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<p>Bacterial biofilm formation plays a critical role in the pathogenicity and virulence of <i>Pseudomonas aeruginosa</i> posing a significant threat to human health. Previously, the uncharacterized <i>P. aeruginosa</i> gene <i>PA2798</i>, was identified as a contributor to its resistance to antibiofilm peptide. However, the functional role of <i>PA2798</i> and the underlying mechanisms by which it regulates biofilm formation and virulence factor production remain largely unexplored. In this study, a <i>PA2798</i>-deficient mutant&#xa0;(PAO1<i>∆PA2798</i>) was constructed, and aminoglycosides minimum inhibitory concentrations (MICs) were measured to assess the effect of <i>PA2798</i> on antibiotic susceptibility. In addition, both in vitro phenotypic assays and in vivo experiments in chronic and acute lung infection mice models were performed to evaluate the role of <i>PA2798</i> in bacterial biofilm associated infection and its potential as an antimicrobial target. Results demonstrated that deletion of <i>PA2798</i> led to fourfold decreases in MICs for gentamicin, amikacin, tobramycin and netilmicin, and was accompanied by reduced biofilm biomass and virulence factor production in PAO1<i>∆PA2798</i>. Moreover, compromised cellular integrity, reduced bacterial activity, and impaired bacterial motility were observed in PAO1∆<i>PA2798</i>. Simultaneously, mice infected with this mutant strain were observed with the reduction of bacterial colonization and improved survival in both chronic and acute in vivo models. Conclusively, our findings support a role for <i>PA2798</i> in aminoglycoside resistance, biofilm formation and virulence factor production in <i>P. aeruginosa</i>, highlighting its potential as a target for therapeutic intervention in biofilm-associated infections.</p>

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Role of gene PA2798 on biofilm formation and virulence factors production of Pseudomonas aeruginosa

  • 期刊论文

  • 发表日期：

    2025年10月14日

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  • Hai-Lin Li,
  • Li Chen,
  • Zhi-Wen Ma,
  • Jing Yan,
  • Xiao-Ling Lu,
  • Hao Nie,
  • Qi Yin,
  • Ying-Li Li

摘要

Bacterial biofilm formation plays a critical role in the pathogenicity and virulence of Pseudomonas aeruginosa posing a significant threat to human health. Previously, the uncharacterized P. aeruginosa gene PA2798, was identified as a contributor to its resistance to antibiofilm peptide. However, the functional role of PA2798 and the underlying mechanisms by which it regulates biofilm formation and virulence factor production remain largely unexplored. In this study, a PA2798-deficient mutant (PAO1∆PA2798) was constructed, and aminoglycosides minimum inhibitory concentrations (MICs) were measured to assess the effect of PA2798 on antibiotic susceptibility. In addition, both in vitro phenotypic assays and in vivo experiments in chronic and acute lung infection mice models were performed to evaluate the role of PA2798 in bacterial biofilm associated infection and its potential as an antimicrobial target. Results demonstrated that deletion of PA2798 led to fourfold decreases in MICs for gentamicin, amikacin, tobramycin and netilmicin, and was accompanied by reduced biofilm biomass and virulence factor production in PAO1∆PA2798. Moreover, compromised cellular integrity, reduced bacterial activity, and impaired bacterial motility were observed in PAO1∆PA2798. Simultaneously, mice infected with this mutant strain were observed with the reduction of bacterial colonization and improved survival in both chronic and acute in vivo models. Conclusively, our findings support a role for PA2798 in aminoglycoside resistance, biofilm formation and virulence factor production in P. aeruginosa, highlighting its potential as a target for therapeutic intervention in biofilm-associated infections.