POLYAMINES AS A FACTOR OF CADAVERINE SYNTHESIS REGULATION UNDER ATIBIOTIC TREATMENT

Abstract

E. coli antibiotic susceptibility could come down due to a cadaverine-caused decrease in cell wall permeability. Cadaverine synthesis is at that realized by CadA and/or LdcC lysine decarboxylases. Here we analyze cadaverine synthesis regulation under antibiotic treatment.We found an increase in ldcC and cadA gene expression following fluoroquinolone application. It leads to lysine decarboxylases enzymatic activity growth (LdcC par excellence) and, finally, to high intracellular cadaverine accumulation. Polyamines putrescine and spermidine in these conditions inhibit expression of lysine decarboxylase genes and diminish their enzymatic activity. Nevertheless, they make bacteria more tolerant of antibiotics due to the weakening of the intensity of antibiotic- induced endogenous oxidative stress.Following the application of β-lactams growth in the expression of cadA was found. The expression of ldcC , on the contrary, dropped down. Lysine decarboxylase activity in these conditions grew (due to CadA activity), however, and led to increased cadaverine accumulation. Exogenous polyamines decreased the expression of cadA and CadA enzymatic activity and had no positive effects on bacterial viability.Thus, there exist pronounced protective effects of putrescine and spermidine under fluoroquinolone treatment and the lack of such effects in response to β-lactams. The physiological role of cadaverine, which is synthesized in a bacterial cell in response to antibacterial compounds, is yet to be specified.