Bambirra E A, da Cruz M Q, Campos D S, Lima A O
Mem Inst Oswaldo Cruz. 1984 Oct-Dec;79(4):433-7. doi: 10.1590/s0074-02761984000400006.
Mice infected with T. cruzi, Y strain, acquire a high level of susceptibility to the effects of bacterial gram-negative LPS. The LD50 of adult female SW mice to LPS from S. typhosa, decreases from 450 to 2,5 mcg 10-12 days after T. cruzi infection. This hyperreactivity to LPS induced by T. cruzi presents all the characteristics of that found in infection caused by many other agents. During the acute phase of experimental infection with T. cruzi Y strain, mice generally die with a hypovolemic shock very similar to that induced in uninfected animals injected with an adequate dose of bacterial endotoxin. There is evidence for and against the hypothesis that LPS absorbed from the intestinal tract may be involved in the mechanism of death of mice during the acute phase of T. cruzi infection.
感染克氏锥虫Y株的小鼠对革兰氏阴性菌脂多糖(LPS)的作用高度敏感。成年雌性SW小鼠对伤寒沙门氏菌LPS的半数致死剂量(LD50)在感染克氏锥虫后10 - 12天从450微克降至2.5微克。克氏锥虫诱导的对LPS的这种高反应性具有许多其他病原体感染所发现的所有特征。在用克氏锥虫Y株进行实验性感染的急性期,小鼠通常死于低血容量性休克,这与注射适当剂量细菌内毒素的未感染动物所诱导的休克非常相似。关于在克氏锥虫感染急性期肠道吸收的LPS可能参与小鼠死亡机制的假说,有支持和反对的证据。