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首页> 外文期刊>Journal of endotoxin research >Apolipoproteins modulate the inflammatory response to lipopolysaccharide.
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Apolipoproteins modulate the inflammatory response to lipopolysaccharide.

机译：载脂蛋白调节对脂多糖的炎症反应。

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摘要

An increasing body of evidence demonstrates a close interplay between lipoprotein metabolism and sepsis. Sepsis results in an increase of plasma triglycerides within VLDL as a consequence of an enhanced hepatic VLDL production and/or inhibited peripheral and hepatic VLDL clearance. In contrast, sepsis decreases plasma cholesterol within LDL and mainly HDL. The decrease in HDL is accompanied by a loss of mainly apoAI-containing particles, an almost total loss of apoCI, and an increase in apoE-containing HDL, as related to the effect of LPS on a wide range of apolipoproteins, plasma enzymes, lipid transfer factors, and receptors that are involved in HDL metabolism. Reciprocally, all lipoprotein classes have been shown to bind LPS and to attenuate the biological response to LPS in vitro and in rodents. Moreover, triglyceride-rich lipoproteins protect rodents against death from LPS and bacterial sepsis. Accumulating evidence indicates that apolipoproteins such as apoE and apoAI, and not the lipid moieties of the particles, may be responsible for these protective effects of lipoproteins. Therefore, to increase our understanding of the complex interaction between lipoprotein metabolism and sepsis, further studies that address the specific roles of apolipoproteins in sepsis are warranted.
机译：越来越多的证据表明脂蛋白代谢和败血症之间存在密切的相互作用。脓毒症由于增强的肝VLDL产生和/或抑制的外周和肝VLDL清除而导致VLDL中的血浆甘油三酯增加。相反，败血症可降低LDL和HDL中的血浆胆固醇。 HDL的降低伴随着主要是含apoAI的颗粒的损失，apoCI的几乎全部损失以及含apoE的HDL的增加，这与LPS对多种载脂蛋白，血浆酶，脂质的作用有关转移因子和参与HDL代谢的受体。相反，在体外和啮齿动物中，所有脂蛋白类别均已显示与LPS结合并减弱对LPS的生物学反应。此外，富含甘油三酸酯的脂蛋白可保护啮齿动物免受LPS和细菌性败血症的死亡。越来越多的证据表明，载脂蛋白（例如apoE和apoAI）而不是颗粒的脂质部分可能是脂蛋白的这些保护作用的原因。因此，为了增加我们对脂蛋白代谢与脓毒症之间复杂相互作用的理解，有必要进一步研究载脂蛋白在脓毒症中的特殊作用。

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