Вирусный маркетинг в туристской индустрии: проблемы и перспективы

Материалы XII Междунар. науч.-техн. конф. (науч. чтения, посвящ. П. О. Сухому), Гомель, 22–23 нояб. 2018 г

Increased Eotaxin and MCP-1 Levels in Serum from Individuals with Periodontitis and in Human Gingival Fibroblasts Exposed to Pro-Inflammatory Cytokines

Periodontitis is a chronic inflammatory disease of tooth supporting tissues resulting in periodontal tissue destruction, which may ultimately lead to tooth loss. The disease is characterized by continuous leukocyte infiltration, likely mediated by local chemokine production but the pathogenic mechanisms are not fully elucidated. There are no reliable serologic biomarkers for the diagnosis of periodontitis, which is today based solely on the degree of local tissue destruction, and there is no available biological treatment tool. Prompted by the increasing interest in periodontitis and systemic inflammatory mediators we mapped serum cytokine and chemokine levels from periodontitis subjects and healthy controls. We used multivariate partial least squares (PLS) modeling and identified monocyte chemoattractant protein-1 (MCP-1) and eotaxin as clearly associated with periodontitis along with C-reactive protein (CRP), years of smoking and age, whereas the number of remaining teeth was associated with being healthy. Moreover, body mass index correlated significantly with serum MCP-1 and CRP, but not with eotaxin. We detected higher MCP-1 protein levels in inflamed gingival connective tissue compared to healthy but the eotaxin levels were undetectable. Primary human gingival fibroblasts displayed strongly increased expression of MCP-1 and eotaxin mRNA and protein when challenged with tumor necrosis factor-alpha (TNF-alpha and interleukin-1 beta (IL-1 beta), key mediators of periodontal inflammation. We also demonstrated that the upregulated chemokine expression was dependent on the NF-kappa B pathway. In summary, we identify higher levels of CRP, eotaxin and MCP-1 in serum of periodontitis patients. This, together with our finding that both CRP and MCP-1 correlates with BMI points towards an increased systemic inflammatory load in patients with periodontitis and high BMI. Targeting eotaxin and MCP-1 in periodontitis may result in reduced leukocyte infiltration and inflammation in periodontitis and maybe prevent tooth loss

Pearson correlation coefficients between serum CRP, MCP-1, eotaxin, and BMI in periodontitis (PD) and in periodontally healthy (PH) subjects.

<p>1) Log10 values</p><p>Pearson correlation coefficients between serum CRP, MCP-1, eotaxin, and BMI in periodontitis (PD) and in periodontally healthy (PH) subjects.</p

Characteristics of study participants describing periodontitis (PD) and periodontally healthy (PH) subjects.

<p>a) Distribution of numbers was tested with Chi² test.</p><p>b) Differences between means were tested with Student´s <i>t</i>-test.</p><p>c) Standardized for sex, age and education using general linear modeling.</p><p>d) Standardized for sex, age, education and number of teeth using general linear modeling.</p><p>Characteristics of study participants describing periodontitis (PD) and periodontally healthy (PH) subjects.</p

Time- and dose-dependent increase of eotaxin and MCP-1 protein expression in gingival fibroblasts stimulated by TNF-α and IL-1β.

<p><b>(A and C)</b> TNF-α (50 ng/ml) stimulates eotaxin and MCP-1 protein expression, and <b>(B and D)</b> IL-1β (100 pg/ml) stimulates eotaxin and MCP-1 protein expression a time-dependent manner. <b>(E and G)</b> TNF-α stimulates eotaxin and MCP-1 protein expression, and <b>(F and H)</b> IL-1β stimulates eotaxin and MCP-1 protein expression in a dose-dependent manner.</p

Schematic figure of the canonical versus non-canonical NF-κB signaling pathways, and downstream targets of inhibitors.

<p>Schematic figure of the canonical versus non-canonical NF-κB signaling pathways, and downstream targets of inhibitors.</p