Gm-csf regulates protein and lipid catabolism by alveolar macrophages

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

Research output: Contribution to journalArticlepeer-review

121 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)L379-L386
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number3 24-3
StatePublished - Mar 2001

All Science Journal Classification (ASJC) codes

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology


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