For years, doctors and scientists have sought to understand a complicated mechanism that triggers an over-aggressive immune response in many patients who suffer from severe microbial infections. This immune system overreaction often leads to septic shock, for which no reliable treatments have been found.
Recent data from the Centers for Disease Control and Prevention in Atlanta show that mortality from infectious diseases in the United States has been increasing in recent years, and the number of deaths due to septicemia almost doubled from 4.2 to 7.7 per 100,000, between 1980 and 1992. Infectious diseases now rank third among leading causes of death in the United States, following only cardiovascular diseases and cancer. Furthermore, recent research has linked even cardiovascular diseases and some cancers to infectious diseases.
In a study headed by researchers at Cedars-Sinai Medical Center, scientists have for the first time identified in actual human cells a "receptor" that may be a key component of the process that leads to septic shock, confirming suspicions raised in other recently published studies. In fact, the existence of these receptors -- called Toll-like receptors -- has been the subject of a recent flurry of research.
Data showing this latest evidence was accepted for rapid publication in the March 19 issue of the Journal of Biological Chemistry. Doctors hope this breakthrough may lead to new and more effective approaches for the treatment of severe bacterial infections and endotoxin-associated septic shock that claim thousands of lives each year.
When bacteria from an infection at any site in the body invade the bloodstream,
a condition known as septicemia, patients typically experience a variety of
symptoms, including chills and fever, and the bacteria are able to travel
throughout the body. In 40 to 70 percent of these cases, septic shock follows,
characterized by a drop in the blood pressure, multiple organ failure,
circulatory
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Contact: Sandra Van
Sandy@VanCommunications.com
1-800-396-1002
Cedars-Sinai Medical Center
30-Mar-1999