ArticleNature communications2026
Collagen binding adhesin restricts Staphylococcus aureus skin infection.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Comparative genomics reveals polyphyletic emergence of methicillin-resistant Staphylococcus aureus ST152 from a diverse methicillin-susceptible population in ghana.BMC microbiology · 2026Article
- Nanofibrous Platforms for Advanced Wound Therapeutics: Mechanisms, Materials, and Clinical Horizons.Macromolecular bioscience · 2026Review
- Microbial allies in skin trauma recovery: from immune modulation to engineered probiotic therapeutics.Burns & trauma · 2026Review
- Extracellular adherence proteins reduce matrix porosity and enhanceInfection and immunity · 2025Article
- Glycan-mediated adhesion mechanisms in antibiotic-resistant bacteria.BBA advances · 2025Article
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9 authors.
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Abstract
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, LTB
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