INHIBITION OF ENDOTOXIN-INDUCED ACTIVATION OF HUMAN-MONOCYTES BY HUMAN LIPOPROTEINS
INHIBITION OF ENDOTOXIN-INDUCED ACTIVATION OF HUMAN-MONOCYTES BY HUMAN LIPOPROTEINS
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DOI：
10.1128/iai.57.7.2237-2245.1989
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发表时间：
1989-07-01
影响因子：
3.1
通讯作者：
NORTHOFF, H
中科院分区：
文献类型：
--
作者：
FLEGEL, WA;WOLPL, A;NORTHOFF, H
内毒素的毒性在很大程度上是由单核/巨噬细胞的激活和随后释放的单因子如白介素1(IL-1)和肿瘤坏死因子α(TNF-α)介导的。众所周知，内毒素很容易与血清脂蛋白结合，而且内毒素-脂蛋白复合体的毒性比未结合的内毒素小。在这里，我们提供了在细胞水平上分析内毒素-血清相互作用的影响的数据。通过检测IL-1、TNF-α和IL-6，可以证明不同的LPS或脂质A与人血清的相互作用可以阻止人单核细胞的激活。正常人血清灭活内毒素的量不超过10 ng/ml，血清灭活内毒素的能力与脂蛋白有关。其他血清成分，如天然产生的抗脂多糖免疫球蛋白G、补体或营养脂质，在我们的系统中没有显著影响。我们的实验表明，血清脂蛋白控制内毒素诱导的单核细胞活化和单核细胞因子的释放。
Toxicity of lipopolysaccharide (LPS) (endotoxin) is, to a large extent, mediated by the activation of monocytes/macrophages and subsequent release of monokines, such as interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-.alpha.). It is known that LPS binds readily to serum lipoproteins and that LPS-lipoprotein complexes are less toxic than unbound LPS. Here we present data analyzing the impact of the LPS-serum interaction at the cellular level. by measuring IL-1 TNF-.alpha., and IL-6, the interaction of different LPSs or lipid A with human serum could be shown to prevent the activation of human monocytes. The amounts of LPS inactivated by normal human serum did not exceed 10 ng/ml. The LPS-inactivating capacity of serum was shown to be a function of the lipoproteins. Other serum components, such as naturally occurring anti-LPS immunoglobulin G, complement, or nutritive lipids, had no significant influence in our system. Our experiments suggest that serum lipoproteins control endotoxin-induced monocyte activation and monokine release.