Molecular regulatory mechanisms of Escherichia coli O157:H7 in response to ultrasonic stress revealed by proteomic analysis.

• Proteome revealed molecular regulatory mechanisms under ultrasonic stress. • Ultrasonic filed influenced various metabolic pathways in E. coli O157:H7 cells. • RpoS protein, MS channels, SOS response protein RecA were up-regulated. • Free radicals might enter into cells via activated mechanosensitive channels. • All-or-nothing effect might due to destruction of crucial cell defensive systems. The antimicrobial effects of ultrasonic filed have been studied for years at the phenotypic level, but there is little research to reveal the molecular regulatory mechanisms underlying the phenotypes. In this study, isobaric tag for relative and absolute quantification (iTRAQ) proteome was applied to analyze the regulatory networks of Escherichia coli O157:H7 in response to ultrasonic stress in whole-genome scale. A total of 1856 differentially expressed proteins were identified, of which 1141 were significant up-regulated and 715 down-regulated compared with live control cells. The comprehensive proteome coverage analysis showed that ultrasonic filed influenced various metabolic pathways in Escherichia coli O157:H7 cells. The ultrasound-induced up-regulation of global stress response regulator RpoS, bacterial mechanosensitive channels and SOS response protein RecA were described from the molecular level for the first time. In addition, we proposed a possible action mechanism that the free radicals produced by acoustic cavitation might enter into cells via the activated mechanosensitive channels, leading to the elevated intracellular ROS level and subsequent cell death. Last but not the least, we illustrated the all-or-nothing phenomenon of power ultrasound might due to the destruction of crucial cell defensive systems, including heat shock proteins and oxidative response regulators. These new findings can let us understand the ultrasonic effects more deeply and will contribute to this area. [ABSTRACT FROM AUTHOR]