旁路活化补体降低PMN吞杀绿脓杆菌力的实验研究

为证明论题,本文做了3项实验:(1)人血PMN培养单层加上酵母多糖活化人血清(ZAHS)。PMN的超氧离子(O_2~-)、特殊颗粒(SG)与胞内杀菌力(ICBA)明显平行下降,于6 h最低,0.05 ml的作用最强。(2)经小鼠尾静脉注射0.5ml ZAHS/鼠,6 h后活杀。肺和血内PMN的上述指标均明显降低;肺内病变明显:急性间质炎,灶性水肿出血和萎陷,肺血屏障亚微结构损伤。(3)经抗人C_3、C_5血清(AHC_(3.5)S)体外中和的ZAHS,在体内外实验中均失去其有害作用。提示:ZAHS的有害作用与C_3、C_5碎片有关,在剂量适中且吞菌前作用时间较长的条件下方显极效。有害作用的可能机制:杀菌且能致炎的O_2~-与SG大多已于吞菌前排放在胞外,所以PMN的ICBA下降;累积于组织内的则损害PMN自身及其邻近的肺血屏障。这便于MOF与感染发生。

Experimental study on the loss of PMN's bactericidal capacity induced by bypass-activated complement

In order to verify that bypass-activated complement can enable polymorphonuclear neutrophils (PMN) to lose their bactericidal capacity,3 experiments were performed as follows:(DA monolayer culture of human PMN was added with zymosan-activated human serum (ZAHS).then the superoxide ion (O2-,the specific granules,and the intracellular bactericidal activity of the cultured PMNs were signigicantly decreased and reached the lowest point in the 6th hour after the adding of ZAHS.0.05 ml of ZAHS showed the maximal effects on the PMNs.(2)Mice were injected intravenously with 0.5 ml of ZAHS and were killed 6 hours later.All the 3 parameters mentioned above dropped markedly in the PMNs isolated from the blood and the lungs of the mice.Pathologically,the lungs of the rats showed acute interstitial inflammation,focal edema,hemorrhage and atelectasis.and subcellular damages on the pulmonary blood-barrier.(3)ZAHS,after neutralization in vitro with antiserum against human C3 and C5,lost most of its harmful effects mentioned above.The findings suggest that the harmful effects of ZAHS originate from the fragments of C3 and Cs and they are most effective when its dosage is suitable and there must be a sufficient length of time to react before the phagocytosis of PMNs.The possible mechanism of the origination of the harmful effects of ZAHS is as follows:Before PMNs undertake phagocytosis,they releas the bactericidal and inflamnagenic (O2-and specific granules extra-cellularly.So the intracellular bactericidal activity of PMNs is decreased.The accumulation of PMNs in the pulmonary tissues can damage the PMNs themselves and the adjacent pulmonary blood-barrier,which will leads to the occurrence of infection and multiple organ failure.