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Granulocyte-colony stimulating factor (G-CSF) stimulates a variety of biological activities in bone marrow neutrophil granulocyte precursors. It is known that some of these activities may be independent of G-CSF binding to its receptor. Therefore, we tested the hypothesis that the G-CSF-induced mobilization of neutrophils to the peripheral blood stream may be explained by an independent G-CSF receptor on the bone marrow neutrophil granulocyte precursor. We therefore studied the effects of anti-G-CSF monoclonal antibody on neutrophil mobilization induced by G-CSF. The dose-response relationships for G-CSF and granulocyte-macrophage colony-stimulating factor were studied in mice after the administration of anti-G-CSF antibody or control IgG. Our results show that G-CSF doses of less than 1 microgram/kg, but not doses of greater than 1 microgram/kg, resulted in a significant depletion of neutrophil numbers in the peripheral blood. The administration of 2.5 micrograms/kg G-CSF in combination with anti-G-CSF did not result in the depletion of the neutrophil pool, although this effect was observed when anti-G-CSF was administered in doses of 0.25 and 0.5 microgram/kg. No depletion of neutrophil numbers was observed in mice treated with either 2.5 micrograms/kg or 5 micrograms/kg G-CSF alone. However, neutrophil numbers were significantly depleted in mice treated with 12 micrograms/kg G-CSF plus anti-G-CSF. These studies show that the mobilization of bone marrow neutrophil granulocyte precursors to the peripheral blood can be induced by high doses of G-CSF but not by lower doses of G-CSF. We conclude that G-CSF-induced neutrophil mobilization to the blood stream is dependent on the interaction of a high-affinity G-CSF receptor on the bone marrow granulocyte precursor. The biological role of this receptor is not known but may be
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