ArticleInfection and immunity2014
Activation of NLRP3 and AIM2 inflammasomes by Porphyromonas gingivalis infection.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers, 1 of them a synthesis that pooled it.
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Who cites it
122 citing papers in PubMed, 1 synthesis or guideline pooled it, 218 citations in OpenAlex.
- Host-Bacterium Interaction Mechanisms inInternational journal of molecular sciences · 2023Pooled it
- Redefining the Evolution of Pulpal Pathology: Inflammasomes as Central Integrative Hubs and Biological Switches Governing the Transition From Reversible to Irreversible Pulpal Inflammation Beyond Symptom-Based Classification.International endodontic journal · 2026Review
- Polymicrobial-driven NLRP6 inflammasome regulates IL-1β production and alveolar bone loss in a murine model of periodontitis.PLoS pathogens · 2026Article
- Integrating machine learning and multi-omics analysis to identify and validate key genes associated with periodontitis.Acta odontologica Scandinavica · 2026Article
- NLRP3 inflammasome promotes PAD2/PAD4 release and protein citrullination in rheumatoid arthritis.Communications biology · 2026Article
- The Oral-Gut-Brain Axis: From Periodontal Dysbiosis to Neuroinflammation-Mechanistic Pathways, Salivary and Intestinal Biomarkers, and Therapeutic Targets: A Narrative Review.Dentistry journal · 2026Review
- Durumamide A Inhibits NLRP3 Assembly, Limiting Pro-Inflammatory Signaling in Human Gingival Fibroblasts.Journal of periodontal research · 2026Article
- Microbial crosstalk along the oral-gut axis: organ-specific oncogenic adaptations of Porphyromonas gingivalis and Fusobacterium nucleatum.Neoplasia (New York, N.Y.) · 2026Review
- Salivary Biomarkers of Inflammasome Activation in Unstable Periodontitis: A Case-Control Study.European journal of dentistry · 2026Article
- Harnessing Microbiome-Mediated and Macrophage-Driven Mechanisms for Oral Wound Healing.Microorganisms · 2026Review
- Evaluation of the conserved subunit of the pathogenicMicrobiology spectrum · 2026Article
- Targeting pyroptosis in periodontitis: mechanisms and therapeutic strategies.Frontiers in immunology · 2026Review
- The Role of Inflammasomes in Chronic Oral Inflammatory Disease and Oral Cancer: A Narrative Review.Dentistry journal · 2025Review
- Inflammatory parameters in gingival crevicular fluid and saliva of patients with celiac disease: a comparative analysis.Clinical oral investigations · 2025Article
- AIM2 and IFI16 as nucleic acid sensors in Periodontitis-Driven systemic inflammation: emerging evidence and therapeutic implications.Clinical oral investigations · 2025Review
- Effect of nonsurgical periodontal treatment on NLRP3, Nrf2, Caspase-1, interleukin-1B, interleukin-18 in gingival crevicular fluid of severe periodontitis.Clinical oral investigations · 2025Article
- Current Landscape of the Interrelationship Between Periodontitis, Type 2 Diabetes Mellitus, and COVID-19.International journal of molecular sciences · 2025Review
- Dual role mechanisms of regulated cell death in apical periodontitis: from pathogenic destruction to therapeutic potential.Cell death discovery · 2025Review
- What would it take to prove that a chronic infection is a causal agent in Alzheimer's disease?Trends in neurosciences · 2025Review
- Corylin ameliorates inflammaging and pyroptosis in diabetic periodontitis: A preliminaryJournal of dental sciences · 2025Article
62 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porphyromonas gingivalis, a major periodontopathogen, is involved in the pathogenesis of periodontitis. Interleukin-1β (IL-1β), a proinflammatory cytokine, regulates innate immune responses and is critical for the host defense against bacterial infection. However, excessive IL-1β is linked to periodontal destruction. IL-1β synthesis, maturation, and secretion are tightly regulated by Toll-like receptor (TLR) signaling and inflammasome activation. We found much higher levels of inflammasome components in the gingival tissues from patients with chronic periodontitis than in those from healthy controls. To investigate the molecular mechanisms by which P. gingivalis infection causes IL-1β secretion, we examined the characteristics of P. gingivalis-induced signaling in differentiated THP-1 cells. We found that P. gingivalis induces IL-1β secretion and inflammatory cell death via caspase-1 activation. We also found that P. gingivalis-induced IL-1β secretion and pyroptic cell death required both NLRP3 and AIM2 inflammasome activation. The activation of the NLRP3 inflammasome was mediated by ATP release, the P2X7 receptor, and lysosomal damage. In addition, we found that the priming signal via TLR2 and TLR4 activation precedes P. gingivalis-induced IL-1β release. Our study provides novel insight into the innate immune response against P. gingivalis infection which could potentially be used for the prevention and therapy of periodontitis.
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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.