Malik Muhammad, Li Liping, Zhao Xilin, Kerns Robert J, Berger James M, Drlica Karl
Public Health Research Institute, New Jersey Medical School, Rutgers Biomedical and Health Sciences, 225 Warren St., Newark, NJ, USA.
Public Health Research Institute, New Jersey Medical School, Rutgers Biomedical and Health Sciences, 225 Warren St., Newark, NJ, USA Department of Microbiology and Molecular Genetics, New Jersey Medical School, Rutgers Biomedical and Health Sciences, 225 Warren St., Newark, NJ, USA.
J Antimicrob Chemother. 2014 Dec;69(12):3227-35. doi: 10.1093/jac/dku285. Epub 2014 Jul 31.
One way to address the growing problem of antimicrobial resistance is to revive old compounds that may have intrinsic lethal activity that is obscured by protective factors. Bicyclomycin is an old inhibitor of the Rho transcription terminator that by itself shows little rapid lethal activity. However, bicyclomycin participates in bacteriostatic synergy, which raises the possibility that conditions for lethal synergy may exist, perhaps through a suppression of protective factors.
Bicyclomycin was combined with bacteriostatic inhibitors of gene expression, and bactericidal activity was measured with several cultured Gram-negative pathogens.
When used alone, bicyclomycin failed to rapidly kill growing cultures of Escherichia coli; however, the additional presence of bacteriostatic concentrations of tetracycline, chloramphenicol or rifampicin led to rapid killing. Four other pathogen species, Acinetobacter baumannii, Klebsiella pneumoniae, Salmonella enterica serotype Typhimurium and Shigella dysenteriae, also exhibited enhanced killing when bicyclomycin was combined with tetracycline or rifampicin. This lethal synergy was achieved at low concentrations (slightly above the MIC) for all agents tested in combinations. Follow-up work with E. coli indicated that lethal synergy arose from a blockage of transcription elongation. Moreover, lethal synergy was reduced when bicyclomycin was added 60 min before tetracycline, suggesting that bicyclomycin induces a protective factor.
The action of bicyclomycin illustrates the potential present in a largely abandoned antibacterial agent; it exhibits lethal synergy when coadministered with known, bacteriostatic inhibitors of gene expression. The identification of protective factors, which are currently uncharacterized, may reveal new ways to promote the lethal action of some old antibiotics.
应对日益严重的抗菌药物耐药性问题的一种方法是重新启用那些可能具有内在致死活性但被保护因子掩盖的旧化合物。双环霉素是一种古老的Rho转录终止子抑制剂,其本身几乎没有快速致死活性。然而,双环霉素参与抑菌协同作用,这增加了可能存在致死协同作用条件的可能性,或许是通过抑制保护因子来实现的。
将双环霉素与基因表达的抑菌抑制剂联合使用,并用几种培养的革兰氏阴性病原体测定杀菌活性。
单独使用时,双环霉素无法快速杀死生长中的大肠杆菌培养物;然而,抑菌浓度的四环素、氯霉素或利福平的额外存在导致快速杀菌。其他四种病原体,鲍曼不动杆菌、肺炎克雷伯菌、鼠伤寒沙门氏菌和痢疾志贺菌,当双环霉素与四环素或利福平联合使用时也表现出增强的杀菌作用。对于所有联合测试的药物,在低浓度(略高于最低抑菌浓度)时即可实现这种致死协同作用。对大肠杆菌的后续研究表明,致死协同作用源于转录延伸的阻断。此外,当在四环素前60分钟添加双环霉素时,致死协同作用减弱,这表明双环霉素诱导了一种保护因子。
双环霉素的作用说明了一种在很大程度上被废弃的抗菌剂所具有的潜力;当与已知的基因表达抑菌抑制剂共同给药时,它表现出致死协同作用。目前尚未明确的保护因子的鉴定可能会揭示促进一些旧抗生素致死作用的新方法。