Lipid-mediated hemagglutination and its relevance to lectin-mediated agglutination

Abstract

Oleic acid and dioleoyl phosphatidic acid at low concentrations (20 and 0.5 μg/ml, respectively) agglutinate rabbit and rat erythrocytes, while dioleoyl phosphatidylcholine is not hemagglutinating up to 0.5 mg/ml. Palmitic acid is not hemagglutinin and dipalmitoyl phosphatidic acid is a very poor one. A polar lipid fraction obtained from calf thymocytes and a commercial preparation of gangliosides also exhibit pronounced hemagglutinating activity. Modification of the erythocytes by either trypsin or neuraminidase causes a marked increase in agglutination only with oleic acid, whereas glutaraldehyde fixation of the cells significantly decreases agglutination with oleic acid, dioleoyl phosphatidic acid and calf thymocyte lipids. None of the lipids tested agglutinate freshly drawn human and sheep erythrocytes, but agglutination occurs following fixation of the sheep cells with glutaraldehyde. Lipid-mediated hemagglutination is strongly inhibited by fetuin and bovine submaxillary mucin (0.5 mg/ml). Defatted bovine serum albumin, also at 0.5 mg/ml, inhibits agglutination by oleic acid, whereas agglutination by other lipids is only poorly inhibited if at all. Monosaccharides at concentrations up to 0.25 M do not inhibit the hemagglutinating activity of the lipids. Comparison of the hemagglutinating properties of lipids and lectins raises the possibility that the agglutinating activity of crude biological extracts which is not inhibited by mono- or oligosaccharides may be due to lipid constituents. Since agglutination by lipids is species specific, they may serve as mediators in intercellular recognition. The mechanism of lipid-mediated hemagglutination is discussed in terms of current concepts of the fusogenic activity of these compounds.