Hyper-reactive mononuclear cells and neutrophils in chronic periodontitis
- PMID: 16441737
- DOI: 10.1111/j.1600-051X.2005.00883.x
Hyper-reactive mononuclear cells and neutrophils in chronic periodontitis
Abstract
Objectives: Stimulated mono- and polymorphonuclear cells from patients with periodontitis have shown increased release of interleukin-1beta (IL-1beta) and oxygen radicals, respectively. The aim was to study whether this hyper-reactivity could be found both in mono- and polymorphonuclear cells from the same patient, and whether there was a relation to the gene coding for IL-1beta (IL-1beta(+3953)).
Material and methods: Peripheral mononuclear cells from 14 non-smoking and well-treated patients and pair-matched controls were incubated with opsonized Staphylococcus aureus and lipopolysaccharide (LPS). Released IL-1beta and tumour necrosis factor (TNF)-alpha were determined with ELISA. Generation of oxygen radicals from the Fcgamma-receptor-stimulated neutrophils was measured with chemiluminescence and the polymorphism at IL-1beta(+3953) was measured with polymerase chainreaction.
Results: The mononuclear cells from the patients released more IL-1beta after incubation with LPS (p<0.001) and with bacteria (p<0.05). The release of TNF-alpha tended to be higher in the patient group. The peripheral neutrophils from the patients generated more oxygen radicals (p<0.06). We found no differences between the study groups regarding the IL-1beta(+3953) polymorphism.
Conclusion: The similarity in systemic inflammation between patients and controls suggests that the increased release/generation of IL-1beta and oxygen radicals from peripheral leukocytes in periodontitis patients is of a constitutional nature and of pathogenic relevance.
Similar articles
-
Effect of priming in subpopulations of peripheral neutrophils from patients with chronic periodontitis.J Periodontol. 2012 Sep;83(9):1192-9. doi: 10.1902/jop.2012.110584. Epub 2012 Jan 16. J Periodontol. 2012. PMID: 22248218
-
Constitutionally hyperreactive neutrophils in periodontitis.J Periodontol. 2003 Feb;74(2):219-24. doi: 10.1902/jop.2003.74.2.219. J Periodontol. 2003. PMID: 12666711
-
Hyperactivity and reactivity of peripheral blood neutrophils in chronic periodontitis.Clin Exp Immunol. 2007 Feb;147(2):255-64. doi: 10.1111/j.1365-2249.2006.03276.x. Clin Exp Immunol. 2007. PMID: 17223966 Free PMC article.
-
[Polymorphonuclear neutrophilic granulocytes and the defense and damage of periodontal tissues].Minerva Stomatol. 1989 Jul;38(7):783-94. Minerva Stomatol. 1989. PMID: 2677651 Review. Italian.
-
Activation of interleukin 1beta gene transcription by human cytomegalovirus: molecular mechanisms and relevance to periodontitis.Oral Microbiol Immunol. 2003 Apr;18(2):67-71. doi: 10.1034/j.1399-302x.2003.00053.x. Oral Microbiol Immunol. 2003. PMID: 12654093 Review.
Cited by
-
Systemic chemical desensitization of peptidergic sensory neurons with resiniferatoxin inhibits experimental periodontitis.Open Dent J. 2011 Jan 6;5:1-6. doi: 10.2174/1874210601105010001. Open Dent J. 2011. PMID: 21339860 Free PMC article.
-
Gene polymorphisms in chronic periodontitis.Int J Dent. 2010;2010:324719. doi: 10.1155/2010/324719. Epub 2010 Feb 9. Int J Dent. 2010. PMID: 20339487 Free PMC article.
-
Neutrophils Orchestrate the Periodontal Pocket.Front Immunol. 2021 Nov 24;12:788766. doi: 10.3389/fimmu.2021.788766. eCollection 2021. Front Immunol. 2021. PMID: 34899756 Free PMC article. Review.
-
Advances of Oxidative Stress Impact in Periodontitis: Biomarkers and Effective Targeting Options.Curr Med Chem. 2024;31(38):6187-6203. doi: 10.2174/0109298673297545240507091410. Curr Med Chem. 2024. PMID: 38726786 Review.
-
Activation of the Nrf2 Signaling Pathway as a Therapeutic Strategy Against Periodontal Disease: A Narrative Review.Dent J (Basel). 2025 Jul 11;13(7):314. doi: 10.3390/dj13070314. Dent J (Basel). 2025. PMID: 40710159 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources