ArticleInternational journal of oral science2024
Caspase-11 mediated inflammasome activation in macrophages by systemic infection of A. actinomycetemcomitans exacerbates arthritis.
Article in International journal of oral science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Pathogens in rheumatoid arthritis: epidemiological, mechanistic, and clinical insights.Biomarker research · 2026Review
- Periodontitis and Rheumatoid Arthritis: Shared Pathophysiology, Bidirectional Association, and Therapeutic Implications-A Narrative Review.Healthcare (Basel, Switzerland) · 2026Review
- Porphyromonas gingivalis-derived extracellular vesicles aggravate bone destruction in rheumatoid arthritis by promoting Syk-dependent osteoclastogenesis.International journal of oral science · 2026Article
- Periodontitis and MASLD: a narrative review of the direct oral-hepatic pathway.Frontiers in cellular and infection microbiology · 2026Review
- Review
- Salidroside: A Potential Drug Candidate to Treat Rheumatoid Arthritis.Molecules (Basel, Switzerland) · 2025Review
- Hypoxia drives progression of multiple sclerosis by enhancing the inflammasome activation in macrophages with Porphyromonas gingivalis infection.Cell death discovery · 2025Article
- The Oral-Gut Microbiome-Brain Axis in Cognition.Microorganisms · 2025Review
- Immunological landscape of periodontitis and rheumatoid arthritis and their molecular crosstalk.European journal of medical research · 2025Article
- Mechanistic pathways predictive modeling and translational interventions for radiation enteritis in cervical cancer radiotherapy.Frontiers in cellular and infection microbiology · 2025Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Clinical studies have shown that Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) is associated with aggressive periodontitis and can potentially trigger or exacerbate rheumatoid arthritis (RA). However, the mechanism is poorly understood. Here, we show that systemic infection with A. actinomycetemcomitans triggers the progression of arthritis in mice anti-collagen antibody-induced arthritis (CAIA) model following IL-1β secretion and cell infiltration in paws in a manner that is dependent on caspase-11-mediated inflammasome activation in macrophages. The administration of polymyxin B (PMB), chloroquine, and anti-CD11b antibody suppressed inflammasome activation in macrophages and arthritis in mice, suggesting that the recognition of lipopolysaccharide (LPS) in the cytosol after bacterial degradation by lysosomes and invasion via CD11b are needed to trigger arthritis following inflammasome activation in macrophages. These data reveal that the inhibition of caspase-11-mediated inflammasome activation potentiates aggravation of RA induced by infection with A. actinomycetemcomitans. This work highlights how RA can be progressed by inflammasome activation as a result of periodontitis-associated bacterial infection and discusses the mechanism of inflammasome activation in response to infection with A. actinomycetemcomitans.
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Registered trials
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