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Nicotine has undergone an image overhaul, at least biomedically. In the past few years researchers have found that the substance can alleviate symptoms of ailments such as Alzheimer's disease and ulcerative colitis. Just how nicotine battles these foes, however, has remained unclear. Now, by studying sepsis, Luis Ulloa of North Shore University Hospital in Manhasset, N.Y., has evidence elucidating nicotine's biochemical pathways that could lead to more potent anti-inflammatory drugs.
Sepsis, the most lethal of inflammatory conditions, is a bacterial invasion of the bloodstream. The third leading cause of death in the developed world, it accounts for nearly 10 percent of overall deaths in the U.S. every year. Infection causes part of the damage, but what makes patients critically ill is their own fiercely aggressive immune response. Macrophages churn out huge quantities of proinflammatory cytokines. This exaggerated immune response leads to tissue damage, and eventually the patient dies of cardiovascular dysfunction and multiorgan failure.
