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Lysine Decarboxylase Activity as a Factor of Fluoroquinolone Resistance in Escherichia coli

机译:赖氨酸脱羧酶活性是大肠杆菌对氟喹诺酮耐药的一个因素

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Exposure of E. coli cells to sublethal concentrations of fluoroquinolones induced synthesis of lysine decarboxylase LdcC, which was previously considered to be a constitutive enzyme. Under these conditions, a key role in this process is played by RNA polymerase as subunit (RpoS); its quantity increased substantially in the presence of antibiotics. Fluoroquinolones of the second and third generations had a more pronounced effect on rpoS expression and LdcC activity than the first-generation antibiotics. A direct correlation was shown between the level of-cadaverine, the product of lysine decarboxylase reaction in E. coli cells, and their resistance to fluoroquinolones. An increase in endogenous cadaverine reduced effectiveness of the second and third-generation fluoroquinolones, but had no effect on antimicrobial activity of the first-generation antibiotics. This is in good agreement with the hydrophilic properties of antibiotics of different generations and, consequently, with different mechanisms of their penetration into bacterial cells.
机译:将大肠杆菌细胞暴露于亚致死浓度的氟喹诺酮类药物可诱导赖氨酸脱羧酶LdcC的合成,该酶以前被认为是组成性酶。在这些条件下,RNA聚合酶作为亚基(RpoS)发挥了关键作用。在存在抗生素的情况下,其数量大大增加。与第一代抗生素相比,第二和第三代氟喹诺酮类药物对rpoS表达和LdcC活性的影响更为明显。尸胺水平,大肠杆菌细胞中赖氨酸脱羧酶反应产物与它们对氟喹诺酮类药物的耐药性之间存在直接关系。内源尸胺的增加降低了第二代和第三代氟喹诺酮类药物的有效性,但对第一代抗生素的抗菌活性没有影响。这与不同世代的抗生素的亲水特性以及因此其渗透到细菌细胞中的不同机理非常吻合。

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