Abstract: | An experimental model of hypersensitivity pneumonitis in rats was used to analyze ultrastructural changes in cellular elements of the epithelium and alveolar lumen, in an attempt to correlate the immunological mechanisms responsible for these pulmonary lesions. Semifine and ultrafine sections of pulmonary tissue of immunized and intratracheally challenged rats were analyzed and compared with their respective controls. A thickening of the alveolar walls and an increase in the number of macrophages and type II pneumocytes were observed in the semifine sections. The ultrastructural examination revealed appreciable changes in morphology, size and location of both types of cells. The membranes of the macrophages showed evident alterations and the type II pneumocytes, an increase in size and number of cytoplasmic inclusions corresponding to surfactant. The cellular changes observed are consistent with phenomena of cellular activation, which can be attributed to the release of soluble mediators by T lymphocytes. The important delayed hypersensitivity phenomena based on the morphology of pulmonary lesions in this model contribute data to the pathogenic interpretation of hypersensitivity alveolitis. |