Abstract
BACKGROUND. The aim of the study was to investigate the effect of (1→3), (1→6)-β-glucan on the production of interleukin 10 (IL-10) and tumor necrosis factor α (TNF-α) in vitro by peripheral blood leukocytes of patients with periodontitis. MATERIAL AND METHODS. In total, 20 patients suffering from untreated severe chronic generalized periodontitis were enrolled in this study. Periodontitis was confirmed by clinical and radiologic examination. Besides, 20 periodontally healthy patients served as a control group. Peripheral venous blood was sampled from the patients, and isolated leukocytes were treated with (1→3),(1→6)-β-glucan from yeast at different concentrations. The levels of IL-10 and TNF-α secreted by the leukocytes unstimulated and stimulated with unopsonized E. coli in vitro were determined by the enzyme amplified sensitivity immunoassay method. RESULTS. Our data showed that (1→3),(1→6)-β-glucan induced a significant decrease (P<0.05) in the TNF-α level and a significant increase (P<0.001) in the IL-10 level in the media of unstimulated and stimulated leukocytes of the patients with periodontitis in comparison with those of the healthy subjects. CONCLUSIONS. The present in vitro study showed that (1→3),(1→6)-β-glucan modulated the response of leukocytes of the patients with periodontitis differently in comparison with those of the healthy subjects. It increased the release of IL-10, which is protective of the tooth-supporting tissues in patients with periodontal disease, but decreased the release of TNF-α, which is mainly responsible for the destruction of the tooth-supporting tissues during periodontal disease.
Highlights
The development of inflammatory periodontal disease is determined by a number of important interrelated factors: the host immuno-inflammatory response, accumulated dental microbial plaque, genetic environmental and conditionally pathogenic periodontal bacteria and their metabolites, etc. [1, 2]
The present in vitro study showed that (1→3),(1→6)-β-glucan modulated the response of leukocytes of the patients with periodontitis differently in comparison with those of the healthy subjects. It increased the release of interleukin 10 (IL-10), which is protective of the tooth-supporting tissues in patients with periodontal disease, but decreased the release of tumor necrosis factor α (TNF-α), which is mainly responsible for the destruction of the tooth-supporting tissues during periodontal disease
Our data showed that the levels of both TNF-α and IL-10, released by unstimulated control leukocytes from the patients with periodontitis and those of the healthy subjects, did not differ significantly (P>0.05) (Figs. 1 and 2)
Summary
The development of inflammatory periodontal disease is determined by a number of important interrelated factors: the host immuno-inflammatory response, accumulated dental microbial plaque, genetic environmental and conditionally pathogenic periodontal bacteria and their metabolites, etc. [1, 2]. The development of inflammatory periodontal disease is determined by a number of important interrelated factors: the host immuno-inflammatory response, accumulated dental microbial plaque, genetic environmental and conditionally pathogenic periodontal bacteria and their metabolites, etc. The number of leukocytes, which migrate to the gingival sulcus and periodontal pockets, increases with the progression of inflammation. Neutrophils, monocytes/macrophages, T lymphocytes, and B cells accumulate in periodontal lesions, where tissue destruction takes place [3]. Microorganisms produce destruction directly through their endotoxins and indirectly through the activation of host cells, which produce biologically active substances, such as cytokines, arachidonic acid metabolites, and proteolytic enzymes [4,5,6]. Effect of β-Glucan on In Vitro Production of Cytokines by Leukocytes of Patients With Periodontitis 187 health and stability in periodontal tissues [12]. TNF-α and IL-1β are important in causing destructive inflammation [5, 13, 14]
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