ArticleCellular microbiology2016
Fusobacterium nucleatum infection of gingival epithelial cells leads to NLRP3 inflammasome-dependent secretion of IL-1β and the danger signals ASC and HMGB1.
Article in Cellular microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.
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Who cites it
81 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The oral bacterial microbiota change in oral squamous cell carcinoma: a systematic review and meta-analysis.BMC oral health · 2026Pooled it
- IsGut microbes · 2026Review
- Interleukin-6 as an Oral-Vascular Inflammatory Bridge: Integrating CXCL10 and Haptoglobin 2-2 into a Potential Model of Periodontitis-Associated Cardiovascular Risk.International journal of molecular sciences · 2026Review
- Dual-Targeting, Hybrid Antifungal Agents Targeting Candida albicans-An Overview.Chemical biology & drug design · 2026Review
- Integrative analysis identifies the intratumoral Fusobacterium nucleatum as a driver of cervical cancer malignancy.BMC biotechnology · 2026Article
- Fusobacterium nucleatum exacerbates chronic atrophic gastritis in rats via mitochondrial dysfunction and inflammatory activation.BMC gastroenterology · 2026Article
- Fusobacterium nucleatum in cancer: Interactions with microbiota, tumour colonisation and cancer progression.Clinical and translational medicine · 2026Review
- Targeted repair of oral mucosal injury: emerging applications of biomaterials-based drug delivery systems.Journal of nanobiotechnology · 2026Review
- Emerging Role of the NLRP3 Inflammasome in the Onset of Oral Diseases and Its Potential as a Therapeutic Target.International journal of molecular sciences · 2026Review
- Salivary and serum levels of high mobility group box protein 1 in periodontitis: a cross-sectional observational study.BMC oral health · 2025Observational
- 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
- Recent advancements in artificial intelligence-powered cancer prediction from oral microbiome.Periodontology 2000 · 2025Review
- Matrix Dynamics and Microbiome Crosstalk: Matrix Metalloproteinases as Key Players in Disease and Therapy.International journal of molecular sciences · 2025Review
- Review
- Periodontal pathogens and cancer development.Periodontology 2000 · 2024Review
- NLRP3 inflammasome activity and periodontal disease pathogenesis-A bidirectional relationship.Oral diseases · 2024Review
- Dying for a cause: The pathogenic manipulation of cell death and efferocytic pathways.Molecular oral microbiology · 2024Review
- Frankincense (Current issues in molecular biology · 2024Article
- Insights into the oral microbiota in human systemic cancers.Frontiers in microbiology · 2024Review
- Oral microbiota and oral squamous cell carcinoma: a review of their relation and carcinogenic mechanisms.Frontiers in oncology · 2024Review
21 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Fusobacterium nucleatum is an invasive anaerobic bacterium that is associated with periodontal disease. Previous studies have focused on virulence factors produced by F. nucleatum, but early recognition of the pathogen by the immune system remains poorly understood. Although an inflammasome in gingival epithelial cells (GECs) can be stimulated by danger-associated molecular patterns (DAMPs) (also known as danger signals) such as ATP, inflammasome activation by this periodontal pathogen has yet to be described in these cells. This study therefore examines the effects of F. nucleatum infection on pro-inflammatory cytokine expression and inflammasome activation in GECs. Our results indicate that infection induces translocation of NF-κB into the nucleus, resulting in cytokine gene expression. In addition, infection activates the NLRP3 inflammasome, which in turn activates caspase-1 and stimulates secretion of mature IL-1β. Unlike other pathogens studied until now, F. nucleatum activates the inflammasome in GECs in the absence of exogenous DAMPs such as ATP. Finally, infection promotes release of other DAMPs that mediate inflammation, such as high-mobility group box 1 protein and apoptosis-associated speck-like protein, with a similar time-course as caspase-1 activation. Thus, F. nucleatum expresses the pathogen-associated molecular patterns necessary to activate NF-κB and also provides an endogenous DAMP to stimulate the inflammasome and further amplify inflammation through secretion of secondary DAMPs.
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