Price R M, Jacobs D M
Biochim Biophys Acta. 1986 Jul 10;859(1):26-32. doi: 10.1016/0005-2736(86)90314-7.
We have modeled the initial interaction of bacterial lipopolysaccharide (endotoxin) with mammalian cells as consisting of two steps. The first step, adherence, we have previously shown to be ionic in nature and contains the necessary elements to determine the observed cell specificity of lipopolysaccharide interactions. The second step, coalescence, is the hypothetical insertion of the Lipid A component of lipopolysaccharide into the cell membrane lipid bilayer. Using small, unilamellar vesicles composed of phosphatidylcholine to model the cell membrane lipid bilayer, we found that lipopolysaccharide interacted with these vesicles to change the fluidity of the lipid bilayer, as measured by an increase in the fluorescence anisotropy of diphenylhexatriene in the vesicles. Since this increase in diphenylhexatriene anisotropy could not be attributed to a transfer of diphenylhexatriene between non-interacting lipopolysaccharide aggregates and vesicles, we concluded that the lipopolysaccharide aggregate coalesced with the lipid bilayer.
我们已将细菌脂多糖（内毒素）与哺乳动物细胞的初始相互作用模拟为两个步骤。第一步是黏附，我们之前已表明其本质上是离子性的，并且包含决定脂多糖相互作用中所观察到的细胞特异性的必要元素。第二步是聚结，即脂多糖的脂质A成分假设性地插入细胞膜脂质双层。使用由磷脂酰胆碱组成的小单层囊泡来模拟细胞膜脂质双层，我们发现脂多糖与这些囊泡相互作用以改变脂质双层的流动性，这通过囊泡中二苯基己三烯荧光 anisotropy 的增加来衡量。由于二苯基己三烯 anisotropy 的这种增加不能归因于非相互作用的脂多糖聚集体与囊泡之间二苯基己三烯的转移，我们得出结论，脂多糖聚集体与脂质双层聚结。
