| 0212 Molecular Mechanisms of Endothelial Destruction by P. gingivalis | ||
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E. KOZAROV1, D. SIEMANN1, Y.-H. SONG2, A. VALLE1, D. ROOKE1, and A. PROGULSKE-FOX1, 1University of Florida, Gainesville, USA, 2Chonbuk National University, Chonju, South Korea Vascular thombosis is the main event leading to myocardial infarction and stroke. Atheromatous plaques occlude the lumen and increase the risk of acute thromboembolic events. There is an emerging body of evidence linking periodontal infections with cardiovascular disease (CVD). Periodontitis is a chronic inflammatory disease caused by gram-negative bacteria, of which Porphyromonas gingivalis is considered a causative agent. Hemorrhage at the infected site is the hallmark of periodontal disease. In addition, P. gingivalis has a potent platelet-aggregating activity. Objective: To investigate the possible involvement of P. gingivalis proteolytic activity in vascular disruption via degradation of the endothelial cell layer. Methods: Cell cultures, microscopy and immunochemistry were employed to quantitate P. gingivalis-mediated destruction of human endothelial cell layers. Results: Using soluble protein extracts from P. gingivalis W83, time-dependent detachment of both growing and quiescent endothelial cells was demonstrated. As seen on phase contrast micrographs, exposure of identical concentrations of either the P. gingivalis whole cells or a 60%-ammonium sulfate culture liquor precipitate to the basolateral side of a polarized endothelial monolayer resulted in complete destruction of the polarized monolayer. However, exposure of bacteria or precipitate to the apical side resulted in no destruction. Apical application of trypsin resulted in faster destruction than basolateral application. Immunochemical analysis demonstrated that a secreted protein of P. gingivalis mediated degradation of human vascular occludin and integrin. Conclusion: These data suggest that the secreted proteolytic activities of P. gingivalis could be involved in hemorrhage, plaque rupture and acute thromboembolic events such as MI and stroke via initial tissue destruction. Identifying the bacterial traits important in the vascular pathogenesis and the mechanism of P. gingivalis-mediated destruction of human endothelium will be beneficial in understanding the epidemiological link between periodontal disease and CVD as well as in developing novel therapeutics for prevention and treatment of CVD. | ||
| Seq #36 - Porphyromonas gingivalis 9:00 AM-11:00 AM, Thursday, 7 March 2002 San Diego Convention Center Room 16A (Mezzanine Level) | ||
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