An international research team has identified a lung protein that appears to play a key role in smoking-related emphysema and have crafted an antibody to block its activity, Indiana University scientists reported.
The research, conducted in mice, suggests that the protein, a cytokine named EMAPII, could provide a target for drugs to treat emphysema, said Irina Petrache, M.D., associate professor of medicine at the Indiana University School of Medicine. The research was posted online May 16 for the June edition of The Journal of Clinical Investigation.
Emphysema, a form of chronic obstructive pulmonary disease (COPD) that affects nearly 5 million people in the U.S alone, is caused by the destruction of cells that transfer oxygen from the lungs to the blood, along with inflammation in the lungs. Cigarette smoking is the most common cause of emphysema.
The cytokine EMAPII a type of cell-signaling molecule is normally part of the process of early lung development. Research had previously found that EMAPII could cause the death of cells that line blood vessels endothelial cells and inflammation, but it had not been identified as the molecular culprit at work when cigarette smoking inflicted its damage on the lungs.
"The fact that we could have a single target affecting two major processes made us excited about looking for it in response to smoking," said Dr. Petrache, the Floyd and Reba Smith Investigator in Respiratory Disease at IU.
When the researchers induced emphysema in mice exposed to cigarette smoke, tests showed the mice had elevated levels of the EMAPII cytokine. In other tests, the scientists also found elevated levels of the cytokine in the lungs of patients with COPD.
The researchers also found that the cell death caused by the EMAPII resulted in the release of enzymes that cause more production of EMAPII, causing a vicious cycle of elevated cytokine levels and more cell death.
|Contact: Eric Schoch|
Indiana University School of Medicine