antigen (2-4). The most successful treatment is avoidance of the antigen. When this is not possible, corticosteroids have been used to alleviate symptoms of the disease (2). Farmer\u27s lung disease, first described by Campbell (5) in 1932, is the most prominent example of hypersensitivity pneumonitis. The causative agent is believed to be a thermopbilic actinomycete (Micropolyspora faeni) growing in moldy bay (6). Other diseases similarly classified as hypersensitivity pneumonitis, along with their suspected causative agents, are listed in Table I (1). The mechanism by which hypersensitivity pneumonitis occurs is quite puzzling. The observation bat only 6 to 10% of individuals similarly exposed develop the disease seems to rule out nonspecific inflammatory reactions as a central factor and may indicate a genetic predisposition (7)