Particular cell surface molecules sense runaway inflammation and tissue damage, say researchers, Michail Sitkovsky, and his coworkers at the National
Particular cell surface molecules sense runaway inflammation and tissue damage, say researchers, Michail Sitkovsky, and his coworkers at the National Institute of Allergy and infectious Diseases (NIAID).The finding appeared in Nature. Inflammation, tissue swelling is accompanied by pain and heat, is the body’s response to a host of insults: invasion by bacteria or viruses, injury, or reactions to one’s own tissues.
Chronic inflammation is characteristic of such disorders as asthma, chronic hepatitis, lupus and rheumatoid arthritis. Little is known about the body,s own mechanism for controlling inflammation and the tissue damage that accompanies it. According to Dr.Sitkovsky, there must be some way for the body to shout. The signal must be sensed and responded to so that inflammatory activity abates. Adenosine and its membrane-bund receptor made attractive cnadidates 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. Despite its numerous roles adenosine has received little attention from immunologists, says Sitkovsky. This much is known: when tissue damage mounts due to prolonged inflammation oxygen levels in the damaged area fall. This leads to increased amounts of adenosine outside cells. Dr. Sitkovsky theorised that the excess adenosine binds to the adenosine receptors, which then initiate a chain reaction that slows and eventually stops inflammation.
