Centre for Infection and Immunity, Queen's University Belfast, Medical Biology Centre, Belfast, United Kingdom.
Antimicrob Agents Chemother. 2012 Aug;56(8):4466-7. doi: 10.1128/AAC.06224-11. Epub 2012 May 29.
Tigecycline resistance in Klebsiella pneumoniae results from ramA upregulation that causes the overexpression of the efflux pump, AcrAB-TolC. Tigecycline mutants, derived from Ecl8ΔramA, can exhibit a multidrug resistance phenotype due to increased transcription of the marA, rarA, acrAB, and oqxAB genes. These findings support the idea that tigecycline or multidrug resistance in K. pneumoniae, first, is not solely dependent on the ramA gene, and second, can arise via alternative regulatory pathways in K. pneumoniae.
肺炎克雷伯菌对替加环素的耐药性源于 ramA 的上调,导致外排泵 AcrAB-TolC 的过度表达。源自 Ecl8ΔramA 的替加环素突变体由于 marA、rarA、acrAB 和 oqxAB 基因转录增加,可表现出多药耐药表型。这些发现支持以下观点:首先,肺炎克雷伯菌对替加环素或多药耐药性并非仅依赖于 ramA 基因,其次,可通过肺炎克雷伯菌中的替代调控途径产生。