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Genes Discovered That Allow Gum Disease Bacterium To Invade Arteries

May 29, 2006 — Researchers have identified the genes in gum-disease bacteria that allow them to invade and infect human arterial cells, offering one possible explanation for a perceived connection between gum disease and heart disease. Scientists from the University of Florida, Gainesville, present their findings today at the 106th General Meeting of the American Society for Microbiology in Orlando, Florida.


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"Aside from lifestyle and genetic factors, there is increasing evidence that bacterial infections may play a role in heart disease. Porphyromas gingivalis, an important bacterium that causes gum disease, is also linked to cardiovascular disease. In this study we have identified and studied four genes of P. gingivalis that allow it to infect and survive inside artery cells," says Paulo Rodrigues, a researcher on the study.

Rodrigues and his colleagues had previously discovered that P. gingivalis had the ability to invade and survive inside human artery cells. In this study they examined the role four different genes play in this ability. They created four strains of the bacterium, each with a different gene mutated to disable it, and tested their ability to invade and survived in artery cells compared to a fully functioning strain of P. gingivalis.

"Our study showed that all four mutated strains were defective in invasion of the artery cells and that their ability to survive inside of the cells was diminished. These results show that these four genes play a role in the invasion and survival of P. gingivalis inside artery cells," says Rodrigues. "The knowledge of how this pathogenic bacterium interacts with artery cells is important and may lead to the development of therapeutics and diagnostic tools for the detection and possibly prevention of heart diseases caused by this association."

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The above story is reprinted from materials provided by American Society for Microbiology, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


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