Triglyceride-rich lipoproteins as agents of innate immunity
Triglyceride-rich lipoproteins as agents of innate immunity
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DOI：
10.1086/432005
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发表时间：
2005-11-15
影响因子：
11.8
通讯作者：
Harris, HW
中科院分区：
文献类型：
--
作者：
Barcia, AM;Harris, HW
细菌内毒素（即，脂多糖[LPS]）在宿主中引起显著的反应，包括由于肝脏合成和分泌富含脂多糖的脂蛋白增加以及抑制脂蛋白脂肪酶而导致的血浆脂质水平升高。这种由精氨酸诱导的高脂蛋白血症，临床上称为“脓毒症脂血症”，通常认为涉及脂质储存的动员，以刺激宿主对感染的反应。然而，由于脂蛋白也可以结合和中和LPS，我们长期以来一直假设富含脂蛋白的脂蛋白（极低密度脂蛋白和乳糜微粒）也是先天性非适应性宿主感染免疫反应的组成部分。最近的研究表明脂蛋白结合LPS的能力，保护免受LPS诱导的毒性，并调节宿主对这种细菌毒素的整体反应。
Bacterial endotoxin ( i.e., lipopolysaccharide [LPS]) elicits dramatic responses in the host, including elevated plasma lipid levels due to increased synthesis and secretion of triglyceride-rich lipoproteins by the liver and inhibition of lipoprotein lipase. This cytokine-induced hyperlipoproteinemia, clinically termed the "lipemia of sepsis," was customarily thought to involve the mobilization of lipid stores to fuel the host response to infection. However, because lipoproteins can also bind and neutralize LPS, we have long postulated that triglyceride-rich lipoproteins ( very-low-density lipoproteins and chylomicrons) are also components of an innate, nonadaptive host immune response to infection. Recent research demonstrates the capacity of lipoproteins to bind LPS, protect against LPS-induced toxicity, and modulate the overall host response to this bacterial toxin.