Related Experiment Videos

R-plasmid RP1 increases sensitivity of Proteus mirabilis to normal body defences

J A Onaolapo1, R M Klemperer

  • 1Department of Pharmaceutical Sciences, Aston University, Birmingham.

Insights

The R-plasmid RP1 enhances bacterial killing by non-immune whole blood, primarily through increased phagocytosis. This plasmid-mediated sensitivity is influenced by nutrient depletion and bacterial growth phase.

Area of Science:

  • Microbiology and Immunology
  • Bacterial Pathogenesis
  • Host-Pathogen Interactions

Background:

  • Non-immune whole blood possesses bactericidal activity against various pathogens.
  • Bacterial plasmids can influence interactions with the host immune system.
  • Nutritional status and growth phase affect bacterial susceptibility.

Purpose of the Study:

  • To investigate the effect of the R-plasmid RP1 on the bactericidal activity of non-immune whole blood against Proteus mirabilis.
  • To determine the mechanisms underlying plasmid-mediated changes in bacterial sensitivity.
  • To assess the influence of environmental factors like nutrient depletion and growth phase.

Main Methods:

  • Assays measuring the bactericidal activity of non-immune whole blood against Proteus mirabilis strains with and without the R-plasmid RP1.
  • Phagocytosis assays to quantify bacterial uptake by immune cells.
  • Comparison of bacterial sensitivity under different nutrient-depleted conditions (iron vs. carbon) and growth phases (stationary vs. exponential).

Main Results:

  • The R-plasmid RP1 significantly increased the bactericidal action of non-immune whole blood on Proteus mirabilis.
  • Increased phagocytosis was identified as the primary mechanism for this enhanced killing.
  • Iron-depleted stationary-phase cells exhibited greater sensitivity compared to carbon-depleted cells, and plasmid-containing cells were generally more sensitive.

Conclusions:

  • The R-plasmid RP1 confers increased sensitivity to non-immune whole blood killing in Proteus mirabilis, mainly via enhanced phagocytosis.
  • Bacterial nutrient status and growth phase modulate this plasmid-mediated immune evasion or susceptibility.
  • Outer membrane alterations, potentially involving glycosylated proteins, may contribute to the R-plasmid-mediated increase in phagocytosis sensitivity.

Related Concept Videos