Ultrastructural Features of Alveolar Cells in Experimental Hypersensitivity Pneumonitis

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.

From granuloma to fibrosis in interstitial lung diseases: molecular and cellular interactions

“…Inflammatory and interstitial cells can then enter the alveolar spaces, initiating intra-alveolar fibrosis, and leading to alveolar collapse and/or coalescence and intramural incorporation of the intra-alveolar fibrosis. This sequence of events has been shown by analysis of the pathology in hypersensitivity pneumonitis [84][85][86], and histiocytosis X [87]. In contrast, less epithelial cell damage is observed in sarcoidosis [88].…”

BN 52021 (a platelet activating factor‐receptor antagonist) decreases alveolar macrophage‐mediated lung injury in experimental extrinsic allergic alveolitis

“…39 Measure ment of this enzyme activity in the BALF has been used as an index of lesion and/or proliferation of these cells. 40,41 Since in acute EAA there is an hypertrophy of type II pneumocytes as well as notable structural alte rations in these cells, 42 we used this measure ment to evaluate their involvement. Our results show a marked rise in alkaline phosphatase activity in acute EAA w ith respect to both control groups.…”

Role of lysosomal enzymes released by alveolar macrophages in the pathogenesis of the acute phase of hypersensitivity pneumonitis

“…Alkaline phosphatase activity in the lower respiratory tract is limited to type II pneumocytes 5 and levels of this enzyme in BALF has been used as an index of pneumocyte lesion and/or proliferation. 29, Since in acute HP there is a hypertrophy of type II pneumocytes as well as marked structural alterations in these cells, 37 we used this measurement to evaluate these events. Our results revealed a marked rise in BALF alkaline phosphatase activity in acute HP with respect to both control groups.…”