Some bacterial stress responses are involved in survival under antibiotic treatment and contribute to less susceptible microbial forms selection. Here, we tested the role of cadaverine, one of the biogenic polyamines considered as universal adaptogens, in the processes. The expression of ldcC and cadA genes, encoding cadaverine-producing lysine decarboxylase, increased in Escherichia coli cells exposed to β-lactams and fluoroquinolones but not aminoglycosides. The transcriptional regulators RpoS and SoxS controlled the expression of ldcC and cadA, respectively, in response to antibiotics. Exogenous cadaverine had little effect on E. coli antibiotic susceptibility, whereas non-antibiotic-induced endogenous cadaverine contributed to its tolerance to β-lactams, fluoroquinolones, and aminoglycosides. Antibiotic-induced cadaverine synthesis promoted bacterial survival under fluoroquinolone exposure, as well as could contribute to low-resistant bacterial forms development. Selection under the fluoroquinolone levofloxacin exposure toward bacteria with an increased ability to synthesize cadaverine and negative correlation between LdcC activity and fluoroquinolone susceptibility in the selected forms were demonstrated. The same correlation in a special group of low-level resistant clinical E. coli isolates was revealed. So, cadaverine biosynthesis appeared to be a significant player in decreased E. coli antibiotic susceptibility development.

一些细菌应激反应与抗生素治疗下的生存有关，并有助于选择较不敏感的微生物形式。在这里，我们测试了尸胺（被认为是通用适应原的生物多胺之一）在该过程中的作用。在暴露于β-内酰胺类药物和氟喹诺酮类药物（而非氨基糖苷类药物）的大肠杆菌细胞中，编码产生尸胺的赖氨酸脱羧酶的ldcC和cadA基因的表达增加。转录调节因子 RpoS 和 SoxS 分别控制ldcC和cadA的表达，以响应抗生素。外源尸胺对大肠杆菌抗生素敏感性影响不大，而非抗生素诱导的内源尸胺有助于其对β-内酰胺类、氟喹诺酮类和氨基糖苷类药物的耐受性。抗生素诱导的尸胺合成促进了细菌在氟喹诺酮暴露下的存活，并可能有助于低耐药细菌形式的发展。证明了在氟喹诺酮左氧氟沙星暴露下对合成尸胺能力增加的细菌的选择，以及所选形式中 LdcC 活性与氟喹诺酮敏感性之间的负相关性。在一组特殊的低水平耐药临床大肠杆菌分离株中也发现了相同的相关性。因此，尸胺生物合成似乎是降低大肠杆菌抗生素敏感性发展的重要因素。