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2002 JAN 16 - (NewsRx.com & NewsRx.net) -- After a decade of research, Michail Sitkovsky, PhD, and his coworkers at the National Institute of Allergy and Infectious Diseases (NIAID) may have answered one of the most perplexing questions in immunology: how the body limits inflammation.
Inflammation, tissue swelling usually accompanied by pain and heat, is the body's generic response to a host of insults: invasion by bacteria or viruses, injury, or reactions to one's own tissues.
Within limits, inflammation is a valuable ally in the body's fight against invaders. But left unchecked, inflammation exposes a decidedly dangerous side. Chronic inflammation is characteristic of such disorders as asthma, chronic hepatitis, lupus and rheumatoid arthritis.
Although many drugs lessen or halt inflammation, very little is known about the body's own mechanism for controlling inflammation and the tissue damage that accompanies it.
"Clearly, there must be some way for the body to shout, 'Enough already! Stop the inflammation,'" explains Sitkovsky. The shout, or signal, must be sensed and responded to so that inflammatory activity abates. "We wanted to learn what the signals and sensors are in living organisms," he says.
Their finding, that particular cell surface molecules sense runaway inflammation and tissue damage, appears in the December 20, 2001, issue of the journal Nature.
Adenosine and its membrane-bound receptor made attractive candidates for signal and sensor, Sitkovsky notes. A simple molecule that leads a busy life, adenosine is the core of the cell's energy-containing compound, ATP, and elevated levels of it in the brain appear to cause sleep.