Expression of the soxRS regulon in bacterial cells exposed to various stress factors

Background. Some stress responses contribute to the formation of bacterial antibiotic resistance, including the soxRS oxidative defense regulon. Elevation of reactive oxygen species production and oxidative stress was detected in bacterial cells exposed to various environmental stresses. It can be supposed that a stress-mediated increase in the level of reactive oxygen species will activate the expression of the soxRS regulon genes, which may provide pre-adaptation to antibiotics.The aim. To study changes in the expression of soxRS regulon genes in Escherichia coli cells exposed to NaCl, acetic acid, and heating.Materials and methods. Gene expression was measured in cells bearing reporter gene fusions (soxS::lacZ, nfo::lacZ). An overnight broth culture was diluted in fresh LB broth to OD600 = 0.1 and cultivated at 37 °C without stirring until OD600 = 0.3, then the stressors were applied.Results. Exposure to NaCl and acetic acid activated the expression of soxRS regulon genes, while heating caused a decrease in gene expression. An increase in the expression level was observed in cells subjected to stresses of low intensity (which did not cause a decrease in the number of colony-forming units (CFU) by the 4th hour of exposure compared to the beginning of the stress exposure) and medium intensity (which caused a 10-fold decrease in the number of CFU), whereas high-intensity stresses (which caused a decrease in the number of CFU by more than 10 times), regardless of their nature, were accompanied by a decrease in the expression of the soxRS regulon genes.Conclusion. Under the conditions studied, only the osmotic stress caused by the addition of NaCl was accompanied by a significant activation of the soxRS regulon genes. Sublethal exposure to NaCl, causing an increase in the expression of soxRS regulon genes by 2–2.5 times, may provide pre-adaptation of bacteria to the factors that this regulon is aimed at counteracting, including antibacterial drugs.