Abstract
Survival and function of immune subsets in the oral blood, peripheral blood and gingival tissues of patients with periodontal disease and healthy controls were assessed. NK and CD8 + T cells within the oral blood mononuclear cells (OBMCs) expressed significantly higher levels of CD69 in patients with periodontal disease compared to those from healthy controls. Similarly, TNF-α release was higher from oral blood of patients with periodontal disease when compared to healthy controls. Increased activation induced cell death of peripheral blood mononuclear cells (PBMCs) but not OBMCs from patients with periodontal disease was observed when compared to those from healthy individuals. Unlike those from healthy individuals, OBMC-derived supernatants from periodontitis patients exhibited decreased ability to induce secretion of IFN-γ by allogeneic healthy PBMCs treated with IL-2, while they triggered significant levels of TNF-α, IL-1β and IL-6 by untreated PBMCs. Interaction of PBMCs, or NK cells with intact or NFκB knock down oral epithelial cells in the presence of a periodontal pathogen, F. nucleatum, significantly induced a number of pro-inflammatory cytokines including IFN-γ. These studies indicated that the relative numbers of immune subsets obtained from peripheral blood may not represent the composition of the immune cells in the oral environment, and that orally-derived immune effectors may differ in survival and function from those of peripheral blood.
Highlights
Periodontitis is an inflammatory disease affecting the supporting tissues of the tooth, and is characterized by a wide range of clinical, microbiological and immunological manifestations [1]
Limited knowledge is available about the function, biology and phenotypic properties of oral blood and immune cells infiltrating the gingival tissues, and their comparison with immune cells within the peripheral blood; it is clear that pathogenesis of periodontitis is complex and involves both innate and adaptive immune responses [6,7]
In this paper we investigated the cell surface receptor expression, activation markers, cytokine secretion and cell death profiles of mononuclear cells obtained from peripheral blood, oral blood and gingival tissues of healthy individuals and patients with periodontitis when they were left untreated or treated with interleukin 2 (IL-2), interferon-gamma (IFNγ) and phorbol myristate acetate (PMA)/ionomycin (I)
Summary
Periodontitis is an inflammatory disease affecting the supporting tissues of the tooth, and is characterized by a wide range of clinical, microbiological and immunological manifestations [1]. Several established causes of periodontitis relate to the imbalance in microbial organisms, heightened host’s inflammatory and immune responses and a series of environmental and genetic factors [1,4,5]. Limited knowledge is available about the function, biology and phenotypic properties of oral blood and immune cells infiltrating the gingival tissues, and their comparison with immune cells within the peripheral blood; it is clear that pathogenesis of periodontitis is complex and involves both innate and adaptive immune responses [6,7]. Many NF-kB-induced pathways are known to be involved in periodontal diseases [9,10]
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