Wassef N M, Alving C R
Department of Membrane Biochemistry, Walter Reed Army Institute of Research, Washington, DC 20307-5100.
Chem Phys Lipids. 1993 Sep;64(1-3):239-48. doi: 10.1016/0009-3084(93)90068-e.
In this article we describe an in vitro model for complement-dependent phagocytosis of liposomes. We have previously reported that complement-opsonized liposomes are avidly ingested by murine peritoneal or bone marrow-derived cultured macrophages. However, when the liposomes contained certain lipids, including phosphatidylinositol, ganglioside GM1, and sulfogalactosyl ceramide, that have been identified as causing prolonged circulation time in vivo, complement-dependent phagocytosis of the liposomes was greatly suppressed. We identify certain additional factors associated with suppressed complement-dependent phagocytosis, including, liposomal negative charge and liposomal prostaglandin E2 or thromboxane B2. Possible mechanisms responsible for suppression of complement dependent phagocytosis are suggested. We propose that suppression of complement-dependent phagocytosis could be a contributing factor in the promotion of increased circulation time of 'stealth' liposomes and that complement opsonization probably plays a role in vivo in removing liposomes from the circulation.
在本文中，我们描述了一种用于脂质体补体依赖性吞噬作用的体外模型。我们之前曾报道，补体调理的脂质体被小鼠腹膜或骨髓来源的培养巨噬细胞大量摄取。然而，当脂质体含有某些已被确定可导致体内循环时间延长的脂质时，包括磷脂酰肌醇、神经节苷脂GM1和硫代半乳糖神经酰胺，脂质体的补体依赖性吞噬作用会受到极大抑制。我们确定了与补体依赖性吞噬作用受抑制相关的某些其他因素，包括脂质体负电荷以及脂质体前列腺素E2或血栓素B2。文中提出了补体依赖性吞噬作用受抑制的可能机制。我们认为，补体依赖性吞噬作用的抑制可能是促进“隐形”脂质体循环时间延长的一个因素，并且补体调理作用可能在体内从循环中清除脂质体方面发挥作用。
