Stop Cell Death, Help Treat Sepsis?

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A body-wide syndrome triggered by sepsis infection is a leading cause of death in hospital intensive care units, striking 750,000 people every year and killing more than 210,000.(1) The most severe form of sepsis occurs when bacteria leak into the bloodstream, spilling their poisons and leading to a dangerous condition called septic shock. Blood pressure plunges dangerously low, the heart has difficulty pumping enough blood, and body temperature climbs or falls rapidly. In many cases, multiple organs fail and the patient dies. In recent years, researchers have come to realize that the intestinal tract plays an important role in sepsis. Scientists have found that after a severe infection or injury, cells in the intestinal lining die off in a process called apoptosis.

Researchers now suspect that blocking apoptosis in the intestines of critically ill patients may help prevent death from sepsis. The strategy looks promising in mice, suggesting that it may someday be effective in people. Dr. Craig Coopersmith of Washington University in St. Louis genetically engineered laboratory mice to produce large amounts of a cell death-blocking protein called bcl-2 in their intestines. He then exposed the experimental mice to the bacterium Pseudomonas aeruginosa, which can cause sepsis in susceptible people. Remarkably, 40 percent of the mice with bcl-2 escaped infection and survived, compared to only 4 percent of the mice without bcl-2.

This study suggests that minimizing apoptosis in intestinal cells may prevent death in people with sepsis. Effective prevention and treatments are urgently needed, since the death rate from sepsis has climbed more than 90 percent over 20 years(2), costing the nation $16.7 billion per year(1).


1Angus DC, Linda-Zwirble WT, Lidicker J, Clermont G, Carcillo J, Pinsky MR. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Crit Care Med 2001;29:1303-10.

2Murphy SL. Deaths: final data for 1998. Natl Vital Stat Rep 2000;48:1-105.