Baccarini M, Bistoni F, Puccetti P, Garaci E
Infect Immun. 1983 Oct;42(1):1-9. doi: 10.1128/iai.42.1.1-9.1983.
We have recently reported the in vivo modulation of resistance to experimental Candida albicans infection by cyclophosphamide (150 mg/kg intraperitoneally) in mice and have shown that increased resistance to the microbial challenge occurs 12 to 21 days after treatment with the drug (Bistoni et al., Infect. Immun. 40: 46-55, 1983). The event is accompanied by the appearance of a highly candidacidal cell population in the spleen and the activation of a subpopulation of natural cytotoxic effectors reactive in vitro against YAC-1 tumor cells. We now provide evidence that these anti-YAC-1 cytotoxic effectors are clearly distinct from the cyclophosphamide-induced candidacidal effectors, which seem to belong to a macrophage-monocyte lineage. The enhanced cytotoxic activity induced by cyclophosphamide was not restricted to C. albicans but was also exerted against a panel of Candida strains.
我们最近报道了环磷酰胺(150毫克/千克腹腔注射)对小鼠实验性白色念珠菌感染抵抗力的体内调节作用,并表明在用该药物治疗后12至21天,对微生物攻击的抵抗力增强(比斯托尼等人,《感染与免疫》40: 46 - 55,1983年)。这一事件伴随着脾脏中出现高度杀念珠菌细胞群以及体外对YAC - 1肿瘤细胞有反应的自然细胞毒性效应子亚群的激活。我们现在提供证据表明,这些抗YAC - 1细胞毒性效应子与环磷酰胺诱导的杀念珠菌效应子明显不同,后者似乎属于巨噬细胞 - 单核细胞谱系。环磷酰胺诱导的增强的细胞毒性活性不仅限于白色念珠菌,还对一组念珠菌菌株起作用。