Salmonella typhimurium resistance on pulsed electric fields associated with membrane fluidity and gene regulation

Abstract

Abstract Effects of different growth temperatures on cytoplasmic membrane fluidity and phospholipids phase transition temperature (T m ) of Salmonella typhimurium and resistance to pulsed electric field (PEF) inactivation, as well as the expression of stress-related genes and fatty acid biosynthesis-associated genes were investigated. Results indicated that the PEF resistance of S . typhimurium increased as growth temperature increased. S . typhimurium cultivated at 10 °C exhibited the lowest PEF resistance with the reduction of 4.23 log 10 CFU/mL, while the reduction of 2.10 log 10 CFU/mL was found in S . typhimurium cultivated at 45 °C under the same PEF treatment, due to the up-regulation of the expression of fabA gene, which was characterized by the lowest T m of membrane phospholipids and the greatest membrane fluidity. Although the expression of alternative sigma factors were altered by growth temperature, these genes were not essential for S . typhimurium to develop PEF resistance, suggesting that the PEF resistance modified by growth temperature could be caused by alterations in membrane fluidity. Industrial relevance Pulsed electric fields (PEF) treatment has been widely applied in nonthermal pasteurization and increasingly focused on synergistic combinations with other techniques such as thermal treatment, sonication and antibacterial agents to improve the efficacy of PEF to inactivate micro-organisms. Our results indicated that S . typhimurium cultivated at relatively lower temperature was easily inactivated by PEF, due to the up-regulation of the expression of fabA gene, which was characterized by the lowest phase transition temperature of cytoplasmic membrane phospholipids and the greatest membrane fluidity. Therefore, the underlying mechanism of alterations in PEF resistance of S . typhimurium induced by growth temperature was explored to achieve better understanding of microbial inactivation by PEF.