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首页> 外文期刊>Applied Microbiology >Potential Risk of Spreading Resistance Genes within Extracellular-DNA-Dependent Biofilms of Streptococcus mutans in Response to Cell Envelope Stress Induced by Sub-MICs of Bacitracin
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Potential Risk of Spreading Resistance Genes within Extracellular-DNA-Dependent Biofilms of Streptococcus mutans in Response to Cell Envelope Stress Induced by Sub-MICs of Bacitracin

机译：在甲硝丙嘧啶亚麦克白素诱导的细胞包络应力响应链球菌依赖于链球菌的细胞外 - DNA依赖性生物膜内扩散基因的潜在风险

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Antibiotics are used to treat or prevent some types of bacterial infection. The inappropriate use of antibiotics unnecessarily promotes antibiotic resistance and increases resistant bacteria, and controlling these bacteria is difficult. While the emergence of drug-resistant bacteria is a serious problem, the behavior of drug-resistant bacteria is not fully understood. In this study, we investigated the behavior of Streptococcus mutans , a major etiological agent of dental caries that is resistant to bacitracin, which is a cell wall-targeting antibiotic, and focused on biofilm formation in the presence of bacitracin. S. mutans UA159 most strongly induced extracellular DNA (eDNA)-dependent biofilm formation in the presence of bacitracin at 1/8× MIC. The Δ mbrC and Δ mbrD mutant strains, which lack bacitracin resistance, also formed biofilms in the presence of bacitracin at 1/2× MIC. This difference between the wild type and the mutants was caused by the induction of atlA expression in the mid-log phase. We also revealed that certain rgp genes involved in the synthesis of rhamnose-glucose polysaccharide related to cell wall synthesis were downregulated by bacitracin. In addition, glucosyltransferase-I was also involved in eDNA-dependent biofilm formation. The biofilm led to increased transformation efficiencies and promoted horizontal gene transfer. Biofilms were also induced by ampicillin and vancomycin, antibiotics targeting cell wall synthesis, suggesting that cell envelope stress triggers biofilm formation. Therefore, the expression of the atlA and rgp genes is regulated by S. mutans , which forms eDNA-dependent biofilms, promoting horizontal gene transfer in response to cell envelope stress induced by sub-MICs of antibiotics.IMPORTANCE Antibiotics have been reported to induce biofilm formation in many bacteria at subinhibitory concentrations. Accordingly, it is conceivable that the MIC against drug-sensitive bacteria may promote biofilm formation of resistant bacteria. Since drug-resistant bacteria have spread, it is important to understand the behavior of resistant bacteria. Streptococcus mutans is bacitracin resistant, and the 1/8× MIC of bacitracin, which is a cell wall-targeted antibiotic, induced eDNA-dependent biofilm formation. The Δ mbrC and Δ mbrD strains, which are not resistant to bacitracin, also formed biofilms in the presence of bacitracin at 1/2× MIC, and biofilms of both the wild type and mutants promoted horizontal gene transfer. Another cell wall-targeted antibiotic, vancomycin, showed effects on biofilms and gene transfer similar to those of bacitracin. Thus, treatment with cell wall-targeted antibiotics may promote the spread of drug-resistant genes in biofilms. Therefore, the behavior of resistant bacteria in the presence of antibiotics at sub-MICs should be investigated when using antibiotics.
机译：抗生素用于治疗或预防某些类型的细菌感染。不当使用抗生素不必要地促进抗生素抗性并增加抗性细菌，并控制这些细菌很难。虽然抗药性细菌的出现是一个严重的问题，但抗药性细菌的行为尚未完全理解。在这项研究中，我们研究了链球菌变异的行为，这是一种耐药蛋白的龋齿的主要原因，这是一种细胞壁靶向抗生素，并在甲硝丁酸存在下聚焦生物膜形成。 S.UA159最强烈诱导的细胞外DNA（EDNA） - 依赖生物膜在1/8×MIC在甲硝丙肽存在下形成。 δMBRC和δMBRD突变菌株，其缺乏双硝基肽抗性，也在1/2×MIC在甲硝肽存在下形成生物膜。野生型和突变体之间的这种差异是由中木阶段中的阿特拉表达的诱导引起的。我们还透露，参与与细胞壁合成相关的鼠李糖 - 葡萄糖多糖合成的某些RGP基因通过Bacitracin下调。此外，葡萄糖基转移酶-1也参与了EDNA依赖性生物膜形成。生物膜导致转化效率增加并促进水平基因转移。生物膜也被氨苄青霉素和万古霉素诱导，抗生素靶向细胞壁合成，表明细胞包络应力触发生物膜形成。因此，ATLA和RGP基因的表达由S. mutAns调节，其形成依赖于依赖的生物膜，促进响应于抗生素亚麦克风诱导的细胞包络应力的水平基因转移。据报道，鉴定抗生素诱导生物膜形成在亚抑制浓度的许多细菌。因此，可以想到的是对药物敏感的细菌MIC可促进抗性细菌的生物膜形成。由于耐药细菌已经扩散，必须了解耐药菌的行为是很重要的。变形链球菌的抗杆菌肽，杆菌肽的1/8×MIC，其为细胞壁靶向抗生素诱导的eDNA依赖性生物膜形成。的ΔMBRC和ΔmbrD菌株，这是不耐杆菌肽，也以1/2×MIC形成在杆菌肽的存在生物膜，和野生型和突变体两者的生物膜促进水平基因转移。另一种细胞壁靶向抗生素，万古霉素，表现出对生物膜和类似的杆菌肽的基因转移的效果。因此，与细胞壁靶向抗生素治疗可以促进的药物抗性基因在生物膜中的传播。因此，耐药细菌的在抗生素在子的MIC存在下的行为应该使用抗生素时进行调查。

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