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高密度脂蛋白的新功能。它们参与细菌脂多糖的血管内反应。

New function for high density lipoproteins. Their participation in intravascular reactions of bacterial lipopolysaccharides.

作者信息

Ulevitch R J, Johnston A R, Weinstein D B

出版信息

J Clin Invest. 1979 Nov;64(5):1516-24. doi: 10.1172/JCI109610.

Abstract

The addition of bacterial lipopolysaccharide (LPS) from Escherichia coli 0111:B4 or Salmonella minnesota R595 to plasma (or serum) resulted in a marked reduction of the hydrated buoyant density of the parent LPS (0111:B4 [d = 1.44 g/cm3] and R595 [d = 1.38 g/cm3]), to d less than 1.2 g/cm3. This reduction in buoyant density to less than 1.2 g/cm3 of the LPS required plasma (or serum) lipid. Delipidation of plasma (or serum) by extraction with n-butanol/diisopropyl ether (40/60, vol:vol) prevented the conversion of the parent LPS to a form with d less than 1.2 g/cm3. Reversal of the effect of delipidation was accomplished by the addition of physiologic concentrations of high density lipoprotein (HDL). In contrast, as much as two times normal serum concentration of low density or very low density lipoprotein were ineffective. The ability of normal plasma (or serum) to inhibit the pyrogenic activity of LPS, lost after delipidation, was also restored after the addition of HDL. Preliminary results suggested that prior modifications of the LPS, probably disaggregation, may be required before interaction with HDL.

摘要

向血浆(或血清)中添加来自大肠杆菌0111:B4或明尼苏达沙门氏菌R595的细菌脂多糖(LPS),导致母体LPS(0111:B4 [d = 1.44 g/cm³]和R595 [d = 1.38 g/cm³])的水合浮力密度显著降低,降至d小于1.2 g/cm³。LPS的浮力密度降至小于1.2 g/cm³需要血浆(或血清)脂质。用正丁醇/二异丙醚(40/60,体积比)萃取使血浆(或血清)脱脂,可防止母体LPS转化为d小于1.2 g/cm³的形式。添加生理浓度的高密度脂蛋白(HDL)可逆转脱脂的效果。相比之下,低密度或极低密度脂蛋白的浓度高达正常血清浓度的两倍也无效。正常血浆(或血清)抑制LPS热原活性的能力在脱脂后丧失,添加HDL后也得以恢复。初步结果表明,在与HDL相互作用之前,可能需要对LPS进行预先修饰,可能是解聚。

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