Cedars-Sinai Medical Center Physicians And Scientists Present Findings At Annual Meeting Of The Pediatric Academic Societies

and often leads to septic shock. More than 20,000 people in the United States die each year from septic shock resulting from Gram-negative septicemia.

Gram-negative bacteria contain a toxin, called lipopolysaccharide (LPS) or endotoxin, on their outer membranes. Even tiny amounts of endotoxin shed from the bacteria into the blood are recognized by the immune system, which activates various types of cells, including white blood cells that produce inflammatory molecules called cytokines. Cytokines destroy invading pathogens but if the production of cytokines continues unchecked, they actually become toxic themselves. Patients suffering from septicemia who progress to septic shock actually may die as a result of the excessive immune response rather than from the initial bacterial infection alone.

In this study, headed by Dr. Arditi and involving researchers at Cedars-Sinai and several other institutions, scientists have for the first time identified in actual human cells a "receptor" that may be a key component of this process.

Scientists had previously discovered that a "Toll receptor" found in the cells of fruit flies and even in a number of plants is responsible for triggering the "innate" or primitive immune system to fend off invading organisms. Suspicions and evidence have been mounting over the past several years that similar "Toll-like receptors" exist in humans. In fact, five Toll-like receptors have recently been cloned and several others have been identified.

In this study using human endothelial cells (cells that line the blood vessels) and human monocytes (blood cells that are important in fighting infection), the researchers provided proof that endotoxin uses a Toll-receptor signaling pathway within human cells to induce NF-kappa B (a protein that turns on genes that make cytokines and trigger inflammatory responses). They also were able to show the presence of Toll-like receptors (TLR2 and TLR4) on the surface of the human cells. Identi

Contact: Sandra Van
Cedars-Sinai Medical Center

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