The Role of ptsH in Stress Adaptation and Virulence in Cronobacter sakazakii BAA-894

Cronobacter sakazakii, an emerging foodborne pathogen that was isolated primarily from powdered infant formula, poses an important issue in food safety due to its high stress tolerance and pathogenicity. The Hpr (encoded by ptsH gene) has been shown to regulate carbon metabolism as well as stress response and virulence. However, the functional properties of ptsH in C. sakzakii have not been investigated. In this study, we clarified the role of ptsH in the C. sakzakii stress response and virulence, and explored its possible regulatory mechanism by RNA-seq. Compared with wild-type, the Delta ptsH mutant showed a slower growth rate in the log phase but no difference in the stationary phase. Moreover, the resistance to heat stress (65 degrees C, 55 degrees C), simulated gastric fluid (pH = 2.5), biofilm formation and adhesion to HT-29 cells of Delta ptsH mutant were significantly decreased, whereas the oxidative resistance (1, 5, 10 mM H2O2), osmotic resistance (10%, 15%, 20% NaCl), and superoxide dismutase activity were enhanced. Finally, RNA-seq analysis revealed the sulfur metabolism pathway is significantly upregulated in the Delta ptsH mutant, but the bacterial secretion system pathway is dramatically downregulated. The qRT-PCR assay further demonstrated that the Delta ptsH mutant has elevated levels of genes that are related to oxidative and osmotic stress (sodA, rpoS, cpxA/R, osmY). This study provides a great understanding of the role of ptsH in diverse stress responses and virulence in C. sakazakii, and it contributes to our understanding of the genetic determinant of stress resistance and pathogenicity of this important foodborne pathogen.

Automated summary

This study investigates the role of ptsH in stress response and virulence in C. sakazakii. The Delta ptsH mutant displays slower growth rate, decreased resistance to various stresses, and altered gene expression patterns compared to the wild-type. Furthermore, RNA-seq analysis reveals the upregulation of sulfur metabolism pathway and downregulation of bacterial secretion system pathway in the Delta ptsH mutant.