Study Suggests How Oral Bacterium Might Cause Cardiovascular Disease

May 18, 2006
At the center of the debate over whether certain oral pathogens might contribute to the onset of cardiovascular disease is the issue of mechanism. How exactly do the bacteria colonize the heart? And how does their colonization trigger an immune response, causing the inflammation often associated with cardiovascular disease?


In the May issue of the journal Cellular Microbiology, NIDCR grantees and colleagues provide a possible answer. They demonstrated in studies with human cells that the oral bacterium Porphyromonas gingivalis relies on its major fimbria, the heavier of its two outer, finger-like appendages, to attach to and efficiently invade the endothelial cells that line the interior surface of the human aorta.


The scientists then found that the lighter so-called minor fimbria appear to play an important role in helping the bacterium gain entry into the endothelial cells. Thereafter, the scientists detected various elements of the inflammatory response, including the release of several signaling proteins by immune cells and the production of adhesion molecules by the endothelial cells. Interestingly, the researchers suggested that alterations in the expression of the fimbria may help P. gingivalis elicit inflammatory changes within the endothelium that predispose the aorta to forming clogging plaques.


The authors concluded, "Although definitive proof of a casual role of infectious agents contributing to atherosclerosis is still lacking . . . 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."