Flegel W A, Baumstark M W, Weinstock C, Berg A, Northoff H
Abteilung für Transfusionsmedizin, Universität Ulm, Germany.
Infect Immun. 1993 Dec;61(12):5140-6. doi: 10.1128/iai.61.12.5140-5146.1993.
Interaction of endotoxin (lipopolysaccharide [LPS]) with human lipoproteins is known to prevent the LPS-induced activation of human monocytes and release of cytokines (monokines). LPS was exposed to lipoprotein classes separated by ultracentrifugation and to apolipoprotein A-I. Then monocytes were added, and the LPS activation of monocytes was determined by measuring the induced monokines. Failure of LPS to induce monokine release was called LPS inactivation caused by lipoproteins or apolipoproteins. The LPS inactivation is shown to be a function of low-density lipoproteins. High-density lipoproteins inactivate LPS to a much lesser extent. The very-low-density lipoproteins cannot inactivate LPS. Lipid components seemed not absolutely required for LPS inactivation, because purified human apolipoprotein A-I without its physiological lipid complement also inhibits LPS-induced monokine release.
已知内毒素（脂多糖[LPS]）与人脂蛋白的相互作用可阻止LPS诱导的人单核细胞活化及细胞因子（单核因子）释放。将LPS分别与经超速离心分离的脂蛋白类别以及载脂蛋白A-I接触。然后加入单核细胞，并通过测量诱导产生的单核因子来确定LPS对单核细胞的激活作用。LPS未能诱导单核因子释放被称为脂蛋白或载脂蛋白导致的LPS失活。结果表明，LPS失活是低密度脂蛋白的一种功能。高密度脂蛋白使LPS失活的程度要小得多。极低密度脂蛋白不能使LPS失活。LPS失活似乎并非绝对需要脂质成分，因为去除了生理脂质成分的纯化人载脂蛋白A-I也能抑制LPS诱导的单核因子释放。
