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Subversive strep bug strategy revealed

Researchers at the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health (NIH), have discovered how Streptococcus pyogenes (S. pyogenes), the bacterium responsible for "flesh-eating" infections, gains a foothold in the body by subverting a key immune system cell.

"The ability of this very common bug, which causes strep throat and other infections, to modulate the gene activity of an immune system cell is remarkable and has never before been seen on this scale," says Frank R. DeLeo, Ph.D., a researcher at NIAID's Rocky Mountain Laboratories (RML) in Hamilton, MT. The findings are scheduled to be published in Proceedings of the National Academy of Sciences, USA this week.

Insight into streptococcal infection is one product of a comprehensive picture of immune cellbacteria interactions developed by the RML scientists. Using microarray technology, Dr. DeLeo and his colleagues created a "snapshot" of how all the genes in a type of white blood cell, called a neutrophil, react following exposure to a variety of bacteria.

"This is work of seminal importance," says NIAID Director Anthony S. Fauci, M.D. "By demonstrating that neutrophils respond with altered gene expression to bacterial invasion, the investigators have exposed dozens of possible targets for drug therapies. These findings are likely to be broadly applicable to many types of microorganisms that cause disease in humans, and could lead to new treatments that augment the immune response against multiple pathogens," he adds.

Neutrophils are the most abundant type of white blood cell and a central player in the body's innate immune system. Like a S.W.A.T. team, neutrophils swarm to the site of infection in the first few minutes after a bacterial attack. Quickly they engulf the invading organisms and destroy them.

Neutrophils are genetically programmed to shut themselves down after they engulf and kill microbes. Because o
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Contact: Anne A. Oplinger
aoplinger@niaid.nih.gov
301-402-1663
NIH/National Institute of Allergy and Infectious Diseases
28-Aug-2003


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