Pourahmad Jaktaji Razieh, Pasand Shirin
Genetics at Faculty of Science, Biotechnology Center, University of Shahrekord, Iran.
Genetics, University of Shahrekord, Iran.
Gene. 2016 Jan 15;576(1 Pt 1):115-8. doi: 10.1016/j.gene.2015.09.069. Epub 2015 Oct 2.
Fluoroquinolones are important antibiotics for the treatment of urinary tract infections caused by Escherichia coli. Mutational studies have shown that ciprofloxacin, a member of fluoroquinolones induces SOS response and mutagenesis in pathogenic bacteria which in turn develop antibiotic resistance. However, inhibition of SOS response can increase recombination activity which in turn leads to genetic variation.
The aim of this study was to measure 5 SOS genes expressions in nine E. coli mutants with different MICs for ciprofloxacin following exposure to ciprofloxacin.
Gene expression was assessed by quantitative real time PCR. Gene alteration assessment was conducted by PCR amplification and DNA sequencing.
Results showed that the expression of recA was increased in 5 mutants. This overexpression is not related to gene alteration, and enhances the expression of polB and umuCD genes encoding nonmutagenic and mutagenic polymerases, respectively. The direct relationship between the level of SOS expression and the level of resistance to ciprofloxacin was also indicated.
It was concluded that novel therapeutic strategy that inhibits RecA activity would enhance the efficiency of common antibiotics against pathogenic bacteria.
氟喹诺酮类药物是治疗由大肠杆菌引起的尿路感染的重要抗生素。突变研究表明，氟喹诺酮类药物成员环丙沙星可在致病细菌中诱导SOS反应和诱变，进而产生抗生素耐药性。然而，抑制SOS反应会增加重组活性，进而导致遗传变异。
本研究旨在测定九株对环丙沙星具有不同最低抑菌浓度（MIC）的大肠杆菌突变体在暴露于环丙沙星后5个SOS基因的表达情况。
通过定量实时PCR评估基因表达。通过PCR扩增和DNA测序进行基因改变评估。
结果显示，5个突变体中recA的表达增加。这种过表达与基因改变无关，并分别增强了编码非诱变和诱变聚合酶的polB和umuCD基因的表达。还表明了SOS表达水平与对环丙沙星的耐药水平之间的直接关系。
得出结论，抑制RecA活性的新型治疗策略将提高常用抗生素对致病细菌的疗效。
