Smoking role in inflammation explained

BIRMINGHAM, Ala., Sept. 6 (UPI) -- Smoking shuts off a key enzyme in airways that regulates the body's response to inflammation, U.S. researchers say.

The study, published online in Science Express ahead of print in the journal Science, finds smoke inhibits the enzyme -- Leukotriene A4 Hydrolase. The shutdown means white blood cells are not stopped after successfully responding to inflammation.

University of Alabama at Birmingham researchers identified a previously unknown substrate of LTA4H -- proline-glycine-proline. PGP recruits neutrophils -- white blood cells -- that rush to the scene and attack the cause of the inflammation. When the job is over, LTA4H shuts off PGP and ends the body's neutrophils response.

"We found, however, that cigarette smoke inhibited LTA4H, preventing it from shutting down PGP," J. Edwin Blalock said in a statement. "A continued presence of PGP means a continued response of neutrophils, a never-ending cycle that supports chronic inflammation."

Blalock notes PGP is a biomarker for several lung diseases involving chronic inflammation including chronic obstructive pulmonary disease and cystic fibrosis. Defining the role of PGP may have important ramifications for the design of new anti-inflammatory drugs.