Dexamethasone enhances macrophage colony stimulating factor- and granulocyte macrophage colony stimulating factor-stimulated proliferation of bone marrow-derived macrophages

Glucocorticoids are effective repressors of the immune system. We haveexamined the effect of glucocorticoids on the proliferation of murinemacrophages. Dexamethasone by itself did not affect proliferation ofdifferentiated or undifferentiated bone marrow-derived macrophages (BMM)and elicited peritoneal macrophages. However, dexamethasone enhanced theproliferation induced by macrophage colony stimulating factor (M-CSF) ofthese cells. The effect of dexamethasone was not restricted toM-CSF-dependent proliferation. Similarly, dexamethasone enhancedgranulocyte macrophage colony stimulating factor (GM-CSF)- dependentproliferation of BMM. In agreement, macrophages transfected with theglucocorticoid receptor showed an enhancement of M-CSF- dependentproliferation. The enhancement of proliferation by dexamethasone or theglucocorticoid receptor was abolished by RU 486, an antagonist of theglucocorticoid receptor. Moreover, the addition of antibodies against M-CSFinhibits the effect of dexamethasone, suggesting that dexamethasoneincreases the autocrine production of M- CSF. This only occurs when M-CSFor GM-CSF, which induce M-CSF, are present in the media. In tissues,dexamethasone may enhance macrophage proliferation and contribute to theresolution of the inflammatory states.