| 0864 Porphyromonas gingivalis lipopolysaccharide induces pro-atherogenic cytokines in human endothelial cells | ||
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L. KOCGOZLU1, R. ELKAIM2, H. TENENBAUM1, and S. WERNER1, 1ERT 1061, Unite INSERM 595, Dental Faculty, University Louis Pasteur, Strasbourg, France, 2Parogène, Strasbourg, France Objectives: To characterize the role of Porphyromonas gingivalis, a major etiological agent of chronic periodontal diseases, lipopolysaccharide (P. gingivalis LPS) in the atherosclerotic process, we investigated cytokine production induced by P. gingivalis LPS stimulation of endothelial cells. Methods: We used human umbilical vein endothelial cells (HUVEC) as a cellular model for endothelial cells and human oral epithelial cells (HOEC) as a control since epithelial cells are the first cell target for periodontopathogens in the periodontal pocket.Cells were stimulated by P. gingivalis LPS for 24 hours. Then, supernatants were collected and submitted to cytokine array analysis. Results: Endothelial and epithelial cells were both strongly stimulated by P. gingivalis LPS to produce pro-inflammatory cytokines. Patterns of cytokine expression were remarkably similar in both cell types, although some cytokines were more specific to one cell type. The comparison of cytokine secreted by HUVEC and HOEC highlighted that most of the detected cytokines were involved in the innate immunity. Several cytokines could play a role in both periodontitis and atherosclerosis, such as IL-1áand IL-6 which are involved in the acute-phase reaction. Very interestingly, RANTES, MIP-1 á,â,ä, and adhesion factors such as ICAM-1which is involved in the recruitment and the adhesion of leukocytes to sites of vascular lesions, and M-CSF which is involved in the differentiation of macrophages into foam cells, are produced by both HUVEC and HOEC. Conclusions: These results are compatible with a model in which bacterial byproducts such as LPS are released, and may either stimulate pro-inflammatory cytokine production by epithelial cells or directly penetrate the blood circulation through degradated gingival tissues and interact with endothelial cells. In both cases, cytokines, chemokines and acute phase mediators may be shed into the vasculature and could contribute to the inflammatory reaction that shift endothelial cells from an anti-thrombotic state to a pro-thrombotic one. | ||
| Seq #90 - Periodontal Research: Microbiology, Immunology 11:30 AM-1:00 PM, Friday, September 12, 2008 Queen Elizabeth II Conference Centre Poster Hall 2 | ||
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