Suppr超能文献

苯并恶嗪诺利霉素KRM-1648、克拉霉素和左氧氟沙星对小鼠腹腔巨噬细胞吞噬的细胞内鸟分枝杆菌复合群的抗菌活性。

Antimicrobial activities of benzoxazinorifamycin KRM-1648, clarithromycin and levofloxacin against intracellular Mycobacterium avium complex phagocytosed by murine peritoneal macrophages.

作者信息

Sato K, Akaki T, Tomioka H

机构信息

Department of Microbiology and Immunology, Shimane Medical University, Japan.

出版信息

J Antimicrob Chemother. 1998 Jan;41(1):77-83. doi: 10.1093/jac/41.1.77.

Abstract

The in-vitro activities of KRM-1648, a new benzoxazinorifamycin, clarithromycin and levofloxacin against clinical isolates of Mycobacterium avium complex (MAC) were measured using various methods of assay and compared with their in-vivo therapeutic activities against MAC infection in mice. The MICs varied according to drug in the order KRM-1648 << clarithromycin < levofloxacin. However, KRM-1648 and clarithromycin but not levofloxacin had similar therapeutic outcomes in MAC-infected mice. KRM-1648 and clarithromycin given at clinical dosages caused 1 to 2 log unit reductions in bacterial loads in the lungs of host mice. The values of Cmax (lung)/MBC were more closely related to the therapeutic efficacy of these drugs in mice than were MICs and MBCs alone. Potent microbicidal activity was observed with KRM-1648 and clarithromycin but not with levofloxacin against extracellularly growing MAC (EG-MAC) in a liquid medium. These two agents caused more than 3 log unit killing of MAC during a 5 day incubation, when added at concentrations equivalent to Cmax (lung). The anti-EG-MAC bactericidal activity of these drugs was greater than their efficacy in mice in vivo. KRM-1648 and clarithromycin but not levofloxacin caused respectively 2 and 0.5 log unit killing of intracellularly growing MAC (IG-MAC) in murine peritoneal macrophages. The profiles of bacterial killing effects of these agents against IG-MAC accurately reflected their therapeutic effects in mice, although the in-vivo activity of KRM-1648 was still overestimated using even this parameter.

摘要

使用多种检测方法测定了新型苯并恶嗪利福霉素KRM - 1648、克拉霉素和左氧氟沙星对鸟分枝杆菌复合群(MAC)临床分离株的体外活性,并将其与它们对小鼠MAC感染的体内治疗活性进行了比较。MICs因药物而异,顺序为KRM - 1648 <<克拉霉素<左氧氟沙星。然而,KRM - 1648和克拉霉素在MAC感染的小鼠中具有相似的治疗效果,而左氧氟沙星则不然。以临床剂量给予KRM - 1648和克拉霉素可使宿主小鼠肺部的细菌载量降低1至2个对数单位。与单独的MICs和MBCs相比,Cmax(肺)/MBC值与这些药物在小鼠中的治疗效果更密切相关。在液体培养基中,观察到KRM - 1648和克拉霉素对细胞外生长的MAC(EG - MAC)具有强大的杀菌活性,而左氧氟沙星则没有。当以相当于Cmax(肺)的浓度添加时,这两种药物在5天的孵育期间可使MAC的杀灭超过3个对数单位。这些药物对EG - MAC的抗杀菌活性大于它们在小鼠体内的疗效。KRM - 1648和克拉霉素而非左氧氟沙星分别使小鼠腹膜巨噬细胞内生长的MAC(IG - MAC)减少2和0.5个对数单位。这些药物对IG - MAC的细菌杀灭作用概况准确反映了它们在小鼠中的治疗效果,尽管即使使用该参数,KRM - 1648的体内活性仍被高估。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验