ArticleInfection and immunity2003
Streptococcus pyogenes infection induces septic arthritis with increased production of the receptor activator of the NF-kappaB ligand.
Article in Infection and immunity, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 41 citations in OpenAlex.
- Streptococcal Toxic Shock Syndrome (STSS) Secondary to Monoarticular Septic Arthritis Leading to Multiorgan Failure in a Patient without Underlying Comorbidities: Emphasizing Early Diagnosis and Management Strategies.Infectious disorders drug targets · 2025Article
- Exploring the role of bacterial virulence factors and host elements in septic arthritis: insights from animal models for innovative therapies.Frontiers in microbiology · 2024Review
- Echinacoside Inhibits Osteoclast Function by Down-Regulating PI3K/Akt/C-Fos to Alleviate Osteolysis Caused by Periprosthetic Joint Infection.Frontiers in pharmacology · 2022Article
- Degenerative Joint Damage Is Not a Risk Factor for Streptococcal Sepsis and Septic Arthritis in Mice.Life (Basel, Switzerland) · 2021Article
- Regulation of Bone Cell Differentiation and Activation by Microbe-Associated Molecular Patterns.International journal of molecular sciences · 2021Review
- Inflammatory Joint Disease Is a Risk Factor for Streptococcal Sepsis and Septic Arthritis in Mice.Frontiers in immunology · 2020Article
- Streptolysin O derived from Streptococcus pyogenes inhibits RANKL‑induced osteoclastogenesis through the NF‑κB signaling pathway.Molecular medicine reports · 2019Article
- Defining Host Responses during Systemic Bacterial Infection through Construction of a Murine Organ Proteome Atlas.Cell systems · 2018Article
- Dual neutralization of TNFR-2 and MMP-2 regulates the severity of S. aureus induced septic arthritis correlating alteration in the level of interferon gamma and interleukin-10 in terms of TNFR2 blocking.Immunologic research · 2018Article
- Effect of hyperbaric oxygen therapy on tooth extraction sites in rats subjected to bisphosphonate therapy-histomorphometric and immunohistochemical analysis.Clinical oral investigations · 2017Article
- Brucella abortus invasion of synoviocytes inhibits apoptosis and induces bone resorption through RANKL expression.Infection and immunity · 2013Article
- Specific behavior of intracellular Streptococcus pyogenes that has undergone autophagic degradation is associated with bacterial streptolysin O and host small G proteins Rab5 and Rab7.The Journal of biological chemistry · 2010Article
- The ScpC protease of Streptococcus pyogenes affects the outcome of sepsis in a murine model.Infection and immunity · 2008Article
- CD46 Contributes to the severity of group A streptococcal infection.Infection and immunity · 2008Article
- Inflammatory cells and bone loss in rheumatoid arthritis.Arthritis research & therapy · 2007Review
- The cytolethal distending toxin induces receptor activator of NF-kappaB ligand expression in human gingival fibroblasts and periodontal ligament cells.Infection and immunity · 2005Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bacterial arthritis is a rapidly progressive and highly destructive joint disease in humans, with Staphylococcus aureus and Neisseria gonorrhoeae the major causative agents, although beta-hemolytic streptococci as well often induce the disease. We demonstrate here that intravenous inoculation of CD-1 mice with the group A streptococcus (GAS) species Streptococcus pyogenes resulted in a high incidence of septic arthritis. Signs of arthritis emerged within the first few days after injection, and bacterial examinations revealed that colonization of the inoculated GAS in the arthritic joints persisted for 21 days. Induction of persistent septic arthritis was dependent on the number of microorganisms inoculated. Immunohistochemical staining of GAS with anti-GAS antibodies revealed colonization in the joints of infected mice. Cytokine levels were quantified in the joints and sera of infected mice by using an enzyme-linked immunosorbent assay. High levels of interleukin-1beta (IL-1beta) and IL-6 were detected in the joints from 3 to 20 days after infection. We noted that an increase in the amount of receptor activator of NF-kappaB ligand (RANKL), which is a key cytokine in osteoclastogenesis, was also evident in the joints of the infected mice. RANKL was not detected in sera, indicating local production of RANKL in the infected joints. Blocking of RANKL by osteoprotegerin, a decoy receptor of RANKL, prevented bone destruction in the infected joints. These results suggest that GAS can colonize in the joints and induce bacterial arthritis. Local RANKL production in the infected joints may be involved in bone destruction.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.