In ARDS, patients cannot breathe on their own because fluid gets into the lungs. Essentially, the body’s immune system causes lung inflammation and accumulation of fluid in the air sacs, leading to low blood-oxygen levels. Up to 30 percent of patients in intensive care units can die from ARDS. There is no current therapy other than general life support and putting patients on a breathing machine. If they survive, many people face long-term lung problems.

The identified receptor is called CXCR2. It’s expressed on the endothelial cells that line the blood vessels of the lung and on inflammatory leukocytes. Using animal models, the researchers have found that CXCR2 attracts white blood cells called neutrophils into the lung, a key event in the early development of ARDS. CXCR2 has been characterized in the past, but the endothelial cell effects define a new role for this receptor in the body’s physiology.

“We can’t say yet that if you target this receptor you will stop ARDS,” said Klaus Ley, M.D., Ph.D., director of the cardiovascular research center at the University of Virginia. “But it is reasonable to be hopeful and to pursue this type of research that might one day translate into clinical application.”

Dr. Jörg Reutershan, M.D., an anesthesiologist from Germany doing research in Ley’s lab, discovered that CXCR2 expressed on endothelial cells is involved in acute respiratory syndrome. “Our finding is that expression of this receptor is in the lung itself,” Reutershan said. “Our hope is that drug companies might be able to target the lung with an aerosol, which would have the advantage of hitting receptor without compromising the entire immune system, which is always a problem. Aerosol treatment would be a great advantage.”

MEDICA.de; Source: University of Virginia Health System