Journal
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
Volume 280, Issue 3, Pages L379-L386Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.2001.280.3.L379
Keywords
pulmonary alveolar proteinosis; granulocyte-macrophage colony-stimulating; factor
Categories
Funding
- NHLBI NIH HHS [HL-61646, HL-56387, HL-28623] Funding Source: Medline
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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(2/2)] mice, wild-type mice, and GM(2/2) mice expressing GM-CSF under control of the SP-C promoter element (SP-C-GM). Although binding and uptake of I-125-SP-A were significantly increased in alveolar macrophages from GM(2/2) compared with wild type or SP-C-GM mice, catabolism of I-125-SP-A was markedly decreased in GM(2/2) mice. Association of [H-3] DPPC with alveolar macrophages from GM(2/2), wild-type, and SP-C-GM mice was similar; however, catabolism of DPPC was markedly reduced in cells from GM(2/2) mice. Fluorescence-activated cell sorter analysis demonstrated decreased catabolism of rhodamine-labeled dipalmitoylphosphatidylethanolamine by alveolar macrophages from GM(2/2) 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.
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