February 27, 2008

Research May Yield New Weapons Against Sepsis

WEDNESDAY, Feb. 27 (HealthDay News) -- U.S. researchers say they've spotted several potential new drug targets for the serious blood infection known as sepsis.

Sepsis, caused by a bacterial infection that enters the bloodstream, is a severe, difficult-to-treat, and often fatal condition that kills tens of thousands of Americans a year.

In their research in mice, a team at the Scripps Institute in La Jolla, Calif., discovered an important connection between blood coagulation and the immune system.

The study was published in the Feb. 27 online issue of the journal Nature.

"We have identified a key connection of signaling pathways in the cascade of events leading to sepsis. This defines a crucial point where the immune system spirals out of control to cause severe sepsis and where there is an opportunity for therapeutic intervention," research co-leader Wolfram Ruf, a professor in the department of immunology, said in a prepared statement.

In this study, the Scripps team described its discovery of a new cross-talk mechanism involving the vascular coagulation system and certain cells in the immune system. When the researchers disrupted this cross-talk, they saved the lives of mice with sepsis.

These successful proof-of-principle experiments may help improve the diagnosis of various sepsis syndromes and lead to the development of new drugs to treat sepsis, the researchers said.

The Scripps team is now evaluating which targets would be the best candidates for drug therapy and is also looking at this pathway's potential role in other infectious diseases.

Sepsis, one of the leading causes of death among infants and adults in the United States, killed more than 33,000 people in 2004, according to the Centers for Disease Control and Prevention.

A number of therapies, including antibiotics, have been used to treat sepsis over the years, but they have a number of drawbacks.

More information

The Society of Critical Care Medicine has more about sepsis.

-- Robert Preidt
SOURCE: Scripps Research Institute, news release, Feb. 27, 2008
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