Hamuro J, Röllinghoff M, Wagner H
Immunology. 1980 Apr;39(4):551-9.
Eight distinct polysaccharides (PS) of beta(1 leads to 3) glucan type were tested for their capacity to render murine peritoneal exudate cells (PEC) cytotoxic. After intraperitoneal injection of lentinan, pachymaran and HE-pachyman 3 and 4 highly cytotoxic PEC were induced. Pachyman and HE-pachyman 1 and 2 were of moderate effect, whereas CM-pachymaran and HE-pachyman 3 and 4, highly cytotoxic PEC were induced. Pachyman and HE-pachymacrophages. The induction of PEC-dependent cytotoxicity exhibited a strict dose relationship. Optimal administration of PS resulted in the induction of cytotoxicity, which persisted for more than 25 days. Surprisingly, none of the PS tested was capable of rendering normal or thioglycollate-induced PEC cytoxic under in vitro conditions. It is suggested that the capacity of PS to render in vivo macrophages cytotoxic is related to the potency of these PS to activate the alternative pathway of complement system (APC) in so far as C3b may be the essential component required to render macrophages cytotoxic.
对8种不同的β(1→3)葡聚糖类型的多糖(PS)进行了测试,以评估它们使小鼠腹腔渗出细胞(PEC)产生细胞毒性的能力。腹腔注射香菇多糖、茯苓聚糖和羟乙基茯苓多糖3和4后,诱导出了高细胞毒性的PEC。茯苓聚糖和羟乙基茯苓多糖1和2具有中等效果,而羧甲基茯苓聚糖和羟乙基茯苓多糖3和4诱导出了高细胞毒性的PEC。茯苓聚糖和羟乙基茯苓多糖能诱导巨噬细胞产生细胞毒性。PEC依赖性细胞毒性的诱导呈现出严格的剂量关系。PS的最佳给药导致细胞毒性的诱导,这种毒性持续超过25天。令人惊讶的是,在体外条件下,所测试的PS均不能使正常或经巯基乙酸诱导的PEC产生细胞毒性。有人认为,PS使体内巨噬细胞产生细胞毒性的能力与这些PS激活补体系统替代途径(APC)的能力有关,因为C3b可能是使巨噬细胞产生细胞毒性所需的关键成分。