Abstract
The binding and effects of inhaled or infused concanavalin A (Con A) preparations on rat and mouse pulmonary alveolar epithelium and macrophages were studied by a number of light-and electron-micro-scopical techniques. In comparison with BSA, inhaled Con A persisted considerably longer in the lung indicating the presence of Con A-receptors and mechanisms which prevent its rapid removal. In the lung periphery ferritin-labeled Con A was bound to type I and II pneumonocytes and macrophages. The density of binding sites was greater on type II than type I pneumonocytes. Within the time studied (up to 2 h) comparatively small amounts of the lectin were incorporated by endocytosis into the alveolar epithelium. The pulmonary macrophages bound and incorporated massive amounts of the lectin by endocytosis within 15 min. High doses of Con A lead to morphological deformation of the apical cytoplasmic zone of type II pneumonocytes and to a partial or complete collapse of the alveolar lumen. The possibility that the lectin may suppress surfactant secretion is discussed.