DURHAM, N.C., July 17 (UPI) -- Genetically altering the immune system can protect arteries from clogging, but also makes the body more vulnerable to infection, a new international study revealed Wednesday.
The finding is important, researchers said, because it could pave the path toward a new way of attacking atherosclerosis, a life-threatening hardening of the arteries that can lead to heart disease and other cardiovascular ills.
Scientists at Duke University Medical Center and from Austria and Italy found a genetic variant among a group of chemical receptors located on the surface of immune system cells, the cells that help fight off infections from bacteria and viruses. These receptors also are located on the surface cells in the body's airways and on cells lining the blood vessels. They work by recognizing outside organisms and providing the body with its first warning to the immune system that an invasion has begun inside the body.
However, this particular genetic variant hinders the receptor's ability to signal the body when it is being infected. This reduced ability suppresses the body's inflammation response, which also means a decreased risk for atherosclerosis.
To confirm this association, researchers used data collected on 810 people in Italy from 1990 to 1995 and then followed the same people for five more years. Of the 810, 55 carried the genetic variant, called TLR4 polymorphism. Using three different ultrasound tests to observe the major arteries running through the neck, those who had the genetic variant showed far less arterial inflammation and thickening compared to the rest of the group -- but they also had more infections.
"We were very encouraged by the consistency of our data," lead researcher Dr. David Schwartz, chief of pulmonary medicine at Duke, told United Press International. "This approach or this study indicates there may be another way to decrease the risk in developing heart disease."
If scientists can control this genetic variant, that could become a potential target for new drugs to treat arterial problems, Schwartz explained. Although the variant leaves a person more prone to infection, for people with serious or life-threatening cardiovascular conditions, the trade-off might be worth it, he added. "There's always a risk of trading off toxic effects for something for the beneficial effects."
Dr. Valentin Fuster, director of the Cardiovascular Institute at Mount Sinai Medical School in New York City, and a former president of the American Heart Association, told UPI this discovery could open doors for cardiovascular patients. "It's interesting because it's a new avenue on a receptor that was discovered about two years ago," Fuster said.
While previous studies suggested a single infection, such as Chlamydia pneumoniae contributed to the development of athersclerosis, this study indicates the condition might be the result of numerous infections. "It's becoming more and more clear that it's not single infection that causes atherosclerosis disease. However, you pay a price. If you have a bacteria that comes in and there's no reaction from the body, what is that bacteria going to do?"
Dr. Nieca Goldberg, an AHA spokeswoman and chief of cardiac prevention and rehabilitation at Lenox Hill Hospital in New York, agreed the study appeared promising.
"I think what's very interesting and very exciting about this particular study is that they identified on a cellular level a dampening of the inflammatory response in cells," Goldberg told UPI. "This is exciting research."
The findings are published in the July 18 issue of The New England Journal of Medicine.
(Reported by Katrina Woznicki in Washington.)
