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Friendly FireMichael Glenwood

Friendly Fire

A new wave of research links inflammation to almost all chronic disease

SIXTY YEARS AGO, Patricia Mabe took her first-ever breath, inflating new pink lungs with the air of Carbondale, Pennsylvania, home of the nation’s first underground mine; a town that today, despite a long-ago demise of the anthracite industry, still smolders from burning veins of coal.

Mabe’s subsequent inhalations—even before she acquired, at age 15, a smoking habit that would be lifelong—no doubt contained vestiges of a variety of toxins, no matter whether she was outside or in. Her dad, who worked in a mine, was a smoker. Her mother smoked, too.

Whenever Mabe inhaled anything noxious, her body’s defense system recognized foreign molecules in her lungs as the interlopers they were and mounted a functional inflammatory response. Brawny cells called macrophages, among others, stormed her lungs to do away with pathogens and debris while unleashing a barrage of molecular messengers that orchestrated strategic battles and mended damaged cells. Then—and this is every bit as important as their SWAT-team-like arrival—the macrophages would leave with all their assorted artillery in tow once the mission was over. In a healthy system, inflammatory cells are both highly regulated and self-disciplined; they go where ordered, expertly distinguish friend from foe, exert only necessary firepower, tidy up after themselves and then retreat, ultimately restoring calm—also known as homeostasis.

Precise though the immune system may be, some level of self-attack occurs even when all parts are working well. The key is keeping the collateral damage in check.

In fact, how effectively and efficiently any one person controls inflammation is a key determinant of health and disease. Some individuals regulate inflammation better than others. It’s likely that many of us are able to control inflammation at certain times of our lives better than at other times. Why—and how—is the focus of intriguing research that’s implicating how nutrition and inflammation interact in just about every major chronic disease.

 “There appear to be windows of opportunity when we are good at adapting to what is in our environment, which is intimately related to how we meet and greet and defend ourselves from potential invaders,” says Keith West, DrPH ’86, MPH ’79, the George G. Graham Professor of Infant and Child Nutrition. “We get less good at that as life goes on.”

Over time—likely in response to the toxicity and persistence of cigarette smoke in her lungs—Mabe’s inflammatory response turned pathological. The composition of immune molecules and cells became qualitatively and quantitatively different. Inflammation became too too: There was too much of it; it was too strong for too long. Complicating that scenario, macrophages also became unfit and lingered incompetently in her lungs, clogging her airways.

What once defended her from disease now was causing it.

"The inflammatory system is like the ocean. It’s beautiful, but also deadly."
—Josef Coresh

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