Schlievert P M, Bettin K M, Watson D W
Infect Immun. 1980 Feb;27(2):542-8. doi: 10.1128/iai.27.2.542-548.1980.
Group A streptococcal pyrogenic exotoxins (SPEs) A, B, and C and alpha-amanitin enhance host susceptibility to lethal endotoxin shock. The capacity of SPE C and alpha-amanitin to prepare rabbits for the enhancement phenomenon required pretreatment of the animals 1 to 2 h before giving endotoxin. Endotoxin clearance from the circulation of rabbits pretreated with either SPE C or alpha-amanitin was reduced. Even at the time of death, significant amounts of endotoxin remained in the circulation. It is proposed that the SPE and alpha-amanitin inhibit ribonucleic acid synthesis in Kupffer cells with concomitant alteration in reticuloendothelial clearnace function, allowing endotoxin to persist in the circulation and produce host injury. All three SPE types and alpha-amanitin inhibited ribonucleic acid synthesis by 50% or greater in whole liver cells. Kupffer cells, liver cell nuclei, and liver nuclear extracts; inhibition was observed liver cells from both mice and rabbits. The inhibitory effect by SPEs was dose dependent and was observed after as little as 15 min of preincubation with liver cells. The content of ribonucleic acid in liver nuclei of mice pretreated with either SPE C or alpha-amanitan was reduced, whereas total deoxyribonucleic acid and protein content remained unaltered.
A组链球菌致热外毒素(SPEs)A、B和C以及α-鹅膏蕈碱可增强宿主对内毒素致死性休克的易感性。SPE C和α-鹅膏蕈碱使家兔出现这种增强现象的能力,要求在给予内毒素前1至2小时对动物进行预处理。用SPE C或α-鹅膏蕈碱预处理的家兔循环中内毒素清除率降低。甚至在死亡时,循环中仍有大量内毒素残留。有人提出,SPE和α-鹅膏蕈碱抑制库普弗细胞中的核糖核酸合成,同时网状内皮系统清除功能发生改变,使内毒素持续存在于循环中并导致宿主损伤。所有三种类型的SPE和α-鹅膏蕈碱在全肝细胞中均能抑制核糖核酸合成达50%或更高。在库普弗细胞、肝细胞核和肝核提取物中;在小鼠和家兔的肝细胞中均观察到抑制作用。SPE的抑制作用呈剂量依赖性,与肝细胞预孵育仅15分钟后即可观察到。用SPE C或α-鹅膏蕈碱预处理的小鼠肝细胞核中核糖核酸含量降低,而总脱氧核糖核酸和蛋白质含量保持不变。