Aepfelbacher M, Ziegler-Heitbrock H W, Lux I, Weber P C
Institut für Prophylaxe und Epidemiologie, Kreislaufkrankheiten, München, Germany.
J Immunol. 1992 Apr 1;148(7):2186-93.
When human monocytic Mono Mac 6 cells were treated with bacterial LPS (10 ng/ml, 72 h), they showed an increase in phagocytic activity, superoxide anion production, and expression of monocyte/macrophage-associated cell surface Ag. In these more mature (LPS-treated) cells but not in untreated cells, platelet-activating factor (PAF) (100 nM) produced a three- to fourfold increase in cytosolic free Ca2+ concentration. The cytosolic free Ca2+ concentration increase was inhibited by the PAF receptor antagonist L-659,989 (10 microM) and by EGTA (2 mM), indicating receptor-dependent Ca2+ influx. Furthermore, L-659,989 (10 microM), as well as PAF (1 microM), inhibited specific [3H]PAF binding in LPS-treated but not in untreated cells. Consistent with these results, PAF (100 nM) stimulated release of arachidonic acid and thromboxane B2 only in LPS-treated cells, and this could be inhibited by L-659,989 (10 microM) and EGTA (2 mM). Our data indicate that LPS up-regulates PAF-induced Ca2+ influx, resulting in arachidonic acid and eicosanoid release in Mono Mac 6 cells.
当人单核细胞系Mono Mac 6细胞用细菌脂多糖（10 ng/ml，72小时）处理时，它们的吞噬活性、超氧阴离子产生以及单核细胞/巨噬细胞相关细胞表面抗原的表达均增加。在这些更成熟的（经脂多糖处理的）细胞中，而非未处理的细胞中，血小板活化因子（PAF）（100 nM）使胞质游离Ca2+浓度增加了三到四倍。胞质游离Ca2+浓度的增加被PAF受体拮抗剂L-659,989（10 microM）和EGTA（2 mM）抑制，表明是受体依赖性的Ca2+内流。此外，L-659,989（10 microM）以及PAF（1 microM）抑制了经脂多糖处理的细胞而非未处理细胞中的特异性[3H]PAF结合。与这些结果一致，PAF（100 nM）仅在经脂多糖处理的细胞中刺激花生四烯酸和血栓素B2的释放，并且这可被L-659,989（10 microM）和EGTA（2 mM）抑制。我们的数据表明，脂多糖上调PAF诱导的Ca2+内流，导致Mono Mac 6细胞中花生四烯酸和类二十烷酸的释放。
