Granulocyte/macrophage colony-stimulating factor-deficient mice show no major perturbation of hematopoiesis but develop a characteristic pulmonary pathology

Edouard Stanley, Graham J. Lieschke, Dianne Grail, Donald Metcalf, George Hodgson, John A.M. Gall, Darryl W. Maker, Jonathan Cebon, Vincent Sinickas, Ashley R. Dunn

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Mice homozygous for a disrupted granulocyte/macrophage colony-stimulating factor (GM-CSF) gene develop normally and show no major perturbation of hematopoiesis up to 12 weeks of age. While most GM-CSF-deficient mice are superficially healthy and fertile, all develop abnormal lungs. There is extensive peribronchovascular infiltration with lymphocytes, predominantly B cells. Alveoli contain granular eosinophilic material and lamellar bodies, indicative of surfactant accumulation. There are numerous large intraalveolar phagocytic macrophages. Some mice have subclinical lung infections involving bacterial or fungal organisms, occasionally with focal areas of acute purulent inflammation or lobar pneumonia. Some features of this pathology resemble the human disorder alveolar proteinosis. These observations indicate that GM-CSF is not essential for the maintenance of normal levels of the major types of mature hematopoietic cells and their precursors in blood, marrow, and spleen. However, they implicate GM-CSF as essential for normal pulmonary physiology and resistance to local infection.

Original languageEnglish
Pages (from-to)5592-5596
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number12
Publication statusPublished - 7 Jun 1994
Externally publishedYes


  • gene targeting
  • hematopoietic growth factors
  • homologous recombination
  • pulmonary diseases

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