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Thioridazine affects transcription of genes involved in cell wall biosynthesis in methicillin-resistant

Mette Bonde1, Dorte H Højland, Hans Jørn Kolmos

  • 1Department of Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark.

FEMS Microbiology Letters
|March 8, 2011
PubMed

Insights

Thioridazine resensitizes methicillin-resistant Staphylococcus aureus (MRSA) to oxacillin by reducing key cell wall biosynthesis genes. This antipsychotic drug offers a potential new strategy against challenging MRSA infections.

Area of Science:

  • Microbiology
  • Pharmacology
  • Infectious Diseases

Background:

  • Methicillin-resistant Staphylococcus aureus (MRSA) poses a significant treatment challenge.
  • The antipsychotic thioridazine shows potential in combination therapy with oxacillin to overcome MRSA resistance.
  • Previous studies indicated thioridazine abolishes some MRSA resistance gene expression.

Purpose of the Study:

  • To elucidate the mechanism by which thioridazine reverses oxacillin resistance in MRSA.
  • To investigate the impact of thioridazine and oxacillin on genes involved in antibiotic resistance and cell wall biosynthesis.

Main Methods:

  • Testing gene expression in MRSA treated with thioridazine and oxacillin.
  • Analyzing the expression of genes within the VraSR regulon.
  • Evaluating the effect of thioridazine on virulence and toxin gene expression.

Main Results:

  • Thioridazine addition reduced oxacillin-induced expression of VraSR regulon genes.
  • This reduction likely weakens the bacterial cell wall, impacting oxacillin efficacy.
  • Thioridazine also decreased the expression of selected virulence genes without inducing toxin genes.

Conclusions:

  • The reversal of MRSA resistance by thioridazine is linked to the downregulation of specific cell wall biosynthesis genes.
  • Thioridazine's multifaceted effects on gene expression present a promising therapeutic avenue against MRSA.

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