Toll样受体抗体抑制脂多糖激活巨噬细胞的吞噬活性

The Inhibition on Phagocytosis of Lipopolysaccharide-stimulated Macrophages by Polyclone Antibody of TLR2

应用脂多糖 (LPS)激活巨噬细胞后其吞噬能力大大增强 ,以此为模型发现TLR2的多抗能部分抑制LPS激活巨噬细胞吞噬金葡萄球菌的能力 ,也能部分阻断对U937细胞的吞噬活性 .TRAIL或TNFα多克隆抗体同样能起到类似作用 .实验还发现低浓度血清培养亦在一定程度上抑制LPS激活巨噬细胞的吞噬作用 .结果证实TLR2能介导LPS的功能 ,而某些血清因子参与了介导LPS的信号转导过程 。

The phagocytosis to Staphylococcus aureus (SA) and cultivated U937 cells by macrophages derived from PBMC was enhanced significantly under lipopolysaccharide(LPS) stimulation. The present experiment showed that the application polyclone antibodies to TLR2 suppressed partly the phagocytosis of macrophages in this model. The LPS enhanced phagocytosis could be further blocked partly by polyclone antibodies to TRAIL or TNFα. Cells cultivated in a lower serum concentration(1%) was also shown to be a decreased phagocytosis. The results confirmed that TLR2 was a LPS receptor which mediated its signal transduction, while some serum factors participated in the binding of LPS to its membrane receptors. It further suggested that LPS induced effectors such as TRAIL and TNFα might be the key mediators involved in the mechanisms of LPS enhanced phagocytosis.