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<p><i>Staphylococcus aureus</i> causes approximately 80% of skin and soft tissue infections (SSTIs). Collagen is the most abundant human extracellular matrix protein with critical roles in wound healing, and <i>S. aureus</i> encodes a collagen binding adhesin (Cna). The role of this protein during skin infections is unknown. Here we report that inability to bind collagen results in worsened pathology of intradermal Δ<i>cna S. aureus</i> infection. WT/Cna+ <i>S. aureus</i> shows reduced infection severity, aggregate formation, and significantly improves clearance of bacteria. Cna binds to the collagen-like domain of serum C1q protein to reduce its opsonophagocytic functions. We demonstrate that infection of C1qKO mice with WT bacteria show results similar to the Δ<i>cna</i> group. Conversely, inability to bind collagen results in an amplified inflammatory response caused in part by macrophage and neutrophil small molecule mediators released at the infection site (MMP-9, MMP-12, LTB<sub>4</sub>), leading to increased immune cell infiltration and death.</p>

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Collagen binding adhesin restricts Staphylococcus aureus skin infection

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月23日

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  • Mohini Bhattacharya,
  • Brady L. Spencer,
  • Jakub M. Kwiecinski,
  • Magdalena Podkowik,
  • Gregory Putzel,
  • Alejandro Pironti,
  • Bo Shopsin,
  • Kelly S. Doran,
  • Alexander R. Horswill

摘要

Staphylococcus aureus causes approximately 80% of skin and soft tissue infections (SSTIs). Collagen is the most abundant human extracellular matrix protein with critical roles in wound healing, and S. aureus encodes a collagen binding adhesin (Cna). The role of this protein during skin infections is unknown. Here we report that inability to bind collagen results in worsened pathology of intradermal Δcna S. aureus infection. WT/Cna+ S. aureus shows reduced infection severity, aggregate formation, and significantly improves clearance of bacteria. Cna binds to the collagen-like domain of serum C1q protein to reduce its opsonophagocytic functions. We demonstrate that infection of C1qKO mice with WT bacteria show results similar to the Δcna group. Conversely, inability to bind collagen results in an amplified inflammatory response caused in part by macrophage and neutrophil small molecule mediators released at the infection site (MMP-9, MMP-12, LTB4), leading to increased immune cell infiltration and death.