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Involvement of granulocyte-macrophage colony-stimulating factor in pulmonary homeostasis.

The in vivo function of murine granulocyte-macrophage colony-stimulating factor (GM-CSF) was investigated in mice, carrying a null allele of the GM-CSF gene, that were generated by gene targeting techniques in embryonic stem cells. Although steady-state hematopoiesis was unimpaired in homozygous mutant animals, all animals developed the progressive accumulation of surfactant lipids and proteins in the alveolar space, the defining characteristic of the idiopathic human disorder pulmonary alveolar proteinosis. Extensive lymphoid hyperplasia associated with lung airways and blood vessels was also found, yet no infectious agents could be detected. These results demonstrate that GM-CSF is not an essential growth factor for basal hematopoiesis and reveal an unexpected, critical role for GM-CSF in pulmonary homeostasis.

Pubmed ID: 8171324


  • Dranoff G
  • Crawford AD
  • Sadelain M
  • Ream B
  • Rashid A
  • Bronson RT
  • Dickersin GR
  • Bachurski CJ
  • Mark EL
  • Whitsett JA


Science (New York, N.Y.)

Publication Data

April 29, 1994

Associated Grants

  • Agency: NHLBI NIH HHS, Id: HL37569

Mesh Terms

  • Animals
  • Bronchoalveolar Lavage Fluid
  • Granulocyte-Macrophage Colony-Stimulating Factor
  • Hematopoiesis
  • Homeostasis
  • Humans
  • Hyperplasia
  • Lung
  • Mice
  • Mice, Inbred C57BL
  • Mutation
  • Proteolipids
  • Pulmonary Alveolar Proteinosis
  • Pulmonary Alveoli
  • Pulmonary Surfactant-Associated Proteins
  • Pulmonary Surfactants