Influence of serum-derived chemotactic factors and bacterial products on human neutrophil chemotaxis
Influence of serum-derived chemotactic factors and bacterial products on human neutrophil chemotaxis
复制标题
血清来源的趋化因子和细菌产物对人中性粒细胞趋化性的影响
作者：
A. Issekutz;W. Biggar
中性粒细胞的趋化性已被证明受到血清因子、组织因子、细菌产物和许多其他物质的调节。在体内，这些因素可能相互作用来改变中性粒细胞的运动。我们研究了聚集的丙种球蛋白激活血清（AS）、细菌因子和内毒素单独或联合使用对人中性粒细胞趋化性的影响。中性粒细胞暴露于 AS 会导致 AS 失活，但不会导致大肠杆菌或表皮葡萄球菌培养滤液失活。中性粒细胞暴露于表皮葡萄球菌或大肠杆菌 CF 或大肠杆菌内毒素会导致 AS 或 C5a 失活，但不会导致大肠杆菌或表皮葡萄球菌培养滤液失活。与单独的 AS 相比，向 AS 或 C5a 添加内毒素导致未处理的中性粒细胞对该组合的趋化性受到抑制。这些结果表明，当血清或细菌趋化因子启动人中性粒细胞趋化性时，可能涉及不同的机制。此外，内毒素对 AS 趋化性的有效但特异性的抑制作用可能具有临床意义。
The chemotaxis of neutrophils has been shown to be modulated by serum factors, tissue factors, bacterial products, and a host of other substances. In vivo, these factors may act in concert with each other to modify neutrophil movement. We examined the effect of aggregated gamma globulin-activated serum (AS), bacterial factors, and endotoxin either alone or in combination with each other, on human neutrophil chemotaxis. Exposure of neutrophils to AS resulted in deactivation to AS but not to Escherichial coli or Staphylococcus epidermis culture filtrate. Exposure of neutrophils to S. epidermis or E. coli CF or E. coli endotoxin resulted in deactivation to AS or C5a but not to E. coli or S. epidermis culture filtrate. Addition of endotoxin to AS or C5a resulted in inhibition of chemotaxis by untreated neutrophils toward this combination as compared with AS alone. These results suggest that separate mechanisms may be involved when serum or bacterial chemotactic factors initiate human neutrophil chemotaxis. Furthermore, the potent but specific inhibitory effect of endotoxin on chemotaxis toward AS may be of clinical significance.