When a person develops a sore or a boil, it erupts, drawing to it immune system cells that fight the infection. Then it resolves and flattens into the skin, often leaving behind a mark or a scar.
A similar scenario plays out in the blood vessels. However, when there is a defect in the resolution response the ability of blood vessels to recover from inflammation atherosclerosis or hardening of the arteries can result, said researchers at Baylor College of Medicine in Houston and Harvard Medical School in Boston in a report that appears online today in The Journal of the Federation of American Societies for Experimental Biology. The major factor in this disease is a deficiency in the chemical signals that encourage resolution (pro-resolution signals). These signals are produced in the blood vessel where the inflammation occurs, the researchers said.
Chronic inflammation of the artery wall can cause atherosclerosis, a major risk factor for heart disease and heart attack. However, said Dr. Lawrence C.B. Chan, professor of medicine and molecular and cellular biology and chief of the division of division of diabetes, endocrinology and metabolism at BCM, in many instances, the lesions or little sores inside the artery arise and then resolve, often from a very young age. The mystery is why some lesions do not heal.
What he and his colleagues from BCM and Harvard found was that genetically increasing the production of the pro-resolution signals would cool down the inflammation and give the "sores" a chance to heal or the atherosclerosis to slow down. However, genetically clamping down on these signals would fan the fire of inflammation and speed up the progression of atherosclerosis.
"Inflammation is a two-edged sword. If resolution fails and the response gets out of hand there is a never ending civil war in the body," said Dr. Aksam J. Merched, assistant professor of molecular and cellular biology at BCM and lead author
|Contact: Dipali Pathak|
Baylor College of Medicine