Barrett T J, Potter M E, Wachsmuth I K
Division of Bacterial Diseases, Centers for Disease Control, Atlanta, Georgia 30333.
Infect Immun. 1989 Nov;57(11):3434-7. doi: 10.1128/iai.57.11.3434-3437.1989.
The ability of bacterial lipopolysaccharide (LPS) to enhance the toxicity of Shiga-like toxin II (SLT-II) was investigated in rabbits and mice. Rabbits were continuously infused with 0.5 50% lethal dose (LD50) of SLT-II per day. Rabbits that received a 30-micrograms/kg dose of LPS (0.02 LD50) on day 3 of infusion were significantly more likely to die than were rabbits receiving SLT-II only. Rabbits receiving SLT-II and a lower dose of LPS (3 micrograms/kg) did not die but lost an average 3.3% +/- 1.0% of initial body weight during the first 5 days of infusion, compared with weight gains of 4.2% +/- 0.6% and 17.1% +/- 0.9% for rabbits receiving only SLT-II or LPS, respectively. Rabbits that were pretreated with LPS 20 h before challenge with a single dose of SLT-II showed highly significant protection from both the diarrheagenic and lethal effects of SLT-II. Pretreatment of endotoxin-responsive C3H/HeN mice protected the animals from challenge with an LD50 but not an LD100 of SLT-II. LPS enhanced the lethal toxicity of SLT-II for C3H/HeN mice when it was given at 8 or 24 h but not 0 or 72 h after SLT-II challenge. LPS did not affect the lethal toxicity of SLT-II for endotoxin-resistant C3H/HeJ mice. These results suggest that LPS enhances the effects of SLT-II in vivo. Since cecal changes that increase mucosal permeability occur in response to SLT in rabbits, this synergy may be directly relevant to disease processes.
研究了细菌脂多糖（LPS）增强志贺样毒素II（SLT-II）毒性的能力，实验对象为兔子和小鼠。兔子每天持续输注0.5倍50%致死剂量（LD50）的SLT-II。在输注第3天接受30微克/千克剂量LPS（0.02 LD50）的兔子比仅接受SLT-II的兔子死亡可能性显著更高。接受SLT-II和较低剂量LPS（3微克/千克）的兔子没有死亡，但在输注的前5天平均体重下降了3.3%±1.0%，而仅接受SLT-II或LPS的兔子体重分别增加了4.2%±0.6%和17.1%±0.9%。在用单剂量SLT-II攻击前20小时用LPS预处理的兔子对SLT-II的致腹泻和致死作用均表现出高度显著的保护作用。对内毒素反应性C3H/HeN小鼠进行内毒素预处理可保护动物免受LD50剂量SLT-II的攻击，但不能抵御LD100剂量的攻击。当在SLT-II攻击后8或24小时给予LPS时，LPS增强了SLT-II对C3H/HeN小鼠的致死毒性，但在攻击后0或72小时给予则无此作用。LPS对耐内毒素的C3H/HeJ小鼠的SLT-II致死毒性没有影响。这些结果表明LPS在体内增强了SLT-II的作用。由于兔子体内因SLT而发生的盲肠变化会增加黏膜通透性，这种协同作用可能与疾病进程直接相关。
