interleukin-8 and Hyperlipoproteinemias

This report describes our findings regarding the potential contribution of periodontitis to atherosclerotic processes using a nonhuman primate model. The goal of the investigations was to target general mechanisms which could describe the association of these disease processes, including: (i) systemic translocation of bacteria/products during periodontitis; (ii) alterations in systemic inflammatory biomarkers during periodontitis; and (iii) the relationship of periodontitis to serum lipids/lipoproteins. Increases in serum endotoxin (e.g. LPS) during ligature-induced periodontitis were observed in these animals. We determined serum levels of various acute phase reactants and chemokines (e.g. CRP, alpha 1-antitrypsin, haptoglobin, fibrinogen, IL-8). A number of these host factors were significantly increased during gingivitis and/or periodontitis. Finally, we observed specific changes in serum lipid levels (cholesterol, triglycerides, HDL, LDL) and lipoproteins (apoA-I) during periodontitis, which were exacerbated by exposure of the animals to a diet with elevated fat content. Thus, we have described systemic manifestations of periodontitis that include detection of bacterial products, inflammatory biomarkers, and dyslipoproteinemia consistent with an increased atherogenic risk.

Topics: alpha 1-Antitrypsin; Animals; Apolipoprotein A-I; Arteriosclerosis; Bacterial Translocation; Biomarkers; C-Reactive Protein; Chemokines; Cholesterol; Cholesterol, HDL; Cholesterol, LDL; Disease Models, Animal; Endotoxins; Fibrinogen; Gingivitis; Haptoglobins; Hyperlipoproteinemias; Inflammation Mediators; Interleukin-8; Lipopolysaccharides; Macaca fascicularis; Periodontitis; Risk Factors; Triglycerides