IgE antibody mediated inflammation of rat lung: histologic and bronchoalveolar lavage assessment.

Pulmonary antigen challenge in sensitized individuals elicits immediate and late phase responses (LPR). While mast cells and tissue inflammation are thought to be vital to the development of the LPR, the precise pathogenesis of these responses remains under investigation. Using the Sprague-Dawley rat as a model to study cutaneous LPR, we have previously demonstrated that rat cutaneous LPR are mast cell-dependent and are histologically characterized by early (1-8 h) neutrophil-rich and late (8-24 h) mononuclear cell-rich infiltrates. To compare and contrast this cutaneous response with IgE-dependent pulmonary inflammatory responses, we performed bronchoalveolar lavage (BAL) analyses of pulmonary inflammation following specific antigen challenge in actively immunized [IgE anti-ovalbumin (OA) antibody] and BAL and histologic analyses in passively sensitized [mouse hybridoma anti-dinitrophenyl (DNP) IgE antibody] rats. Following direct insufflation of OA into the trachea, actively sensitized animals demonstrated an increased number of polymorphonuclear leukocytes (PMNs) at 4 h in BAL fluid. These cell numbers were significantly increased over controls by 24 h following challenge. In addition, rats passively sensitized for 72 h with anti-DNP IgE hybridoma antibody (PCA = 1:10,000) were challenged with DNP-BSA aerosols. Examination of BAL fluid 1 to 2 h following challenge revealed significantly increased numbers of PMNs which returned to normal levels by 24 h. Numbers of lymphocytes and macrophages were unchanged compared to controls. Microscopic examination of lung tissue revealed alveolar and interstitial edema at 2 h following challenge and a focal peribronchiolitis characterized by a predominantly mononuclear cell infiltrate.(ABSTRACT TRUNCATED AT 250 WORDS)