Doctors have long known that smokers rarely suffer from a common form of inflammatory bowel disease (IBD) called ulcerative colitis, but they didn’t know why. A new study in the December 19 issue of The Journal of Experimental Medicine might help explain this apparent resistance. Scott Plevy and his colleagues at the University of Pittsburgh now show that carbon monoxide (CO), a component of cigarette smoke, helps shut down the intestinal inflammation that causes ulcerative colitis.
CO is best known as a toxic air pollutant, but small amounts of this gas are also produced in the human body as a normal byproduct of metabolism, suggesting that the effects of CO must not be all bad. High dose CO gas is lethal, because it robs the body of life-sustaining oxygen. It is this asphyxiant property of CO that has earned it a bad reputation. But recent scientific studies have shown that CO — at least at low concentrations — has a redeeming quality: it acts as an anti-inflammatory agent.
It is this quality, according to Plevy and colleagues, that allowed CO to ease the symptoms of IBD in mice. The group traced the action of inhaled CO to a protein that is produced by immune cells called interleukin (IL)-12. IL-12 is normally produced during infection and helps activate the immune cells that fight off the invading pathogens. But chronic production of IL-12 in the gut also drives the inflammation that causes ulcerative colitis. Inhaled CO inhibited the production of IL-12, short-circuiting the disease-causing inflammation.
The researchers are now trying to unravel the specific cellular components that are required for CO to inhibit IL-12. In the meantime, Plevy thinks that inhaled CO might provide some relief for patients with ulcerative colitis. But non-smokers with IBD shouldn’t necessarily break out the Marlboros, as cigarette smoking is a risk factor not only for heart disease and cancer but also for Crohn’s disease, another form of IBD.
