Saranac Lake, N.Y. New research from the Trudeau Institute may help to explain why anticoagulant therapies have largely failed to extend the lives of patients with sepsis. The study was led by Deyan Luo, a postdoctoral fellow in Stephen Smiley's laboratory. It shows that fibrin, a key product of the blood clotting process, is critical for host defense against Yersinia enterocolitica, a gram-negative bacterium that causes sepsis in humans and experimental mice. The new data will be published in the August 15 issue of The Journal of Immunology and is available now online ahead of print.
"After inoculating a variety of genetically engineered mice with this bacterium, the lab observed that mice lacking fibrin showed dramatically decreased survival and harbored greatly increased numbers of bacteria in their blood and tissues," said Dr. Smiley. "These findings add to a growing body of evidence that fibrin helps to protect our bodies during infection."
Infectious disease remains a leading cause of death worldwide. Many of these deaths actually result, in large part, from our bodies' own excessive responses to certain types of infections. Whether the infectious agents first gain access to our bodies via a wound, intravenous line, or catheter, and whether they first establish infections in our skin, lung or intestine, all too often they evade our natural immune defense mechanisms and then spread, causing a generalized infection throughout much of the body.
Unless effective antibiotics are administered promptly, these generalized infections can lead to sepsis, a syndrome in which the immune system unleashes so much infection-fighting inflammation that it causes more damage than good, leading to organ failure, shock and death. With the ever-growing presence of multiple drug resistant bacteria like MRSA, the incidence of sepsis is increasing, even in state-of-the-art hospitals. Typically doctors simply tell family members that th
|Contact: Karen Sharma|