Barcia Anthony M, Harris Hobart W
Department of Surgery, University of California, San Francisco, CA 94143-0104, USA.
Clin Infect Dis. 2005 Nov 15;41 Suppl 7:S498-503. doi: 10.1086/432005.
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.
细菌内毒素（即脂多糖[LPS]）可在宿主体内引发剧烈反应，包括由于肝脏合成和分泌富含甘油三酯的脂蛋白增加以及脂蛋白脂肪酶受到抑制而导致血浆脂质水平升高。这种细胞因子诱导的高脂蛋白血症，临床上称为“败血症性脂血症”，传统上被认为涉及脂质储存的动员，以为宿主对感染的反应提供能量。然而，由于脂蛋白也可以结合并中和LPS，我们长期以来一直推测富含甘油三酯的脂蛋白（极低密度脂蛋白和乳糜微粒）也是宿主对感染的先天性、非适应性免疫反应的组成部分。最近的研究表明脂蛋白具有结合LPS、预防LPS诱导的毒性以及调节宿主对这种细菌毒素的整体反应的能力。
