Altes C, Steele J, Stanford J L, Rook G A
Tubercle. 1985 Dec;66(4):261-6. doi: 10.1016/0041-3879(85)90063-7.
Murine peritoneal macrophages protect Mycobacterium intracellular from amoxycillin added to the culture medium. This protective effect is enhanced by the addition of macrophage-activating lymphokines, although in the absence of amoxycillin these lymphokines cause macrophage-mediated inhibition of the organisms. Thus about 10 times more organisms survive exposure to 100 microgram/ml of amoxycillin for 3 days in the presence of lymphokine-activated macrophages than in their absence, whereas without amoxycillin the reverse is true. These findings suggest that in this in vitro system lymphokines cause stasis rather than kill of the organisms. The possibility that lymphokine-induced bacteriostasis protects mycobacteria from antibiotics in vivo is discussed.
小鼠腹腔巨噬细胞可保护细胞内分枝杆菌免受添加到培养基中的阿莫西林的影响。添加巨噬细胞激活淋巴因子可增强这种保护作用，尽管在没有阿莫西林的情况下，这些淋巴因子会导致巨噬细胞介导的对该微生物的抑制。因此，在存在淋巴因子激活的巨噬细胞的情况下，暴露于100微克/毫升阿莫西林3天存活的微生物数量比不存在时多约10倍，而在没有阿莫西林的情况下情况则相反。这些发现表明，在这个体外系统中，淋巴因子导致微生物停滞而非杀灭。文中讨论了淋巴因子诱导的抑菌作用在体内保护分枝杆菌免受抗生素影响的可能性。
