Wecke J, Johannsen L, Giesbrecht P
Robert Koch-Institut, Berlin, Federal Republic of Germany.
Infect Immun. 1990 Jan;58(1):197-204. doi: 10.1128/iai.58.1.197-204.1990.
Clindamycin treatment of Staphylococcus aureus caused a remarkable thickening of the bacterial cell wall and made the bacterial wall much more resistant against lytic enzymes within bone marrow-derived macrophages as revealed by electron microscopy and radiolabeling experiments. This reduced wall degradability resulted from an increased number of O-acetyl groups in the murein. Furthermore, such clindamycin-treated bacteria were ingested by adherent bone marrow-derived macrophages at a higher rate than untreated bacteria. The medical aspects of these results are discussed.
克林霉素治疗金黄色葡萄球菌导致细菌细胞壁显著增厚,并使细胞壁对骨髓来源巨噬细胞内的裂解酶具有更强的抗性,这通过电子显微镜和放射性标记实验得以揭示。这种细胞壁降解能力的降低是由于胞壁质中O - 乙酰基团数量增加所致。此外,与未处理的细菌相比,这种经克林霉素处理的细菌被贴壁骨髓来源巨噬细胞摄取的速率更高。本文讨论了这些结果的医学意义。