Inflamed lesions release degradation products of
membrane lipids,
lysophospholipids, and inflamed
tumor tissues release alkylglycerols. Macrophages were activated by administration of
lysophosphatidylcholine (
lyso-Pc) or dodecylglycerol (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, followed by 3-h cultivation of adherent cells (macrophages) alone, resulted in greatly enhanced
Fc-receptor mediated phagocytic activity and
superoxide generating capacity of macrophages. The
tumor lipid metabolite, DDG, is far more potent (400-fold) than
lyso-Pc in terms of doses required for the maximal levels of macrophage activation. The
inflammation-primed macrophage activation required a serum factor,
vitamin D binding protein, as a precursor for the macrophage activating factor. Treatment of mouse peritoneal cells with 1 microgram
lyso-Pc/ml or 50 ng DDG/ml in a serum-free 0.1% egg
albumin supplemented medium for 30 min, followed by 3-h cultivation of the treated peritoneal cells in a medium supplemented with a very small amount (0.0005-0.05%) of
ammonium sulfate [20-50% saturated (NH4)2SO4] precipitable
protein fraction of FCS, resulted in greatly enhanced
superoxide generating capacity of macrophages. The
ammonium sulfate precipitable fraction was found to contain
vitamin D binding protein.