It is often assumed that macrophage‐colony stimulating factor (M‐CSF) or CSF‐1, as well as granulocyte macrophage‐CSF (GM‐CSF), can induce inflammatory mediator production by monocytes/macrophages. We demonstrate with elutriation‐purified human monocytes that, in contrast to lipopolysaccharide, recombinant human CSF‐1 does not induce secretion of prostaglandin E₂, interleukin‐6 (IL‐6), IL‐lβ, or tumor necrosis factor a, as measured by immunoassay; however, increased urokinase‐type plasminogen activator (u‐PA) activity in cell lysates and mRNA was observed. Similar results were obtained when the monocytes were treated with recombinant human GM‐CSF. Such increased u‐PA expression may contribute to the function of CSF‐1 at sites of inflammation.