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Study by UCSD gives new insight into how anthrax bacteria can evade a host's immune response

Biologists at the University of California, San Diego have determined how toxin produced by anthrax bacteria blocks a person's normal immune response, a discovery that could lead to new treatments for anthrax infection.

In a paper to be published in the January 15th issue of The Journal of Immunology the UCSD scientists show why, in the presence of anthrax toxin, human immune cells fail to respond normally to lipopolysaccharide--a component of the cell walls of many bacteria including the bacteria that cause anthrax, Bacillus anthracis. Bacterial invasion, or the presence of lipopolysaccharide, usually causes immune cells known as macrophages to release cytokines--chemicals that signal other cells about the presence of an invader. Release of cytokines causes large numbers of immune cells to arrive at the site of infection and destroy the bacteria. By blocking this host immune response, anthrax bacteria are able to multiply unchecked. According to the Centers for Disease Control, approximately 75 percent of people infected with inhalation anthrax die, even with all possible supportive care including appropriate antibiotics.

"Although it was known for quite some time that anthrax toxins can suppress cytokine production, the mechanism by which Bacillus anthracis escapes the immune response isn't really understood," says Michael David, a biology professor at UCSD who headed the research team. "We have identified a protein molecule targeted by the anthrax toxin and determined where it acts in the sequence of steps involved in immune response."

Macrophages have special receptors on their surfaces that bind to lipopolysaccharide. The binding of lipopolysaccharide to this receptor sets off a sequence of events inside the macrophage, in which a series of proteins activate one another in turn. This cascade of proteins activating one another ultimately turns on cytokine genes, causing the macrophage to churn out large quantities of cytokines. <
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Contact: Sherry Seethaler
sseethaler@ucsd.edu
858-534-4656
University of California - San Diego
6-Jan-2004


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