de Azavedo J C, Hartigan P J, de Saxe M, Arbuthnott J P
Prog Clin Biol Res. 1985;189:419-32.
Strains of Staphylococcus aureus isolated from toxic shock syndrome (TSS) produce toxic shock syndrome toxin 1 (TSST1) which causes a shock-like illness in rabbits with many features similar to TSS in humans. TSST1 is lethal per se in rabbits and also acts synergistically with endotoxin to potentiate lethality. The mode of action of TSST1 is as yet unknown; it has been suggested that it may act by inhibiting the reticuloendothelial system thus allowing endotoxic shock to occur. Rabbits pretreated with polymyxin-B, which prevents the effect of endotoxin, were found to be protected from death by TSST1 indicating that endotoxin is indeed implicated in the pathogenesis of TSS. Specific pathogen-free rabbits which presumably have negligible levels of circulating LPS were susceptible to TSST1 suggesting that very small amounts of endotoxin are sufficient to potentiate lethality. The ways in which TSST1 may allow shock to occur is discussed.
从中毒性休克综合征（TSS）中分离出的金黄色葡萄球菌菌株会产生中毒性休克综合征毒素1（TSST1），该毒素会在兔子身上引发类似休克的疾病，其许多特征与人类的TSS相似。TSST1本身对兔子具有致死性，并且还与内毒素协同作用以增强致死性。TSST1的作用方式尚不清楚；有人提出它可能通过抑制网状内皮系统起作用，从而导致内毒素休克的发生。发现用多粘菌素B预处理过的兔子可免受TSST1致死，多粘菌素B可防止内毒素的作用，这表明内毒素确实与TSS的发病机制有关。推测循环LPS水平可忽略不计的无特定病原体兔子对TSST1敏感，这表明极少量的内毒素就足以增强致死性。本文讨论了TSST1可能导致休克发生的方式。
