Fig. 1.

Pathways for lipid clearance by wild type (SP-A +/+) and SP-A gene-targeted (SP-A −/−) mice lungs. Data are adapted from reference [13]. ³H-dipalmitoyl-phosphatidylcholine labeled phospholipid (PL) liposomes (circles) were instilled into the trachea of mice and the lungs placed in an isolated perfused lung system under basal (upper panels) or secretagogue-stimulated (lower panels) conditions. Uptake of liposomes sensitive to the clathrin-inhibitor, amantadine, is “Clathrin-dependent.” Uptake of liposomes that is inhibited by cytochalasin D, an actin blocker, but not affected by amantadine is “Clathrin-independent.” (Left) SP-A, present in the surfactant of wild-type mice, associates with the instilled liposomes, while (Middle) SP-A is absent in the SP-A null mice. (Right) SP-A (−/−) plus SP-A: liposomes containing SP-A were instilled into the lungs of SP-A (−/−) mice. The addition of SP-A to the liposomes served to “rescue” the phenotype of the SP-A (−/−) mice by restoring the clathrin-mediated, secretagogue-sensitive process used by the wild type mice which had SP-A present.