Blanden R V, Mackaness G B, Collins F M
J Exp Med. 1966 Oct 1;124(4):585-600. doi: 10.1084/jem.124.4.585.
Experiments in vitro comparing normal mouse peritoneal macrophages with cells from Salmonella typhimurium-infected mice have shown that the "immune" macrophages have conspicuously enhanced microbicidal properties. Whereas normal macrophages could inactivate only 50 to 60% of intracellular S. typhimurium pretreated with immune serum, cells from infected animals killed virtually all ingested organisms and did so at an accelerated rate. Macrophages from Listeria monocytogenes-infected mice were shown to possess similarly enhanced microbicidal activity against S. typhimurium. Furthermore, the growth of S. typhimurium in the liver and spleen was more effectively restricted in Listeria-infected mice than in animals vaccinated with heat-killed S. typhimurium, even though the Listeria-infected animals possessed no demonstrable cross-reacting antibody to S. typhimurium. The lack of resistance in the mice vaccinated with heat-killed organisms could not be attributed to any deficiency of humoral factors, since the serum from these animals was as effective at promoting phagocytosis and killing by macrophages as serum from actively infected (and demonstrably resistant) mice. Conversely, Salmonella-infected mice were totally resistant to intravenous challenge with L. monocytogenes. The level of resistance in individual animals was related to the numbers of residual Salmonellae remaining in the tissues; mice with heavier residual infections being the more resistant. Specific antiserum from mice vaccinated with heat-killed S. typhimurium was found to be significantly protective only when the intraperitoneal route of challenge was employed. The foregoing studies have been interpreted to mean that enhancement of the microbicidal ability of macrophages is the mechanism of major importance in acquired resistance to S. typhimurium infection in mice.
将正常小鼠腹腔巨噬细胞与感染鼠伤寒沙门氏菌的小鼠细胞进行体外实验比较，结果表明“免疫”巨噬细胞的杀菌特性显著增强。正常巨噬细胞只能使经免疫血清预处理的细胞内鼠伤寒沙门氏菌灭活50%至60%，而感染动物的细胞几乎能杀死所有摄入的细菌，且杀灭速度更快。已证明，来自感染单核细胞增生李斯特菌的小鼠的巨噬细胞对鼠伤寒沙门氏菌也具有类似增强的杀菌活性。此外，在感染李斯特菌的小鼠中，鼠伤寒沙门氏菌在肝脏和脾脏中的生长比接种热灭活鼠伤寒沙门氏菌的动物更有效地受到限制，尽管感染李斯特菌的动物没有可证明的针对鼠伤寒沙门氏菌的交叉反应抗体。接种热灭活菌的小鼠缺乏抵抗力不能归因于体液因子的任何缺陷，因为这些动物的血清在促进巨噬细胞吞噬和杀灭方面与主动感染（且明显有抵抗力）小鼠的血清一样有效。相反，感染沙门氏菌的小鼠对单核细胞增生李斯特菌的静脉内攻击完全有抵抗力。个体动物的抵抗力水平与组织中残留的沙门氏菌数量有关；残留感染较重的小鼠抵抗力更强。仅当采用腹腔内攻击途径时，接种热灭活鼠伤寒沙门氏菌的小鼠的特异性抗血清才具有显著的保护作用。上述研究被解释为意味着巨噬细胞杀菌能力的增强是小鼠对鼠伤寒沙门氏菌感染获得性抵抗力的主要重要机制。
