摘要
内毒素 (脂多糖 ,LPS)可引起机体的急剧变化 ,包括肝三酰甘油脂蛋白的合成和分泌增加。人们通常认为 ,这个LPS诱导的高脂血症———脓毒型脂蛋白血症 ,是机体动员贮存的脂肪以供热能的代偿表现 ,是宿主对感染的反应。但脂蛋白也有结合和中和LPS的能力 ,故高脂血症 (高三酰甘油血症 )可能也是宿主先天性免疫反应的一部分。LPS与脂蛋白的结合是内毒素插入磷脂层类脂A的特定位点。这个结合过程受到CD14和脂多糖结合蛋白(LBP)促进。二者一旦结合 ,LPS对效应细胞和组织的作用就会大大减低。与三酰甘油脂蛋白结合的LPS也会很快被肝细胞清除。进入到肝内的脂蛋白 LPS复合物可削弱细胞因子介导的NF κB活性 ,并由此起到抗炎、调节急性炎症反应的作用。为了更好地了解高脂血症在调节宿主对LPS攻击反应中的作用 。
Bacterial endotoxin elicits dramatic responses in the host including elevated plasma lipid levels due to the increased synthesis and secretion of triglyceride (TG) rich lipoproteins by the liver and the inhibition of lipoprotein lipase. This cytokine induced hyperlipoproteinemia, clinically termed the lipemia of sepsis, was customarily thought to represent the mobilization of lipid stores to provide the fuel for the host’s response to infection. However, since lipoproteins can also bind and neutralize LPS, TG rich lipoproteins (VLDL and chylomicrons) are also components of non adaptive host immune response to infection. The studies are reviewed about the capacity of lipoproteins to bind LPS, protect against LPS induced toxicity and modulate the host response to the bacterial toxin.
出处
《肠外与肠内营养》
CAS
2003年第2期114-118,共5页
Parenteral & Enteral Nutrition
