旁路活化补体降低宿主抗感染条件与机制的实验研究

目的 为证明旁路活化补体降低蚕噬细胞功能,了解宿主抗感染能力下降的条件与机制方法 分离人中性粒细胞和大鼠枯否细胞;ＰＭＮ和ＫＣ培养单层加上酵母多糖活化人血清;观测蚕噬细胞胞内杀菌力,超氧阴离子,酸性磷酸酶指标动态水平;以抗人Ｃ３Ｃ５血清中和阻断ＺＡＨＳ进行反证。

Condition and mechanism of host antiinfect capacity induced by bypass-activated complement: experimental study

OBJECTIVE: To verify host antiinfect capacity induced by bypass-activated complement. METHODS: A monolayer culture of human PMNs and rats kupffer cells (KCs) were added with zymosan-activated human serum (ZAHS) and 3 parameters were measured. ZAHS had been neutralized in tube with antiserum against human C3 and C5. RESULTS: In 0.07-0.09 ml ZAHS and 1-3 h, intracellular bactericidal activity (ICBA) showed a peak but significant top value at 2nd hour. The value dropped markedly with time and significantly in 4-6 h. Superoxide ions (O2-) dynamics was similar to ICBA. Acid phosphatase (ACP) curve distinguished from the former's with monotonous decrease (1-6 h) and more deep. With 0.11 ml ZAHS after 4 h, about 80% of KCs were fallen off. Three parameters of PMNs were decreased and reached the lowest point in the 6th hour after the adding 0.05-0.09 ml of ZAHS. After blocking test with antihuman C3 and C5 serum, the values of ICBA, O2- and ACP surpassed those in the experimental group. CONCLUSION: The possible mechanism of the origination of the harmful effects of ZAHS is suggested. Before KCs and PMNs undertake phagocytosis, they release the bactericidal and inflamagenic (O2- and ACP) so the intracellular bactericidal activity of KCs and PMNs are decreased. The accumulation of KCs and PMNs in tissues can damage themselves and the adjacent tissues barrier, which will lead to the occurrence of infection.