Plasma lipoproteins promote the release of bacterial lipopolysaccharide from the monocyte cell surface
Plasma lipoproteins promote the release of bacterial lipopolysaccharide from the monocyte cell surface
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DOI：
10.1074/jbc.274.48.34116
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发表时间：
1999-11-26
影响因子：
4.8
通讯作者：
Munford, RS
中科院分区：
文献类型：
--
作者：
Kitchens, RL;Wolfbauer, G;Munford, RS
当细菌脂多糖（LPS）进入血液时，它被认为有两种一般的命运。如果LPS与循环中的白细胞结合，它会触发宿主固有的防御机制，并经常引发毒性反应。如果LPS与血浆脂蛋白结合，则其生物活性在很大程度上被中和。当单核细胞负载[H-3]LPS并在血浆中孵育时，它们将超过70%的细胞结合的[H-3]LPS释放为脂蛋白（主要是高密度脂蛋白），而在无血清培养基中，[H-3]LPS仍然与细胞紧密结合。在纯天然脂蛋白或重组高密度脂蛋白存在下，转移反应可再现。血浆免疫耗竭实验和使用重组LPS转移蛋白的实验显示可溶性CD 14显著增强LPS从细胞的释放，高浓度的EPS结合蛋白具有适度的作用，并且磷脂转移蛋白不能促进LPS的释放，基本上单核细胞表面上的所有LPS都可以被释放。脂蛋白介导的LPS释放伴随着几种细胞对LPS的反应减少，表明LPS从白细胞进入脂蛋白的运动可能会减弱宿主对LPS的体内反应。
When bacterial lipopolysaccharide (LPS) enters the bloodstream, it is thought to have two general fates. If LPS binds to circulating leukocytes, it triggers innate host defense mechanisms and often elicits toxic reactions. If instead LPS binds to plasma lipoproteins, its bioactivity is largely neutralized. This study shows that lipoproteins can also take up LPS that has first bound to leukocytes, When monocytes were loaded with [H-3]LPS and then incubated in plasma, they released over 70% of the cell-associated [H-3]LPS into lipoproteins (predominantly high density lipoprotein), whereas in serum-free medium the [H-3]LPS remained tightly associated with the cells. The transfer reaction could be reproduced in the presence of pure native lipoproteins or reconstituted high density lipoprotein. Plasma immunodepletion experiments and experiments using recombinant LPS transfer proteins revealed that soluble CD14 significantly enhances LPS release from the cells, high concentrations of EPS-binding protein have a modest effect, and phospholipid transfer protein is unable to facilitate LPS release, Essentially all of the LPS on the monocyte cell surface can be released. Lipoprotein-mediated LPS release was accompanied by a reduction in several cellular responses to the LPS, suggesting that the movement of LPS from leukocytes into lipoproteins may attenuate host responses to LPS in vivo.