PREVENTION OF ENDOTOXIN-INDUCED MONOKINE RELEASE BY HUMAN LOW- AND HIGH-DENSITY-LIPOPROTEINS AND BY APOLIPOPROTEIN-A-I
PREVENTION OF ENDOTOXIN-INDUCED MONOKINE RELEASE BY HUMAN LOW- AND HIGH-DENSITY-LIPOPROTEINS AND BY APOLIPOPROTEIN-A-I
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DOI：
10.1128/iai.61.12.5140-5146.1993
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发表时间：
1993-12-01
影响因子：
3.1
通讯作者：
NORTHOFF, H
中科院分区：
文献类型：
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作者：
FLEGEL, WA;BAUMSTARK, MW;NORTHOFF, H
已知内毒素（脂多糖 [LPS]）与人脂蛋白的相互作用可防止 LPS 诱导的人单核细胞活化和细胞因子（单核因子）释放。 LPS 暴露于通过超速离心分离的脂蛋白类别和载脂蛋白 A-I。然后添加单核细胞，并通过测量诱导的单核因子来确定单核细胞的LPS活化。 LPS 不能诱导单核因子释放称为脂蛋白或载脂蛋白引起的 LPS 失活。 LPS 失活被证明是低密度脂蛋白的功能。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脂多糖失活。 LPS 灭活似乎并非绝对需要脂质成分，因为不含其生理脂质补体的纯化人载脂蛋白 A-I 也会抑制 LPS 诱导的单核因子释放。
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.