Kato H, Inoue M, Yamamura Y, Tanigawa M, Sano H, Sugino S, Kondo M
First Department of Internal Medicine, Kyoto Prefectural University of Medicine, Japan.
Nat Immun Cell Growth Regul. 1989;8(5):290-300.
When the streptococcal preparation OK-432 was intraperitoneally injected for the treatment of carcinomatous peritonitis, antitumor polymorphonuclear leukocytes (PMNs) accumulated in the peritoneal cavity. We examined the mechanism of this PMN accumulation using an in vivo system in rats. FUT-175, EDTA and K76 inhibited C5a generation by OK-432 in vitro, but EGTA, prednisolone and inhibitors of arachidonic acid cascade did not. In in vivo experiments, EDTA, FUT-175, antirat C3 serum and K76 reduced the accumulation of PMNs onto filter membranes, when these reagents were reacted with OK-432 for 3 h through filter membranes placed on the turned rat peritoneum. EGTA failed to inhibit PMN accumulation. Prednisolone, indomethacin, OKY046 and AA861 inhibited PMN accumulation in a dose-dependent manner. These inhibitions of PMN accumulation were confirmed by histological examination. It was concluded that complement-derived chemotactic factor C5a generated by OK-432 induced PMN accumulation in association with chemotactic arachidonic acid metabolites.
当将链球菌制剂OK-432腹腔注射用于治疗癌性腹膜炎时，抗肿瘤多形核白细胞（PMN）会在腹腔内积聚。我们使用大鼠体内系统研究了这种PMN积聚的机制。FUT-175、EDTA和K76在体外可抑制OK-432产生C5a，但EGTA、泼尼松龙和花生四烯酸级联反应抑制剂则不能。在体内实验中，当将EDTA、FUT-175、抗大鼠C3血清和K76通过置于翻转大鼠腹膜上的滤膜与OK-432反应3小时后，它们可减少PMN在滤膜上的积聚。EGTA未能抑制PMN积聚。泼尼松龙、吲哚美辛、OKY046和AA861以剂量依赖方式抑制PMN积聚。通过组织学检查证实了这些对PMN积聚的抑制作用。得出的结论是，OK-432产生的补体衍生趋化因子C5a与趋化性花生四烯酸代谢产物相关，诱导了PMN积聚。
