Debate over whether certain oral pathogens might contribute to the onset of cardiovascular disease centers on the issue of mechanism. In the May issue of Cellular Microbiology, NIDCR grantees and colleagues provide a possible answer to how bacteria colonize the heart and how their colonization triggers an immune response, causing the inflammation often associated with cardiovascular disease.
Mouse studies demonstrated that the oral bacterium Porphyromonas gingivalis relies on its major fimbria, the heavier of its 2 outer, finger-like appendages, to attach to and efficiently invade the endothelial cells that line the interior surface of the human aorta. It was found that the lighter so-called minor fimbria appear to help the bacterium gain entry into the endothelial cells. Various elements of the inflammatory response were detected, including the release of several signaling proteins by immune cells and the production of adhesion molecules by the endothelial cells. The researchers suggested that alterations in the ex-pression of the fimbria may help P. gingivalis elicit in-flammatory changes within the endothelium that predispose the aorta to forming clogging plaques.
Though proof of infectious agents’ contributory role to atherosclerosis is lacking, the authors concluded that “…our results propose a mechanism by which both the major and minor fimbria of intact P. gingivalis can facilitate inflammatory responses by endothelial cells through modification of the actin cytoskeleton.”
(Source: NIDCR Web site, Science News in Brief, accessed May 19, 2006)
