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The high-affinity phosphate transporter Pst in Proteus mirabilis HI4320 and its importance in biofilm formation

G A O'May1, S M Jacobsen1, M Longwell2

  • 1Department of Microbial Pathogenesis, University of Maryland - Baltimore, Dental School, 650 W. Baltimore Street, Baltimore, MD 21201, USA.

Microbiology (Reading, England)
|April 18, 2009
PubMed

Insights

The phosphate-specific transport (Pst) system in Proteus mirabilis negatively regulates crystalline biofilm formation, impacting its virulence in complicated urinary tract infections (UTIs). This study highlights the Pst system

Area of Science:

  • Microbiology
  • Urology
  • Pathogenesis

Background:

  • Proteus mirabilis is a key cause of urinary tract infections (UTIs), particularly in patients with long-term indwelling catheters.
  • Virulence of P. mirabilis involves crystalline biofilm formation and nutrient acquisition systems, such as the phosphate-specific transport (Pst) system.
  • The Pst system's role in P. mirabilis pathogenesis and biofilm formation during UTIs is not fully understood.

Purpose of the Study:

  • To investigate the role of the Pst system in P. mirabilis biofilm formation and pathogenesis during UTIs.
  • To compare the proteomes of P. mirabilis wild-type and Pst system mutants during planktonic and biofilm growth.
  • To microscopically analyze biofilms formed by Pst mutants.

Main Methods:

  • Construction and characterization of transposon mutants in Pst system components (PstS, PstA).
  • Assessment of UTI pathogenesis using a CBA mouse model.
  • Evaluation of biofilm formation in human urine.
  • Proteomic analysis comparing wild-type and mutant strains under different growth conditions.
  • Microscopic examination of biofilms.

Main Results:

  • Pst system mutants (DeltapstS and DeltapstA) showed significant attenuation in the mouse UTI model.
  • These mutants exhibited defective biofilm formation in human urine.
  • Proteomic analysis revealed significant differences between wild-type and Deltapst mutant proteomes.
  • The Deltapst mutants, especially DeltapstS, were defective in biofilm formation.

Conclusions:

  • The Pst system in P. mirabilis HI4320 negatively regulates biofilm formation.
  • The Pst system is crucial for the pathogenesis of P. mirabilis during complicated UTIs.
  • Targeting the Pst system could be a potential strategy for managing P. mirabilis-associated UTIs.

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