Triggering of the macrophage and neutrophil respiratory burst by antibody bound to a spin-label phospholipid hapten in model lipid bilayer membranes

Abstract

The specific antibody-dependent stimulation of the respiratory burst (cyanide-insensitive oxygen consumption, 1-C-glucose oxidation) of [mouse neoplastic] RAW264 macrophage cells by haptenated lipid vesicles depends strongly on the physical properties of the lipid membrane and the surface density of antibodies on the vesicles. Lipid membranes that are solid at 37.degree. C (dipalmitoylphosphatidylcholine, DPPC) are much more effective, per vesicle bound, than are fluid membranes (dimyristoylphosphatidylcholine, DMPC). Vesicle membranes that have both fluid and solid regions (DPPC containing < 20 mol % cholesterol) show both enhanced binding rates (due to the fluid regions) and enhanced respiratory rates (due to the solid regions). In contrast to these results, the specific antibody-dependent respiratory burst of neutrophils due to haptenated vesicles parallels the antibody-dependent vesicle binding and shows no significant difference between fluid and solid target membranes.