ArticleCommunications biology2025
Staphylococcus aureus thermonuclease NucA is a key virulence factor in septic arthritis.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Osteomyelitis: Epidemiology, Classification, Pathophysiology, Clinical Features, Diagnosis, and Management.MedComm · 2026Review
- Time-associated phenotypic changes related to virulence and immune interaction of Staphylococcus aureus during relapsing infection within individual hosts.BMC infectious diseases · 2026Article
- E2F5 Overexpression in Laryngeal Squamous Cell Carcinoma: Associations With Neutrophil Extracellular Traps in the Tumor Microenvironment.World journal of oncology · 2026Article
- Extracellular Vesicle-Mimetic Nanoplatforms for Integrated Vaccination and Targeted Antibiotic Therapy against MRSA Bacteremia: A Wolf in Sheep's Clothing.Biomaterials research · 2026Article
- Genomic insights into multidrug resistance and virulence of methicillin-resistantFrontiers in veterinary science · 2026Article
- Advancing virulence factor prediction using protein language models.BMC biology · 2025Article
- Bacterial and host interactions inFrontiers in microbiology · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Septic arthritis, primarily caused by Staphylococcus aureus, poses a significant risk of both mortality and morbidity due to its aggressive nature. The nuc1-encoded thermonuclease NucA of S. aureus degrades extracellular DNA/RNA, allowing the pathogen to escape neutrophil extracellular traps (NETs) and maintain the infection unabated. Here we show that in the mouse model for hematogenous septic arthritis, the Δnuc1 mutant is much less pathogenic and the severity of clinical septic arthritis is markedly reduced, including decreased weight loss, lower kidney bacterial load, reduced bone erosion, and much less IL-6 production. In vitro, S. aureus genomic DNA induces a robust TNF-α response in macrophage-like RAW 264.7 cells abrogated when the DNA is degraded by NucA. Moreover, the wild type induces high levels of TNF-α, IL-10, and IL-6 in neutrophils and osteoblast-like SAOS-2 cells, respectively. NucA exacerbates septic arthritis by increasing extracellular and intracellular survival of bacteria.
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