Acute inflammation and infection maintain circulating phospholipid levels and enhance lipopolysaccharide binding to plasma lipoproteins
Acute inflammation and infection maintain circulating phospholipid levels and enhance lipopolysaccharide binding to plasma lipoproteins
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DOI：
10.1194/jlr.m300228-jlr200
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发表时间：
2003-12-01
影响因子：
6.5
通讯作者：
O'Keefe, GE
中科院分区：
文献类型：
--
作者：
Kitchens, RL;Thompson, PA;O'Keefe, GE
循环脂蛋白被认为通过将脂多糖（LPS）的生物活性脂质A部分结合到脂蛋白表面而在LPS的解毒中起重要作用。据推测，低胆固醇血症通过损害LPS中和而导致危重病期间的炎症。我们测试了危重病是否损害LPS与脂蛋白的结合，并发现，相反，LPS结合增强，LPS与脂蛋白类的结合与其磷脂含量相关。而低血清胆固醇几乎完全是由于酯化胆固醇（脂蛋白核心成分）的损失，磷脂（主要脂蛋白表面脂质）维持在接近正常水平，并增加在败血症患者的高脂血症子集。发现在LDL和VLDL组分中的磷脂水平与HDL组分中的磷脂水平成反比，并且当HDL水平低时，LPS主要与LDL和VLDL组分中的脂蛋白结合。从脓毒症患者血清中分离的脂蛋白中和了与之结合的LPS的生物活性。我们的研究结果表明，宿主对急性炎症和感染的反应倾向于维持脂蛋白磷脂水平，并且尽管低胆固醇血症和HDL水平降低，循环脂蛋白仍保持其结合和中和重要细菌激动剂LPS的能力。克特河L.，P. A.汤普森河，巴西-地S. Munford和G. E.奥基夫急性炎症和感染维持循环磷脂水平并增强脂多糖与血浆脂蛋白的结合。
Circulating lipoproteins are thought to play an important role in the detoxification of lipopolysaccharide (LPS) by binding the bioactive lipid A portion of LPS to the lipoprotein surface. It has been assumed that hypocholesterolemia contributes to inflammation during critical illness by impairing LPS neutralization. We tested whether critical illness impaired LPS binding to lipoproteins and found, to the contrary, that LPS binding was enhanced and that LPS binding to the lipoprotein classes correlated with their phospholipid content. Whereas low serum cholesterol was almost entirely due to the loss of esterified cholesterol (a lipoprotein core component), phospholipids (the major lipoprotein surface lipid) were maintained at near normal levels and were increased in a hypertriglyceridemic subset of septic patients. The levels of phospholipids found in the LDL and VLDL fractions varied inversely with those in the HDL fraction, and LPS bound predominantly to lipoproteins in the LDL and VLDL fractions when HDL levels were low. Lipoproteins isolated from the serum of septic patients neutralized the bioactivity of the LPS that had bound to them. Our results show that the host response to acute inflammation and infection tends to maintain lipoprotein phospholipid levels and that, despite hypocholesterolemia and reduced HDL levels, circulating lipoproteins maintain their ability to bind and neutralize an important bacterial agonist, LPS.-Ktchens, R. L., P. A. Thompson, R. S. Munford, and G. E. O'Keefe. Acute inflammation and infection maintain circulating phospholipid levels and enhance lipopolysaccharide binding to plasma lipoproteins.