ArticleCellular microbiology2010
ATP-dependent activation of an inflammasome in primary gingival epithelial cells infected by Porphyromonas gingivalis.
Article in Cellular microbiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
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Who cites it
89 citing papers in PubMed, 146 citations in OpenAlex.
- Host-microbiome-immune disequilibrium in oral disease: mechanisms, dysbiosis, and precision therapeutics.Frontiers in immunology · 2026Review
- Shear stress-triggered adenosine triphosphate regulates angiogenic properties of human periodontal ligament stem cells.Scientific reports · 2025Article
- Porphyromonas gingivalis Induces Chronic Kidney Disease through Crosstalk between the NF-κB/NLRP3 Pathway and Ferroptosis in GMCs.Current medical science · 2024Article
- NLRP3 inflammasome activity and periodontal disease pathogenesis-A bidirectional relationship.Oral diseases · 2024Review
- Frankincense (Current issues in molecular biology · 2024Article
- NFκB and NLRP3/NLRC4 inflammasomes regulate differentiation, activation and functional properties of monocytes in response to distinct SARS-CoV-2 proteins.Nature communications · 2024Article
- Biomaterials Functionalized with Inflammasome Inhibitors-Premises and Perspectives.Journal of functional biomaterials · 2024Review
- Alternatives to β-Lactams as Agents for the Management of Dentoalveolar Abscess.Current topics in medicinal chemistry · 2024Review
- AMPK/mTOR/p70S6K axis prevents apoptosis of Porphyromonas gingivalis-infected gingival epithelial cells via BadApoptosis : an international journal on programmed cell death · 2023Article
- Roles of extracellular adenosine triphosphate on the functions of periodontal ligament cells.BDJ open · 2023Review
- Inhibition of LPS‑induced NLRP3 inflammasome activation by stem cell‑conditioned culture media in human gingival epithelial cells.Molecular medicine reports · 2023Article
- Porphyromonas gingivalis infection promotes inflammation via inhibition of the AhR signalling pathway in periodontitis.Cell proliferation · 2023Article
- Complement Is Required for Microbe-Driven Induction of Th17 and Periodontitis.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- The Role of Inflammasome NLPR3 in the Development and Therapy of Periodontitis.International journal of medical sciences · 2022Review
- Inflammasome Activation in Gingival Epithelial Cells.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Differential involvement of the canonical and noncanonical inflammasomes in the immune response against infection by the periodontal bacteriaCurrent research in microbial sciences · 2021Article
- Key Elements of Gingival Epithelial Homeostasis upon Bacterial Interaction.Journal of dental research · 2021Review
- Periodontal Pathogens Promote Oral Squamous Cell Carcinoma by Regulating ATR and NLRP3 Inflammasome.Frontiers in oncology · 2021Article
- NLRP3 Inflammasome Expression in Gingival Crevicular Fluid of Patients with Periodontitis and Chronic Hepatitis C.Mediators of inflammation · 2021Article
- Inflammasomes in Alveolar Bone Loss.Frontiers in immunology · 2021Review
29 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
Abstract
Production of IL-1beta typically requires two-separate signals. The first signal, from a pathogen-associated molecular pattern, promotes intracellular production of immature cytokine. The second signal, derived from a danger signal such as extracellular ATP, results in assembly of an inflammasome, activation of caspase-1 and secretion of mature cytokine. The inflammasome component, Nalp3, plays a non-redundant role in caspase-1 activation in response to ATP binding to P2X(7) in macrophages. Gingival epithelial cells (GECs) are an important component of the innate-immune response to periodontal bacteria. We had shown that GECs express a functional P2X(7) receptor, but the ability of GECs to secrete IL-1beta during infection remained unknown. We find that GECs express a functional Nalp3 inflammasome. Treatment of GECs with LPS or infection with the periodontal pathogen, Porphyromonas gingivalis, induced expression of the il-1beta gene and intracellular accumulation of IL-1beta protein. However, IL-1beta was not secreted unless LPS-treated or infected cells were subsequently stimulated with ATP. Conversely, caspase-1 is activated in GECs following ATP treatment but not P. gingivalis infection. Furthermore, depletion of Nalp3 by siRNA abrogated the ability of ATP to induce IL-1beta secretion in infected cells. The Nalp3 inflammasome is therefore likely to be an important mediator of the inflammatory response in gingival epithelium.
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Registered trials
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.