Phagocytosis of liposomes by human platelets.

We have shown that platelets are capable of phagocytosing liposomes rather than simply sequestering particles as previously postulated. Incubation of human platelets with small neutral unilamellar liposomes (approximately 74 nm) resulted in uptake of the liposomes and retention of the lipid with rapid release of the aqueous-phase components. The lipid label [3H]-cholesterylhexadecyl ether and water-soluble [3H]inulin were used to study the fate of the liposome components. Uptake of liposomes was proportional to the number of liposomes added and to the incubation time. Approximately 250 liposomes per platelet were taken up within a 5-hr incubation period. Uptake of the liposomes occurred through the open-channel system, as evidenced by thin-section electron microscopy, and was followed by accumulation and degradation in acid- and esterase-containing vesicles, as determined by changes in fluorescence of the pH-sensitive probe, pyranine (1-hydroxypyrene-3,6,8-trisulfonic acid), and hydrolysis of the cholesteryl [14C]oleate membrane marker. Uptake was inhibited by the addition of EDTA, cytochalasin B, or 2,4-dinitrophenol and iodoacetate to the medium. Results from the serotonin release assay, micro-aggregation assay, fluorescein diacetate membrane integrity assay, and electron microscopy indicate that neither the conditions for loading nor phagocytosis of liposomes significantly alter platelet function or morphology.