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Expression of Pls (plasmin sensitive) in Staphylococcus aureus negative for pls reduces adherence and cellular

Muzaffar Hussain1, Daniel Schäfer, Katri M Juuti

  • 1Institute of Medical Microbiology, University Hospital of Münster, Münster, Germany.

The Journal of Infectious Diseases
|May 29, 2009
PubMed
Abstract

Insights

The Staphylococcus aureus surface protein Pls reduces bacterial adhesion and invasion, acting through steric hindrance. This mechanism is independent of the methicillin-resistant Staphylococcus aureus (MRSA) background.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Infectious Diseases

Background:

  • Methicillin-resistant Staphylococcus aureus (MRSA) poses a significant health threat.
  • The MRSA surface protein Pls (plasmin sensitive) is known to reduce bacterial adhesion and invasiveness.
  • The precise mechanism by which Pls exerts these effects remains unclear.

Purpose of the Study:

  • To investigate the mechanism of action of the Pls protein in reducing Staphylococcus aureus adhesion and invasiveness.
  • To determine if the effects of Pls are dependent on the specific MRSA or methicillin-susceptible Staphylococcus aureus (MSSA) background.
  • To elucidate the role of Pls expression in bacterial-host interactions.

Main Methods:

  • Transformation of three distinct Staphylococcus aureus strains (MSSA and MRSA) with different Pls constructs (full-length, no sortase motif, no SD repeats).
  • Quantification of bacterial adherence to fibronectin and invasion of host cells using photometric and flow cytometry methods.
  • Analysis of gene and surface protein expression via real-time RT-PCR and ELISA.

Main Results:

  • Pls expression significantly reduced adherence to fibronectin (approx. 20-25%) and invasion of host cells (up to 85%).
  • While transcription of fnbA and spa was upregulated, clfA and hla were downregulated; Pls and FnBP surface expression increased.
  • Invasiveness was primarily reduced by competition with FnBPA, suggesting Pls acts independently of FnBP binding.

Conclusions:

  • Cell wall-anchored Pls effectively reduces Staphylococcus aureus adherence and invasiveness across different genetic backgrounds.
  • The mechanism of Pls action is attributed to steric hindrance, not other known pathways.
  • These findings provide a clearer understanding of Pls function in bacterial pathogenesis.

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