Newborg M F, North R J
Infect Immun. 1979 Jun;24(3):667-72. doi: 10.1128/iai.24.3.667-672.1979.
Intravenous injection of bacterial endotoxin into mice at any time during ongoing infection with Listeria monocytogenes resulted in a markedly increased multiplication of this organism in the liver and spleen. Experiments designed to investigate the basis of this infection-enhancing effect revealed that endotoxin was also capable of inhibiting the expression of adoptive T-cell-mediated anti-Listeria immunity if given to normal recipient mice up to 48 h before they were infused with protective T-cells. On the other hand, endotoxin had only a marginal effect on the expression of adoptive immunity if given to donor mice before their spleen cells were harvested for adoptive transfer. Taken together, these results indicate that endotoxin probably interferes with the antibacterial function of macrophages rather than with mediator lymphocytes. The additional finding that the infection-enhancing action of endotoxin could be greatly reduced by making mice "tolerant" to endotoxin suggests that the acquisition of tolerance to this effect of endotoxin may be an important adaptive mechanism in acquired resistance to infection with gram-negative bacteria.
在小鼠感染单核细胞增生李斯特菌的任何阶段,静脉注射细菌内毒素都会导致该菌在肝脏和脾脏中的繁殖显著增加。旨在探究这种感染增强效应机制的实验表明,如果在正常受体小鼠注入保护性T细胞前48小时内给予内毒素,它也能够抑制过继性T细胞介导的抗李斯特菌免疫的表达。另一方面,如果在内毒素供体小鼠的脾细胞被采集用于过继性转移之前给予内毒素,内毒素对过继性免疫的表达仅有轻微影响。综合来看,这些结果表明内毒素可能干扰巨噬细胞的抗菌功能,而非介导淋巴细胞。另外一项发现是,通过使小鼠对内毒素“耐受”,内毒素的感染增强作用可大幅降低,这表明对内毒素这种效应产生耐受性可能是获得性抗革兰氏阴性菌感染的重要适应性机制。