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Interactions between Porphyromonas gingivalis and endothelial cells.


Description

There is an emerging paradigm shift from the belief that cardiovascular disease (CVD) has a purely hereditary/ nutritional etiology to the view that CHD may have an infectious component to its etiology. Among the microorganisms that are suspected to be involved in CHD are pathogens associated with periodontal diseases. Oral bacteria may exacerbate the inflammatory response of atherosclerosis in coronary arteries. The periodontal pathogens gain entry to the circulatory system via minor traumas to the gingival tissues (e.g., flossing). The bacteria may come into contact with the endothelium during this transient bacteremia. This study demonstrates that Porphyromonas gingivalis, a main periodontal pathogen, strains invade endothelial cells. Twenty-six different strains were tested using three different vascular cell lines. Strain 381 exhibited the highest ability to invade, and only strain AJW4 was noninvasive. Once intracellular, P. gingivalis gains access to the autophagic pathway, thus bypassing the cell's normal defense mechanism of routing the bacteria to the lysosome via the endocytic pathway. Entry into the autophagy pathway was assessed morphologically by transmission electron microscopy. The cellular compartments containing P. gingivalis in the absence and presence of the autophagy inhibitor wortmannin were examined using antibodies against different cellular markers. Within its privileged niche, P. gingivalis survives and replicates over 8 hours. However, when autophagy is inhibited, the numbers of viable P. gingivalis decrease. The data indicate that P. gingivalis is able to survive and replicate in a late autophagosome that fails to mature to an autolysosome. If autophagy is inhibited, P. gingivalis proceeds to a lysosome for degradation. These interactions could contribute to arterial disease at sites of atherosclerosis. This study provides a possible molecular mechanism to explain the association between periodontal disease and coronary heart disease.