
Stanley E, Lieschke GJ, Grail D, Metcalf D, Hodgson G, Gall JA, Maher DW, Cebon J, Sinickas V, Dunn AR:
Granulocyte/macrophage colony-stimulating factor-deficient mice show
no major perturbation of hematopoiesis but develop a characteristic
pulmonary pathology.
Proceedings of the National Academy of Sciences of the United States of
America 1994 Jun 7;91(12):5592-6
ABSTRACT
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.