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Am J Physiol Lung Cell Mol Physiol 277: L983-L987, 1999;
1040-0605/99 $5.00
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Vol. 277, Issue 5, L983-L987, November 1999

CCSP deficiency does not alter surfactant homeostasis during adenoviral infection

Machiko Ikegami, Kevin S. Harrod, Jeffrey A. Whitsett, and Alan H. Jobe

Division of Pulmonary Biology, Children's Hospital Medical Center, Cincinnati, Ohio 45229-3039

Clara cell secretory protein (CCSP) deficiency in mice is associated with increased susceptibility to pulmonary inflammation after hyperoxia or viral infection. Because adenoviral exposure perturbs pulmonary surfactant homeostasis in vivo, we hypothesized that CCSP deficiency would influence surfactant metabolism after pulmonary infection. Alveolar and total lung saturated phosphatidylcholine pool sizes were similar in CCSP-deficient [CCSP(-/-)] and wild-type [CCSP(+/+)] mice before and 7 days after intratracheal administration of adenovirus. Radiolabeled choline and palmitate incorporation into saturated phosphatidylcholine was similar, and there was no alteration by previous infection 7 days before the incorporation measurements. Furthermore, CCSP deficiency did not influence clearance of [14C]dipalmitoylphosphatidylcholine and 125I-labeled recombinant surfactant protein C. Increased persistence of alveolar capillary leak was observed in CCSP(-/-) mice after adenoviral infection. Surfactant lipid homeostasis was not influenced by CCSP before or after administration of adenovirus to the lung. Persistence of alveolar capillary leak in CCSP(-/-) mice after adenovirus provides further evidence for the role of CCSP in the regulation of pulmonary inflammation.

phosphatidylcholine; transgenic mice; surfactant protein A; surfactant protein C; Clara cells; Clara cell secretory protein


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