The effect of PmrA/B two-component system on the phenotype and virulence of Salmonella Typhimurium

Cunlei Liu1, Yupeng Fang1, Ziwei Guo1

  • 1Hebei Key Laboratory of Preventive Veterinary Medicine, Hebei Normal University of Science and Technology, Qinhuangdao, Hebei, 066000, China.

Microbial Pathogenesis
|April 16, 2026
PubMed

Insights

The PmrA/B system is crucial for Salmonella Typhimurium virulence, impacting biofilm formation, stress resistance, and infection severity. Its deletion significantly reduces pathogenicity, offering insights into bacterial mechanisms.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Molecular Biology

Background:

  • Salmonella Typhimurium is a significant human pathogen.
  • Two-component systems play vital roles in bacterial adaptation and virulence.
  • The PmrA/B system's specific role in S. Typhimurium pathogenicity requires elucidation.

Purpose of the Study:

  • To investigate the function of the PmrA/B two-component system in Salmonella Typhimurium pathogenicity.
  • To characterize the impact of PmrA/B deletion on bacterial traits related to virulence.

Main Methods:

  • Construction of PmrA, PmrB, and PmrA/B deletion mutants and complemented strains using λ-Red recombination.
  • Systematic evaluation of biological characteristics including growth, antibiotic susceptibility, biofilm formation, stress tolerance, adhesion, invasion, and mouse infection models.
  • Confirmation of mutant construction via PCR and sequencing.

Main Results:

  • PmrA/B deletion mutants showed increased sensitivity to doxycycline, tetracycline, and imipenem.
  • Biofilm formation, adhesion, and invasion capabilities were significantly reduced in PmrA/B mutants.
  • Mutants exhibited decreased tolerance to high osmolarity and acidic conditions, and reduced virulence in a mouse model.

Conclusions:

  • The PmrA/B two-component system is essential for Salmonella Typhimurium's biofilm formation, stress resistance, and overall virulence.
  • Disruption of PmrA/B significantly attenuates S. Typhimurium pathogenicity.
  • Findings provide a foundation for understanding S. Typhimurium pathogenic mechanisms.