PARTICIPATION OF SERUM-PROTEINS IN THE INFLAMMATION-PRIMED ACTIVATIONOF MACROPHAGES

Inflamed lesions release degradation products of membrane lipids, lyso phospholipids, and inflamed tumor tissues release alkylglycerols. Macr ophages were activated by administration of lysophosphatidylcholine (l yso-Pc) or dodecylgrycerol (DDG) to mice. In vitro treatment of mouse peritoneal cells (mixture of nonadherent and adherent cells) with lyso -Pc or DDG in fetal calf serum supplemented medium for 30 min, followe d by 3-h cultivation of adherent cells (macrophages) alone, resulted i n greatly enhanced Fc-receptor mediated phagocytic activity and supero xide generating capacity of macrophages. The tumor lipid metabolite, D DG, is far more potent (400-fold) than lyso-Pc in terms of doses requi red for the maximal levels of macrophage activation. The inflammation- primed macrophage activation required a serum factor, vitamin D bindin g protein, as a precursor for the macrophage activating factor. Treatm ent of mouse peritoneal cells with 1 mu g lyso-Pc/ml or 50 ng DDG/ml i n a serum-free 0.1% egg albumin supplemented medium for 30 min, follow ed by 3-h cultivation of the treated peritoneal cells in a medium supp lemented with a very small amount (0.0005-0.05%) of ammonium sulfate [ 20-50% saturated (NH4)(2)SO4] precipitable protein fraction of FCS, re sulted in greatly enhanced superoxide generating capacity of macrophag es. The ammonium sulfate precipitable fraction was found to contain vi tamin D binding protein.