Experimental lung injury. I. Bacterial pneumonia: ultrastructural, autoradiographic and histochemical observations.
Proteus infection in the rat produces an acute bacterial pneumonia which resolves without necrosis or significant organization within 2 weeks. Ultrastructural changes included widespread damage to type 2 cells and endothelial cells and rapid proliferation of the alveolar epithelial cells, which were the predominant site of labeling with tritiated thymidine. Histochemical staining for lysosomal enzymes showed an initial reduction in type 2 cell reactivity. The majority of proliferating epithelial cells were also unreactive until the normal pattern of staining and morphology returned at 8 to 12 days after infection. The acute inflammatory exudate was reactive, but there was only minimal to moderate staining in the subsequent clusters of alveolar macrophages. These data suggest that resolution with the preservation of the normal architecture of the peripheral airspaces may be correlated with superficial injury and limited reactivity for digestive enzymes.
D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D001345:Autoradiography; D002466:Cell Nucleolus; D002467:Cell Nucleus; D003593:Cytoplasm; D004195:Disease Models, Animal / Q000473:pathology; D004847:Epithelial Cells; D005966:Glucuronidase / Q000378:metabolism; D006965:Hyperplasia / Q000473:pathology; D008168:Lung / Q000473:pathology*; D008264:Macrophages; D008297:Male; D008928:Mitochondria; D011014:Pneumonia / Q000473:pathology*; D011512:Proteus Infections / Q000473:pathology; D011513:Proteus mirabilis; D011650:Pulmonary Alveoli / Q000473:pathology; D051381:Rats; D012270:Ribosomes
D000135:Acid Phosphatase; D005966:Glucuronidase