Like a captain on a shoot a rocket to call for help sinking ship, distressed arteries attract immune cells. But instead of saving the arteries, immune cells appear to accelerate their decline. The findings, reported in today's issue of Journal of Clinical Investigation , suggest that put a damper on some of this distress call may be a new way to treat heart disease.
Everyone knows that "bad" cholesterol tends to accumulate in the arteries and often leads to atherosclerosis. But for many other risk factors - such as cigarette smoke and certain bacterial infections - the cause of the disease mechanism is unclear. One thing these risk factors have in common, however, is that they trigger an inflammatory response and repair, said Robert Terkeltaub Hospital of the Veteran Administration in San Diego. We knew that the precursor macrophages - wandering cells made by the immune system to consume bacteria and dead cells - accelerates the deposition of fat in the arteries bruised
Terkeltaub enlisted colleagues at Scripps Research Institute La Jolla. In California, and the University of California, San Diego, to try to understand how these precursors called monocytes could be attracted to the injury. Working on mice, Linda Curtiss Scripps transplanted bone marrow that churn white blood cells, with or without the mouse version of CXCR-2, a receptor for chemokines - the distress call from the injured cells to the lesion . The team fed two groups of mice a diet of artery hardening ". And a milkshake over it" the equivalent of one hamburger per day, Terkeltaub said, After 4 months, the mice with the receptor exhibited arterial lesions 2.5 times the size of lesions in mice lacking the receptor; the CXCR-2 mice also had significantly higher macrophage account.
The discovery shows that the modification of the immune response can change the course of atherosclerosis, said Alan Greater Columbia University. The implication, he said, is that compounds that block chemokine receptors could someday be used to protect people injured arteries.
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