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  1. Home
  3. Skin Androgens Regulate Staphylococcus Aureus Pathogenicity Via Quorum Sensing.
  1. Home
  3. Skin Androgens Regulate Staphylococcus Aureus Pathogenicity Via Quorum Sensing.

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Skin androgens regulate Staphylococcus aureus pathogenicity via quorum sensing.

Maria Sindhura John1, Mahendran Chinnappan1, Camille I Sturges1

  • 1Department of Dermatology, University of Texas Southwestern Medical Center, Dallas, TX, USA.

Nature Microbiology
|February 27, 2026

View abstract on PubMed

Summary
This summary is machine-generated.

Skin cells produce testosterone, which increases the risk of bacterial skin infections like MRSA. Blocking this effect may offer new ways to treat infections.

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Area of Science:

  • Microbiology
  • Dermatology
  • Biochemistry

Background:

  • Skin cells secrete testosterone, with higher levels in males.
  • Males exhibit increased susceptibility to skin infections compared to females.
  • Methicillin-resistant Staphylococcus aureus (MRSA) is a significant pathogen causing skin infections.

Purpose of the Study:

  • To investigate the role of skin-secreted testosterone in MRSA infections.
  • To elucidate the mechanism by which testosterone influences S. aureus virulence.
  • To explore potential therapeutic strategies targeting the testosterone-AgrC interaction.

Main Methods:

  • Generation of testosterone-deficient skin in mice.
  • Analysis of S. aureus virulence factor expression.
  • Quorum-sensing pathway activation studies (agr pathway).
  • Mutational analysis of S. aureus AgrC.
  • In silico molecular docking simulations.
  • Testing of testosterone isomers for anti-virulence activity.

    • Main Results:

    • Testosterone-deficient skin mice showed resistance to MRSA infections.
    • Testosterone enhanced S. aureus cytotoxic virulence factor expression via the agr pathway.
    • Testosterone's effect was concentration-dependent and independent of auto-inducing peptides.
    • A functional AgrC histidine kinase in S. aureus was essential for testosterone's effect.
    • In silico analysis suggested direct interaction between testosterone and AgrC.
    • Enantiomer-testosterone blocked bacterial quorum sensing and reduced S. aureus-induced cytotoxicity.

    Conclusions:

    • Skin-secreted testosterone promotes S. aureus virulence by activating the AgrC pathway.
    • Testosterone directly interacts with AgrC, influencing bacterial communication and virulence.
    • Targeting the testosterone-AgrC interaction presents a novel therapeutic avenue for managing S. aureus skin infections.