Rickles F R, Rick P D
J Clin Invest. 1977 Jun;59(6):1188-95. doi: 10.1172/JCI108743.
Activation of mononuclear cell tissue factor was examined utilizing lipopolysaccharides obtained from wild-type and both Rc and Re mutants of Salmonella typhimurium. Wild-type (smooth) lipopolysaccharide, galactose-deficient (Rc) lipopolysaccharide, heptose-deficient (Re) lipopolysaccharide, and lipid A preparations were all active in their ability to generate tissue factor activity in human mononuclear cells grown in tissue culture. Polymyxin B has been reported to prevent some of the lethal effects of endotoxin in vivo, and the drug reportedly binds to the 2-keto-3-deoxyoctulosonate-lipid A region of the lipopolysaccharide molecule. Polymyxin B was effective in inhibiting the tissue factor generating activity of wild-type lipopolysaccharide, Re lipopolysaccharide, and lipid A in a dose-dependent fashion. Treatment of lipid A preparations with mild alkali abolished the ability of these preparations to activate tissue factor in cells. Analogous to many of the other biologic properties of lipopolysaccharide, tissue factor activation in human mononuclear cells appears to depend upon the integrity of the lipid A portion of the molecule.
利用从鼠伤寒沙门氏菌的野生型以及Rc和Re突变体中获得的脂多糖,检测单核细胞组织因子的激活情况。野生型(光滑型)脂多糖、半乳糖缺陷型(Rc)脂多糖、庚糖缺陷型(Re)脂多糖以及脂质A制剂,在组织培养中生长的人单核细胞中产生组织因子活性的能力方面均具有活性。据报道,多粘菌素B可预防内毒素在体内的一些致死作用,且据报道该药物可与脂多糖分子的2-酮-3-脱氧辛糖酸-脂质A区域结合。多粘菌素B能以剂量依赖的方式有效抑制野生型脂多糖、Re脂多糖和脂质A的组织因子生成活性。用弱碱处理脂质A制剂可消除这些制剂激活细胞中组织因子的能力。与脂多糖的许多其他生物学特性类似,人单核细胞中的组织因子激活似乎取决于分子中脂质A部分的完整性。