Bakker-Woudenberg I A, Lokerse A F, Vink-van den Berg J C, Roerdink F H
Department of Clinical Microbiology and Antimicrobial Therapy, Erasmus University, Rotterdam.
Infection. 1988;16 Suppl 2:S165-70. doi: 10.1007/BF01639742.
In an experimental infection caused by Listeria monocytogenes in mice a considerable enhancement (90-fold) of the therapeutic activity of ampicillin resulting from liposomal encapsulation was observed. The mechanism by which liposomes improved the therapeutic index of ampicillin in this infection appeared to be an increased delivery of the antibiotic to the site of infection, i.e. the liver and spleen. Substantial amounts of liposomal ampicillin were recovered from isolated Kupffer cells, the target cells of L. monocytogenes after intravenous inoculation. In addition, in studies on the survival of L. monocytogenes within murine peritoneal macrophages in vitro it was found that liposomal encapsulation of ampicillin resulted in an increased availability of the antibiotic for the intracellular bacteria: liposomal ampicillin killed 90% of the intracellular bacteria, whereas a similar concentration of free ampicillin plus empty liposomes had no effect upon the intracellular bacteria.
在小鼠由单核细胞增生李斯特菌引起的实验性感染中,观察到脂质体包封使氨苄西林的治疗活性显著增强(90倍)。脂质体提高氨苄西林在该感染中治疗指数的机制似乎是抗生素向感染部位即肝脏和脾脏的递送增加。从分离的库普弗细胞(静脉接种后单核细胞增生李斯特菌的靶细胞)中回收了大量脂质体氨苄西林。此外,在体外对单核细胞增生李斯特菌在小鼠腹膜巨噬细胞内存活情况的研究中发现,氨苄西林的脂质体包封导致细胞内细菌可获得的抗生素增加:脂质体氨苄西林杀死了90%的细胞内细菌,而相似浓度的游离氨苄西林加空脂质体对细胞内细菌没有影响。