title: Participation of serum proteins in the inflammation-primed activation of macrophages.
abstract: 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.
authors.affiliation: Department of Biochemistry, Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140.
authors.forename: N
authors.initials: N
authors.lastname: Yamamoto
authors.forename: N P
authors.initials: NP
authors.lastname: Willett
authors.forename: D D
authors.initials: DD
authors.lastname: Lindsay
mesh_terms: D000645:Ammonium Sulfate / Q000494:pharmacology; D000818:Animals; D001798:Blood Proteins / Q000502:physiology*; D002417:Cattle / Q000196:embryology; D005591:Chemical Fractionation; D004305:Dose-Response Relationship, Drug; D005260:Female; D005312:Fetal Blood / Q000502:physiology; D005989:Glycerides / Q000494:pharmacology; D007249:Inflammation / Q000473:pathology / Q000503:physiopathology*; D007848:Laurates / Q000494:pharmacology; D008244:Lysophosphatidylcholines / Q000494:pharmacology; D017737:Macrophages, Peritoneal / Q000502:physiology*; D051379:Mice; D008807:Mice, Inbred BALB C; D050178:Monoglycerides; D009994:Osmolar Concentration; D013481:Superoxides / Q000378:metabolism
chemical_list: D001798:Blood Proteins; D005989:Glycerides; D007848:Laurates; D008244:Lysophosphatidylcholines; D050178:Monoglycerides; D013481:Superoxides; C020777:monolaurin; D000645:Ammonium Sulfate