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Molecular mechanism underlaying anthrax infection described by UCSD School Of Medicine researchers

The mechanism by which inhaled anthrax disarms and evades the immune system, enabling the potentially lethal bacteria to rapidly spread throughout the body, has been described by researchers at the University of California, San Diego (UCSD) School of Medicine.

Published online Aug. 29 in Science Express, the website of the journal Science, the lab-culture research with mouse cells describe how a complex of Bacillus anthracis (anthrax) proteins called lethal toxin (LT) inhibits and destroys macrophages, the large white blood cells that act as the body's first defense against pathogens, and also disables the signaling mechanism triggering immune activation. This allows the bacteria to spread through the body unchecked by the immune system, resulting in rapid and potentially lethal anthrax infection.

When the bacterium (b. anthracis) is inhaled, its spores are surrounded by alveolar macrophages in the lung, the beginning stage of normal immune response. But instead of succumbing to the defensive assault, they survive and germinate within the cells, traveling with the macrophages in their normal sentinel duty throughout the body to the lymph nodes, and eventually into the bloodstream, ultimately leading to fatal systemic shock if treatment fails.

In order to understand how anthrax was evading the immune system, the research team led by Michael Karin, Ph.D., UCSD professor of pharmacology and American Cancer Society Research Professor, used a variety of lab tests to determine how LT caused cell death in mouse macrophage cells. They pinpointed a series of steps, and specifically inhibition of an enzyme (a protein kinase) called p38, that lead to macrophage death and prevent secretion of chemokines and cytokines, the signaling agents that alert the immune system to the presence of an invading pathogen.

According to Karin, these findings open the door for development of an antidote that could block the action of a specific toxin called leth
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Contact: Sue Pondrom
spondrom@ucsd.edu
619-543-6163
University of California - San Diego
29-Aug-2002


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