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Comparative analysis of immune cell subsets in peripheral blood from patients with periodontal disease and healthy controls

Research output: Contribution to journalArticle

Original languageEnglish
Pages (from-to)380-390
Number of pages11
JournalClinical & Experimental Immunology
Volume194
Issue number3
Early online date18 Aug 2018
DOIs
Accepted/In press14 Aug 2018
E-pub ahead of print18 Aug 2018
Published2018

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Abstract

Periodontitis is a chronic inflammatory disease caused by the colonisation of teeth by the bacterial plaque biofilm and the resultant host immune responses in adjacent periodontal tissues. Disease severity can vary dramatically between patients with periodontitis, with some subjects displaying inflammation without bony destruction (gingivitis), whilst others experience chronic progressive or rapidly aggressive gingival connective tissue damage and bone loss. To determine whether peripheral immune dysregulation is associated with periodontitis, we performed extensive analysis of immune cell subsets in peripheral blood from patients with chronic or aggressive periodontitis vs. periodontally healthy control subjects. Peripheral blood mononuclear cells (PBMC) from patients with chronic periodontitis or aggressive periodontitis and from periodontally healthy controls were analysed by 8‐10 colour flow cytometry for the frequencies of various lymphocyte subsets, including IL‐17, IFNγ, TNFα and IL‐10 producing cells, and the frequencies and phenotype of monocytes. Cytokine levels in serum from the different groups were determined by Luminex assay. We found no significant differences in the frequencies of major immune cell populations (CD4+ T cells, CD8+ T cells, γδ T cells, CD4+CD45RO+CD25+CD127low regulatory T cells (Tregs), CD19+ B cells, CD14+ monocytes) or of cytokine producing T cells, or in the phenotype of CD14+ monocytes in peripheral blood from these patient cohorts. Additionally, no significant differences were observed in serum levels of prototypical inflammatory cytokines. These results suggest that the local gingival inflammatory response is not reflected by obvious changes in major blood immune cell subset frequencies.

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