[Tests for studying invasive properties of selected Proteus mirabilis strains]

B Bartodziejska1, M Wykrota, A Rózalski

  • 1Zakład Immunobiologii Bakterii, Instytut Mikrobiologii i Immunologii Uniwersytetu Łódzkiego.

Medycyna Doswiadczalna I Mikrobiologia
|January 12, 2002
PubMed

Insights

Proteus mirabilis causes urinary tract infections (UTIs). Lipopolysaccharide (LPS) from these bacteria reduced their invasion of mouse cells over time, suggesting LPS impacts bacterial pathogenicity.

Area of Science:

  • Microbiology
  • Pathogenesis
  • Cell Biology

Background:

  • Proteus mirabilis is a significant cause of urinary tract infections (UTIs).
  • Lipopolysaccharide (LPS), an endotoxin, is a key virulence factor in P. mirabilis pathogenicity.
  • Understanding bacterial invasion mechanisms is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the invasion dynamics of P. mirabilis strains (serogroups O10, O23, O30, O43) into L929 mouse fibroblasts.
  • To assess the impact of bacterial incubation time and lipopolysaccharide (LPS) on bacterial invasiveness and cytotoxicity.
  • To explore the role of HpmA hemolysin in the cytotoxic effects of P. mirabilis.

Main Methods:

  • Invasion assays using L929 mouse fibroblasts and various P. mirabilis serogroups.
  • Time-course experiments to evaluate bacterial invasiveness and cytotoxicity.
  • Treatment of fibroblasts with purified LPS to determine its effect on bacterial invasion.

Main Results:

  • Maximal invasiveness of P. mirabilis into L929 cells was observed between 4-6 hours of incubation.
  • Bacterial cytotoxicity increased with incubation time, potentially due to HpmA hemolysin production.
  • Incubation of L929 fibroblasts with LPS significantly decreased bacterial invasiveness, with longer LPS exposure leading to weaker bacterial penetration.

Conclusions:

  • Bacterial incubation time influences the invasion of P. mirabilis into host cells.
  • Lipopolysaccharide (LPS) plays a role in modulating P. mirabilis invasiveness, potentially reducing its ability to penetrate host cells.
  • Further research into LPS-host cell interactions could reveal novel therapeutic targets for UTIs.

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