Magazine article Science News

Immune Blockade Impedes Blood Poisoning

Magazine article Science News

Immune Blockade Impedes Blood Poisoning

Article excerpt

Each year, roughly a half million people in the United States come down with sepsis--blood poisoning that is usually caused by bacteria. The consequences can be dire: One-third to one-half of these patients die from the disease, despite massive doses of antibiotics.

The body doesn't handle sepsis well in part because key white blood cells called neutrophils, whose job it is to destroy bacteria in the blood, tend to shut down when it strikes. Researchers have now engineered an antibody that blocks this neutrophil deactivation in rats with sepsis, extending their survival. The research, reported in the July NATURE MEDICINE, suggests that a similar antibody might work in human disease.

Sepsis, also called septicemia, is a blood infection that can arise from trauma or disease. In past centuries, plagues, battle wounds, and unsanitary surgery caused many cases.

Neutrophil deactivation in sepsis stems from a tragic misfire in the complement system, a complex cascade of protein interactions that guides many immune responses. In a normal immune response, some complement proteins activate neutrophils to combat bacteria.

Scientists became curious, however, when they found large amounts of a complement-protein fragment called C5a attached to neutrophils in blood from people with sepsis. While C5a normally incites neutrophils to do battle, too much of it shuts them down, says study coauthor Peter A. Ward, a pathologist at the University of Michigan in Ann Arbor.

Despite the complement system's apparent role in sepsis, many scientists have hesitated to tamper with these proteins because their immune functions are critical, if poorly understood, he says. …

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