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本文引用的文献

1
Bacterial lipopolysaccharide binds and stimulates cytokine-producing cells before neutralization by endogenous lipoproteins can occur.细菌脂多糖在被内源性脂蛋白中和之前就会结合并刺激产生细胞因子的细胞。
Cytokine. 1998 Oct;10(10):766-72. doi: 10.1006/cyto.1998.0364.
2
Antiinflammatory effects of reconstituted high-density lipoprotein during human endotoxemia.重组高密度脂蛋白在人类内毒素血症期间的抗炎作用。
J Exp Med. 1996 Nov 1;184(5):1601-8. doi: 10.1084/jem.184.5.1601.
3
Low-density lipoprotein receptor-deficient mice are protected against lethal endotoxemia and severe gram-negative infections.低密度脂蛋白受体缺陷小鼠对致死性内毒素血症和严重革兰氏阴性菌感染具有抵抗力。
J Clin Invest. 1996 Mar 15;97(6):1366-72. doi: 10.1172/JCI118556.
4
Endurance run increases circulating IL-6 and IL-1ra but downregulates ex vivo TNF-alpha and IL-1 beta production.耐力跑会增加循环中的白细胞介素-6和白细胞介素-1受体拮抗剂，但会下调体外肿瘤坏死因子-α和白细胞介素-1β的产生。
J Appl Physiol (1985). 1995 Nov;79(5):1497-503. doi: 10.1152/jappl.1995.79.5.1497.
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A reconstituted, apolipoprotein A-I containing lipoprotein reduces tumor necrosis factor release and attenuates shock in endotoxemic rabbits.
Circ Shock. 1993 May;40(1):14-23.
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In vivo protection against endotoxin by plasma high density lipoprotein.
Proc Natl Acad Sci U S A. 1993 Dec 15;90(24):12040-4. doi: 10.1073/pnas.90.24.12040.
7
Prevention of endotoxin-induced monokine release by human low- and high-density lipoproteins and by apolipoprotein A-I.人低密度脂蛋白、高密度脂蛋白及载脂蛋白A-I对内毒素诱导的单核因子释放的预防作用
Infect Immun. 1993 Dec;61(12):5140-6. doi: 10.1128/iai.61.12.5140-5146.1993.
8
Hyperlipidemic response to endotoxin--a part of the host-defence mechanism.对内毒素的高脂血症反应——宿主防御机制的一部分。
Scand J Infect Dis. 1993;25(6):675-82. doi: 10.3109/00365549309008562.
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Triglyceride-rich lipoproteins prevent septic death in rats.富含甘油三酯的脂蛋白可预防大鼠败血症死亡。
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10
Role for circulating lipoproteins in protection from endotoxin toxicity.循环脂蛋白在抵御内毒素毒性中的作用。
Infect Immun. 1995 May;63(5):2041-6. doi: 10.1128/iai.63.5.2041-2046.1995.

脂蛋白(a)抑制脂多糖诱导人单核细胞产生肿瘤坏死因子α 。

Lipoprotein(a) inhibits lipopolysaccharide-induced tumor necrosis factor alpha production by human mononuclear cells.

作者信息

Netea M G, de Bont N, Demacker P N, Kullberg B J, Jacobs L E, Verver-Jansen T J, Stalenhoef A F, Van der Meer J W

机构信息

Department of Medicine, University Hospital Nijmegen, The Netherlands.

出版信息

Infect Immun. 1998 May;66(5):2365-7. doi: 10.1128/IAI.66.5.2365-2367.1998.

DOI:10.1128/IAI.66.5.2365-2367.1998
PMID:9573133
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC108207/
Abstract

Lipoproteins can bind lipopolysaccharide (LPS) and decrease LPS-stimulated cytokine production. Lipoprotein(a) [Lp(a)] was as potent as low-density lipoproteins (LDL) in inhibiting LPS-stimulated tumor necrosis factor synthesis by human mononuclear cells. The kinetics of LPS inhibition by Lp(a) was similar to that of LDL. This suggests that circulating Lp(a) may be an important factor determining the amplitude of the response to LPS in humans.

摘要

脂蛋白可以结合脂多糖（LPS）并减少LPS刺激的细胞因子产生。脂蛋白(a) [Lp(a)]在抑制LPS刺激人单核细胞合成肿瘤坏死因子方面与低密度脂蛋白（LDL）同样有效。Lp(a)对LPS的抑制动力学与LDL相似。这表明循环中的Lp(a)可能是决定人类对LPS反应幅度的一个重要因素。