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Am J Physiol Lung Cell Mol Physiol 280: L379-L386, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 3, L379-L386, March 2001

EDITORIAL FOCUS
GM-CSF regulates protein and lipid catabolism by alveolar macrophages

Mitsuhiro Yoshida, Machiko Ikegami, Jacquelyn A. Reed, Zissis C. Chroneos, and Jeffrey A. Whitsett

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

Metabolism of surfactant protein (SP) A and dipalmitoylphosphatidylcholine (DPPC) was assessed in alveolar macrophages isolated from granulocyte-macrophage colony-stimulated factor (GM-CSF) gene-targeted [GM(-/-)] mice, wild-type mice, and GM(-/-) mice expressing GM-CSF under control of the SP-C promoter element (SP-C-GM). Although binding and uptake of 125I-SP-A were significantly increased in alveolar macrophages from GM(-/-) compared with wild type or SP-C-GM mice, catabolism of 125I-SP-A was markedly decreased in GM(-/-) mice. Association of [3H]DPPC with alveolar macrophages from GM(-/-), wild-type, and SP-C-GM mice was similar; however, catabolism of DPPC was markedly reduced in cells from GM(-/-) mice. Fluorescence-activated cell sorter analysis demonstrated decreased catabolism of rhodamine-labeled dipalmitoylphosphatidylethanolamine by alveolar macrophages from GM(-/-) mice. GM-CSF deficiency was associated with increased SP-A uptake by alveolar macrophages but with impaired surfactant lipid and SP-A degradation. These findings demonstrate the important role of GM-CSF in the regulation of alveolar macrophage lipid and SP-A catabolism.

pulmonary alveolar proteinosis; granulocyte-macrophage colony-stimulating factor


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