Scholarlink

<p>Skin cells secrete testosterone, with greater amounts secreted at the skin surface of males compared with females. Males are also more susceptible to skin infections than females. Here we report that mice engineered with testosterone-deficient skin are resistant to methicillin-resistant <i>Staphylococcus aureus</i> infections. Testosterone promoted the expression of <i>S. aureus</i> cytotoxic virulence factors by activating the accessory gene regulator (<i>agr</i>) quorum-sensing pathway in a concentration-dependent manner and independent of quorum-sensing-activating auto-inducing peptides. Mutational analysis revealed that a functional histidine kinase AgrC in <i>S. aureus</i> was required for testosterone to exert its effect, with in silico evidence indicating a direct interaction between testosterone and AgrC. An isomer of testosterone, enantiomer-testosterone, that blocked bacterial quorum sensing, inhibited <i>S. aureus</i>-induced cytotoxicity of human cells. These findings advance our understanding of how the skin regulates bacterial virulence and reveals a potential therapeutic strategy for the management of infections.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Skin androgens regulate Staphylococcus aureus pathogenicity via quorum sensing

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月27日

查看全文
  • Maria Sindhura John,
  • Mahendran Chinnappan,
  • Camille I. Sturges,
  • Methinee Artami,
  • Mohini Bhattacharya,
  • Rebecca A. Keogh,
  • Jeffrey S. Kavanaugh,
  • Shivani Jain,
  • Hanna Gedamu,
  • Jessica Komarovsky,
  • Mauricio Velasquez,
  • Tripti Sharma,
  • Jeffrey G. McDonald,
  • Alexander R. Horswill,
  • Tamia A. Harris-Tryon

摘要

Skin cells secrete testosterone, with greater amounts secreted at the skin surface of males compared with females. Males are also more susceptible to skin infections than females. Here we report that mice engineered with testosterone-deficient skin are resistant to methicillin-resistant Staphylococcus aureus infections. Testosterone promoted the expression of S. aureus cytotoxic virulence factors by activating the accessory gene regulator (agr) quorum-sensing pathway in a concentration-dependent manner and independent of quorum-sensing-activating auto-inducing peptides. Mutational analysis revealed that a functional histidine kinase AgrC in S. aureus was required for testosterone to exert its effect, with in silico evidence indicating a direct interaction between testosterone and AgrC. An isomer of testosterone, enantiomer-testosterone, that blocked bacterial quorum sensing, inhibited S. aureus-induced cytotoxicity of human cells. These findings advance our understanding of how the skin regulates bacterial virulence and reveals a potential therapeutic strategy for the management of infections.