Surfactant metabolism in surfactant protein a deficient mice.
Ikegami, Machiko, Thomas R. Korfhagen, Michael D. Bruno, Jeffrey A.
Whitsett, Alan H. Jobe.
Department of Pediatrics, UCLA School of Medicine, Harbor-UCLA
Medical Center, Torrance, CA 90509, Department of Pediatrics,
Division of Pulmonary Biology, Cincinnati Children's Hospital,
Cincinnati, OH 45229
APStracts 3:0199L, 1996.
In the present study we asked if surfactant metabolism was altered in
SP-A deficient mice in vivo. Although previous studies in vitro
demonstrated that SP-A modulates surfactant secretion and reuptake by
Type II cells, mice made SP-A deficient by homologous recombination
grow and reproduce normally and have normal lung function. Alveolar
and lung tissue Sat PC pools were 50% and 26% larger, respectively,
in SP-A (-/-) mice than in SP-A (+/+) mice. Radiolabeled choline and
palmitate incorporation into lung saturated phosphatidylcholine (Sat
PC) was similar both in vivo and for lung tissue slices in vitro from
SP-A (+/+) and SP-A (-/-) mice. Percent secretion of radiolabeled Sat
PC was unchanged from 3 to 15 h, although SP-A (-/-) mice retained
more labeled Sat PC in the alveolar lavages at 48 h (consistent with
the increased surfactant pool sizes). Clearance of radiolabeled
dipalmitoylphosphatidylcholine and SP-B from the airspaces after
intratracheal injection was similar in SP-A (-/-) and SP-A (+/+)
mice. Lack of SP-A had minimal effects on the overall metabolism of
Sat PC or SP-B in mice.
Received 2 August 1996; accepted in final form 25 October 1996.
APS Manuscript Number L249-6.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996