Possible role of sarA in dehydroepiandrosterone-mediated increase in Staphylococcus aureus resistance to vancomycin

Chemotherapy. 2007;53(3):181-4. doi: 10.1159/000100863. Epub 2007 Mar 14.

Abstract

Background: Dehydroepiandrosterone (DHEA), a steroid present throughout life, can induce an increase in resistance to vancomycin in methicillin-sensitive and methicillin-resistant clinical isolates of Staphylococcus aureus.

Methods: The in vitro effect of DHEA on vancomycin killing of S. aureus with mutations in sarA and/or agr was determined by standard microtiter protocols and time to kill determinations.

Results: Of the isolates tested, the strain with a deletion in sarAderived from a DHEA- responsive parent was not protected from vancomycin killing by DHEA. However, DHEA significantly (p < 0.01) slowed the rate of vancomycin killing of sarA-.

Conclusion: These data indicate that sarA may play a role in DHEA-mediated protection from vancomycin killing of S. aureus.

MeSH terms

  • Anti-Bacterial Agents / pharmacology
  • Bacterial Proteins / genetics*
  • Dehydroepiandrosterone / pharmacology*
  • Microbial Sensitivity Tests
  • Staphylococcus aureus / drug effects*
  • Staphylococcus aureus / genetics
  • Trans-Activators / deficiency
  • Trans-Activators / genetics*
  • Vancomycin / pharmacology
  • Vancomycin Resistance / drug effects*
  • Vancomycin Resistance / genetics

Substances

  • Agr protein, Staphylococcus aureus
  • Anti-Bacterial Agents
  • Bacterial Proteins
  • SarA protein, bacterial
  • Trans-Activators
  • Dehydroepiandrosterone
  • Vancomycin