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Am J Physiol Lung Cell Mol Physiol 283: L76-L85, 2002; doi:10.1152/ajplung.00418.2001
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Vol. 283, Issue 1, L76-L85, July 2002

Surfactant protein A regulates surfactant phospholipid clearance after LPS-induced injury in vivo

Omar A. Quintero1, Thomas R. Korfhagen2, and Jo Rae Wright1

1 Department of Cell Biology, Duke University, Durham, North Carolina 27710; and 2 Department of Pediatrics, Division of Pulmonary Biology, Cincinnati Children's Hospital, Cincinnati, Ohio 45529

Previous in vitro studies have suggested that surfactant protein A (SP-A) may play a role in pulmonary surfactant homeostasis by mediating surfactant secretion and clearance. However, mice made deficient in SP-A [SP-A (-/-) animals] have relatively normal levels of surfactant compared with wild-type SP-A (+/+) animals. We hypothesize that SP-A may play a role in surfactant homeostasis after acute lung injury. Bacterial lipopolysaccharide was instilled into the lungs of SP-A (-/-) mice and SP-A (+/+) mice to induce injury. Surfactant phospholipid levels were increased 1.6-fold in injured SP-A (-/-) animals, although injury did not alter [3H]choline or [14C]palmitate incorporation into dipalmitoylphosphatidylcholine (DPPC), suggesting no change in surfactant synthesis/secretion 12 h after injury. Clearance of [3H]DPPC from the lungs of injured SP-A (-/-) animals was decreased by ~40%. Instillation of 50 µg of exogenous SP-A rescued both the clearance defect and the increased phospholipid defect in injured SP-A (-/-) animals, suggesting that SP-A may play a role in regulating clearance of surfactant phospholipids after acute lung injury.

lipopolysaccharide; surfactant secretion; surfactant homeostasis; dipalmitoylphosphatidylcholine


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