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Updated: Jan 25, 2026
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Development and Assessment of Intracellular Infection Models for Staphylococcus aureus
Published on: January 17, 2025
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Collagen binding adhesin restricts Staphylococcus aureus skin infection
Mohini Bhattacharya1, Brady L Spencer1,2, Jakub M Kwiecinski3
1Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, USA.
Nature Communications
|January 23, 2026
Summary
Staphylococcus aureus collagen adhesin (Cna) worsens skin infections by inhibiting immune responses. Blocking Cna binding to collagen improves bacterial clearance and reduces pathology.
Area of Science:
- Microbiology
- Immunology
- Dermatology
Background:
- Staphylococcus aureus is a primary cause of skin and soft tissue infections (SSTIs).
- Collagen, a key extracellular matrix protein, is vital for wound healing.
- S. aureus possesses a collagen adhesin (Cna) whose role in skin infections remains unclear.
Purpose of the Study:
- To investigate the role of Staphylococcus aureus collagen adhesin (Cna) in the pathogenesis of skin infections.
- To elucidate the mechanism by which Cna influences the host immune response during intradermal S. aureus infections.
Main Methods:
- Generation and characterization of a Δcna S. aureus mutant.
- Intradermal infection models using wild-type (WT) and Δcna S. aureus in mice.
- Assessment of bacterial load, pathology, immune cell infiltration, and inflammatory mediators.
- Investigation of Cna interaction with serum C1q protein.
Main Results:
- Loss of Cna binding to collagen resulted in worsened pathology and increased bacterial burden in intradermal infections.
- WT S. aureus expressing Cna exhibited reduced infection severity and enhanced bacterial clearance compared to Δcna mutants.
- Cna was found to bind serum C1q, inhibiting its opsonophagocytic functions.
- Infection of C1q-deficient mice with WT bacteria mimicked the exacerbated pathology observed in Δcna infections.
- Impaired collagen binding led to an amplified inflammatory response, characterized by increased immune cell infiltration and elevated levels of mediators like MMP-9, MMP-12, and LTB4.
Conclusions:
- Staphylococcus aureus collagen adhesin (Cna) plays a significant role in promoting skin infection severity.
- Cna contributes to immune evasion by inhibiting the opsonophagocytic activity of serum C1q.
- Targeting Cna represents a potential therapeutic strategy to enhance bacterial clearance and reduce pathology in S. aureus skin infections.
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