Inflammation kills bacteria // and heals wounds // But what if your body kept fixing something that wasn’t broken? // That’s the problem of an immune system that’s...
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When scientists decry the sharp decline in the number of autopsies, they talk about what medical science may lose by not having the chance, after a patient’s death, to explore the body in a way that wouldn’t have been possible when the patient was alive. One of medicine’s earliest diagnostic tools, autopsies have helped solve myriad medical mysteries—including the link between Alzheimer’s disease and heart disease, and the discovery of the West Nile Virus—and in the 1980s, evidence uncovered during postmortems began solidifying the case for a risk factor that may have a profound role in the development of heart attacks, strokes and a laundry list of other plagues.
During the first half of the twentieth century, the prevailing view of heart disease considered arteries to be simple pipes, and cholesterol the gunk accumulating in those pipes until blood could no longer reach the heart or brain. But research in lab animals during the 1970s began to suggest that there was much more to it than grungy hardware. In 1973, University of Washington researcher Russell Ross proposed that arteries react to cholesterol and other environmental influences. This set the stage for a new view of atherosclerosis, and, in 1979, pathologist Ross Gerrity, then at the Cleveland Clinic Foundation, found some of the first evidence that atherosclerosis emerges in part because our own immune system attacks our arteries. When he examined the arteries of pigs that ate a high-cholesterol diet, he found inflammatory cells called monocytes packing the regions that developed atherosclerotic plaques. In two landmark 1981 papers, he made the case that these inflammatory cells are in fact the most important factors for plaque development: They not only absorb the low-density lipoprotein (LDL, or “bad” cholesterol) that trespasses into the blood vessel wall, but they also become foam cells, which researchers knew to form the core of a plaque.
And when pathologists autopsied patients who had suffered from atherosclerosis, it seemed the disease in humans followed a similar trajectory. Autopsied blood vessels revealed clots, like scabs on cuts, as well as monocytes and macrophages, which are cells that monocytes mature into once they’re in the artery wall.
Soon, Peter Libby, chief of cardiovascular medicine at Brigham and Women’s Hospital in Boston, along with many other scientists across the country, was researching the details of this phenomenon in lab animals. The emerging consensus was that it’s not just cholesterol that causes problems in the bloodstream; it’s also the chronic low-level inflammation that responds to the cholesterol—and to elevated blood sugar, smoking and a diet high in saturated fat, among other “injuries.”
This long-term inflammatory response was very different from acute short-term inflammation, which is a vital part of the so-called innate immune system, the body’s first-line defense against bacteria and viruses. When you slice your finger on a jagged can, vessels dilate to allow more blood into the area. The finger becomes red and hot (from the extra blood), and white blood cells ooze into the wound to combat bacteria. The process accelerates until the site is clear, then stops. Inflammatory cells and proteins go back to their normal patrol in the bloodstream, and the finger heals.
