Nakato H, Shinomiya K, Mikawa H
Scand J Haematol. 1986 Jul;37(1):18-24. doi: 10.1111/j.1600-0609.1986.tb01766.x.
The role of complement in the pathogenesis of marked thrombocytopenia induced in rats by Erysipelothrix rhusiopathiae (E. rhusiopathiae) was examined. In cobra venom factor (CoF)-treated rats thrombocytopenia was not induced by the bacterium. The content of 5-hydroxytryptamine (5-HT) in platelets was decreased significantly after inoculation only in untreated rats. E. rhusiopathiae could bind C3 and generate platelet-bacteria aggregation when incubated in the plasma diluted with veronal-buffered saline containing calcium and magnesium (VBS++) or gelatin-VBS containing magnesium and ethyleneglycol tetra-acetic acid (GVB-Mg-EGTA), but not when incubated in GVB-ethylenediamine tetra-acetic acid (GVB-EDTA) diluted plasma or in CoF-treated or anti rat C3-treated plasma. When platelets were preincubated with activated zymosan, no bacteria could bind to platelets. From the results, we speculate that the alternative complement pathway, activated by E. rhusiopathiae, appears to mediate the formation of platelet-bacterial aggregations that may accelerate the removal of platelets from circulating blood.
研究了补体在猪丹毒杆菌（Erysipelothrix rhusiopathiae，E. rhusiopathiae）诱导大鼠显著血小板减少症发病机制中的作用。在经眼镜蛇毒因子（CoF）处理的大鼠中，该细菌未诱导血小板减少症。仅在未处理的大鼠接种后，血小板中5-羟色胺（5-HT）的含量显著降低。当猪丹毒杆菌在含有钙和镁的巴比妥缓冲盐水（VBS++）或含有镁和乙二醇四乙酸的明胶-VBS（GVB-Mg-EGTA）稀释的血浆中孵育时，它可以结合C3并产生血小板-细菌聚集，但在GVB-乙二胺四乙酸（GVB-EDTA）稀释的血浆或经CoF处理或抗大鼠C3处理的血浆中孵育时则不会。当血小板与活化的酵母聚糖预孵育时，没有细菌能与血小板结合。从结果推测，由猪丹毒杆菌激活的替代补体途径似乎介导了血小板-细菌聚集的形成，这可能加速血小板从循环血液中的清除。
