ArticleClinical and experimental immunology2007
The dual role of p55 tumour necrosis factor-alpha receptor in Actinobacillus actinomycetemcomitans-induced experimental periodontitis: host protection and tissue destruction.
Article in Clinical and experimental immunology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 131 citations in OpenAlex.
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- The Effect of Acknowledged and Novel Anti-Rheumatic Therapies on Periodontal Tissues-A Narrative Review.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Natural Killer-Like B Cells Secreting Interleukin-18 Induces a Proinflammatory Response in Periodontitis.Frontiers in immunology · 2021Article
- Investigation of Antibacterial and Antiinflammatory Activities of Proanthocyanidins fromNutrients · 2019Article
- To P or not to P, is that the question? Rethinking experimental design and data analysis to improve biological significance beyond the statistical significance.Journal of applied oral science : revista FOB · 2019Article
- Levels of Pro and Anti-inflammatory Citokynes and C-Reactive Protein in Patients with Chronic Periodontitis Submitted to Nonsurgical Periodontal TreatmentAsian Pacific journal of cancer prevention : APJCP · 2018Article
- RANKL Triggers Treg-Mediated Immunoregulation in Inflammatory Osteolysis.Journal of dental research · 2018Article
- Interleukin-10 polymorphisms affect the key periodontal pathogens in Chinese periodontitis patients.Scientific reports · 2018Article
- NADPH Oxidase Contributes to Resistance against Aggregatibacter actinomycetemcomitans-Induced Periodontitis in Mice.Infection and immunity · 2017Article
- Genes Critical for Developing Periodontitis: Lessons from Mouse Models.Frontiers in immunology · 2017Review
- Simvastatin modulates gingival cytokine and MMP production in a rat model of ligature-induced periodontitis.Clinical, cosmetic and investigational dentistry · 2017Article
- Porphyromonas gulae Has Virulence and Immunological Characteristics Similar to Those of the Human Periodontal Pathogen Porphyromonas gingivalis.Infection and immunity · 2016Article
- Lack of Proinflammatory Cytokine Interleukin-6 or Tumor Necrosis Factor Receptor-1 Results in a Failure of the Innate Immune Response after Bacterial Meningitis.Mediators of inflammation · 2016Article
- Intragingival injection of Porphyromonas gingivalis-derived lipopolysaccharide induces a transient increase in gingival tumour necrosis factor-α, but not interleukin-6, in anaesthetised rats.International journal of oral science · 2015Article
- IL-4/CCL22/CCR4 axis controls regulatory T-cell migration that suppresses inflammatory bone loss in murine experimental periodontitis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2015Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory immune reactions in response to periodontopathogens are thought to protect the host against infection, but may trigger periodontal destruction. Thus, we examined the mechanisms by which the proinflammatory cytokine tumour necrosis factor (TNF)-alpha modulates the outcome of Actinobacillus actinomycetemcomitans-induced periodontal disease in mice. Our results showed that TNF-alpha receptor p55-deficient mice [p55TNF-knock-out (KO)] developed a less severe periodontitis in response to A. actinomycetemcomitans infection, characterized by significantly less alveolar bone loss and inflammatory reaction. Real-time polymerase chain reaction (PCR) demonstrated that levels of chemokines (CXCL1, 3 and 10; CCL3 and 5) and their receptors (CXCR2 and 3, CCR5) were lower in p55TNF-KO mice, as were matrix metalloproteinase (MMP)-1, 2 and 9 and receptor activator of nuclear factor kB ligand (RANKL) mRNA levels. However, the absence of the TNF-alpha p55 results in an impairment of protective immunity to A. actinomycetemcomitans infection, characterized by increased bacterial load and higher levels of C-reactive protein during the course of disease. Such impaired host response may be the result of the reduced chemoattraction of lymphocytes, neutrophils and macrophages, and reduced inducible nitric oxide synthase expression (iNOS) and myeloperoxidase (MPO) production in periodontal tissues of p55 TNF-KO mice. Our results demonstrate the mechanisms involved determining periodontal disease severity by TNF-alpha receptor p55, and its role in providing immune protection to A. actinomycetemcomitans periodontal infection.
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