Binh Tran Thanh, Suzuki Rumiko, Trang Tran Thi Huyen, Kwon Dong Hyeon, Yamaoka Yoshio
Department of Environmental and Preventive Medicine, Oita University Faculty of Medicine, Yufu, Japan Department of Endoscopy, Cho Ray Hospital, Ho Chi Minh City, Vietnam.
Department of Environmental and Preventive Medicine, Oita University Faculty of Medicine, Yufu, Japan.
Antimicrob Agents Chemother. 2015 Apr;59(4):2343-8. doi: 10.1128/AAC.04852-14. Epub 2015 Feb 2.
Metronidazole resistance is a key factor associated with Helicobacter pylori treatment failure. Although this resistance is mainly associated with mutations in the rdxA and frxA genes, the question of whether metronidazole resistance is caused by the inactivation of frxA alone is still debated. Furthermore, it is unclear whether there are other mutations involved in addition to the two genes that are associated with resistance. A metronidazole-resistant strain was cultured from the metronidazole-susceptible H. pylori strain 26695-1 by exposure to low concentrations of metronidazole. The genome sequences of both susceptible and resistant H. pylori strains were determined by Illumina next-generation sequencing, from which putative candidate resistance mutations were identified. Natural transformation was used to introduce PCR products containing candidate mutations into the susceptible parent strain 26695-1, and the metronidazole MIC was determined for each strain. Mutations in frxA (hp0642), rdxA (hp0954), and rpsU (hp0562) were confirmed by the Sanger method. The mutated sequence in rdxA was successfully transformed into strain 26695-1, and the transformants showed resistance to metronidazole. The transformants containing a single mutation in rdxA showed a low MIC (16 mg/liter), while those containing mutations in both rdxA and frxA showed a higher MIC (48 mg/liter). No transformants containing a single mutation in frxA or rpsU were obtained. Next-generation sequencing was used to identify mutations related to drug resistance. We confirmed that the mutations in rdxA are mainly associated with metronidazole resistance, and mutations in frxA are able to enhance H. pylori resistance only in the presence of rdxA mutations. Moreover, mutations in rpsU may play a role in metronidazole resistance.
甲硝唑耐药是与幽门螺杆菌治疗失败相关的关键因素。尽管这种耐药主要与rdxA和frxA基因的突变有关,但仅由frxA失活导致甲硝唑耐药这一问题仍存在争议。此外,除了这两个与耐药相关的基因外,是否还有其他突变参与其中尚不清楚。通过暴露于低浓度甲硝唑,从甲硝唑敏感的幽门螺杆菌菌株26695-1中培养出一株甲硝唑耐药菌株。通过Illumina下一代测序确定了敏感和耐药幽门螺杆菌菌株的基因组序列,从中鉴定出假定的候选耐药突变。利用自然转化将含有候选突变的PCR产物导入敏感亲代菌株26695-1,并测定各菌株的甲硝唑最低抑菌浓度(MIC)。通过桑格法确认了frxA(hp0642)、rdxA(hp0954)和rpsU(hp0562)中的突变。rdxA中的突变序列成功转化到菌株26695-1中,转化体对甲硝唑表现出耐药性。在rdxA中含有单个突变的转化体显示出低MIC(16毫克/升),而在rdxA和frxA中均含有突变的转化体显示出更高的MIC(48毫克/升)。未获得在frxA或rpsU中含有单个突变的转化体。利用下一代测序来鉴定与耐药相关的突变。我们证实rdxA中的突变主要与甲硝唑耐药相关,而frxA中的突变仅在存在rdxA突变的情况下才能增强幽门螺杆菌的耐药性。此外,rpsU中的突变可能在甲硝唑耐药中起作用。