Department of Biochemistry and Molecular Biology, "Ernesto Quagliariello", University of Bari, Via Orabona 4, 70126, Bari, Italy.
Inflamm Res. 2011 Apr;60(4):329-35. doi: 10.1007/s00011-010-0272-7. Epub 2010 Nov 2.
To examine the role of lipoprotein(a) [Lp(a)] on the inflammatory response of cells in the nervous system by investigating its effect on lipopolysaccharide (LPS)-induced interleukin-6 (IL-6) secretion.
Human astrocytoma U373 cells were treated with recombinant apolipoprotein(a) [r-apo(a)] A10K (175-11 nM), alone or in combination with LPS (100 and 10 ng/ml). IL-6 levels were evaluated by immunoblotting. Statistical analysis was performed by one-way ANOVA.
r-apo(a) caused dose-dependent inhibition of LPS-induced IL-6 secretion (100 ng/ml LPS, p = 0.0205; 10 ng/ml LPS, p = 0.0005). Pre-treatment of cells with 88 nM r-apo(a), rinsing, and activation with 10 ng/ml LPS did not reverse the inhibition (p = 0.0048), which could be reversed by supplementation with excess serum (5-20%) (p = 0.0454) or recombinant CD14 (2.0-0.05 μg/ml) (p = 0.0230).
Our data indicate that apo(a) plays a natural anti-endotoxin role which relies on its interference with cell-associated and serum components of LPS signaling.
通过研究脂蛋白(a) [Lp(a)] 对脂多糖 (LPS) 诱导的白细胞介素 6 (IL-6) 分泌的影响，研究其在神经系统细胞炎症反应中的作用。
用重组载脂蛋白(a) [r-apo(a)] A10K（175-11 nM）单独或与 LPS（100 和 10 ng/ml）处理人星形细胞瘤 U373 细胞。通过免疫印迹法评估 IL-6 水平。采用单因素方差分析进行统计学分析。
r-apo(a) 导致 LPS 诱导的 IL-6 分泌呈剂量依赖性抑制（100ng/ml LPS，p=0.0205；10ng/ml LPS，p=0.0005）。用 88 nM r-apo(a)预处理细胞，冲洗，并用 10ng/ml LPS 激活，不能逆转抑制（p=0.0048），用过量血清（5-20%）（p=0.0454）或重组 CD14（2.0-0.05μg/ml）（p=0.0230）补充可以逆转。
我们的数据表明，apo(a) 发挥天然抗内毒素作用，依赖于其对细胞相关和 LPS 信号转导中血清成分的干扰。
