ArticlePLoS pathogens2012
Direct recognition of Fusobacterium nucleatum by the NK cell natural cytotoxicity receptor NKp46 aggravates periodontal disease.
Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.
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Who cites it
86 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.
- Influence of Natural Killer Cells and Natural Killer T Cells on Periodontal Disease: A Systematic Review of the Current Literature.International journal of molecular sciences · 2020Pooled it
- Amino acid metabolic reprogramming by gut microbiota: a novel metabolic checkpoint in the tumor microenvironment.Gut microbes · 2026Review
- Fusobacterium nucleatum in cancer: Interactions with microbiota, tumour colonisation and cancer progression.Clinical and translational medicine · 2026Review
- The Silent Link: Exploring the Impact of Periodontal Diseases on Head and Neck Carcinogenesis.Clinical and experimental dental research · 2026Review
- RadD fromeLife · 2026Article
- Cadherin-11 serves as a novel receptor for Fusobacterium nucleatum adhesin FadA to exacerbate pulmonary inflammation.PLoS pathogens · 2026Article
- Mucosal immunity in cancer metastasis: roles, mechanisms, and therapeutic implications.Frontiers in immunology · 2026Review
- Exploring Matrix Stiffness-Related Gene in Periodontitis: A Comprehensive Multidataset Analysis.Mediators of inflammation · 2026Article
- The outer membrane autotransporters Fap2 and CmpA facilitate specific coaggregation betweenApplied and environmental microbiology · 2025Article
- Characterization of the OMP biogenesis machinery in Fusobacterium nucleatum.Structure (London, England : 1993) · 2025Article
- Review
- NKp46 recognizes the hyphal form of Candida albicans and mediates protective antifungal immunity.iScience · 2025Article
- Periodontitis-associated Fusobacterium nucleatum promotes ulcerative colitis by ferroptosis-mediated gut barrier disruption.NPJ biofilms and microbiomes · 2025Article
- Infectious and Immunological Links Between Periodontitis and COVID-19: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2025Review
- Linking microRNA to metabolic reprogramming and gut microbiota in the pathogenesis of colorectal cancer (Review).International journal of molecular medicine · 2025Review
- Bioinspired nano-micron hydrogel microspheres for periodontitis therapy through synergistic multi-targeted remodeling of microenvironment.Theranostics · 2025Article
- Investigation of the relationship betweenFrontiers in microbiology · 2025Article
- Proteomics reveals periodontitis-driven oxidative stress and lipid metabolism disruption in NAFLD.Frontiers in endocrinology · 2025Article
- Microbiota-immune dysregulation in cervical cancer patients from Western Mexico: linking gut dysbiosis and NK cell exhaustion as promising biomarkers.Frontiers in immunology · 2025Article
- Inflammation and mechanical force-induced bone remodeling.Periodontology 2000 · 2024Review
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Periodontitis is a common human chronic inflammatory disease that results in the destruction of the tooth attachment apparatus and tooth loss. Although infections with periopathogenic bacteria such as Porphyromonas gingivalis (P. gingivalis) and Fusobacterium nucleatum (F. nucleatum) are essential for inducing periodontitis, the nature and magnitude of the disease is determined by the host's immune response. Here, we investigate the role played by the NK killer receptor NKp46 (NCR1 in mice), in the pathogenesis of periodontitis. Using an oral infection periodontitis model we demonstrate that following F. nucleatum infection no alveolar bone loss is observed in mice deficient for NCR1 expression, whereas around 20% bone loss is observed in wild type mice and in mice infected with P. gingivalis. By using subcutaneous chambers inoculated with F. nucleatum we demonstrate that immune cells, including NK cells, rapidly accumulate in the chambers and that this leads to a fast and transient, NCR1-dependant TNF-α secretion. We further show that both the mouse NCR1 and the human NKp46 bind directly to F. nucleatum and we demonstrate that this binding is sensitive to heat, to proteinase K and to pronase treatments. Finally, we show in vitro that the interaction of NK cells with F. nucleatum leads to an NCR1-dependent secretion of TNF-α. Thus, the present study provides the first evidence that NCR1 and NKp46 directly recognize a periodontal pathogen and that this interaction influences the outcome of F. nucleatum-mediated periodontitis.
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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.