Researchers at the University of Virginia Health System have identified a molecular target, or receptor, for potential drugs to treat acute respiratory distress syndrome (ARDS), a sudden and life-threatening failure of the lung. Interestingly, the receptor is in the same class that gives people their sense of sight, smell and taste (G-protein coupled receptors.)
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, or alveoli, 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. Common causes of ARDS are pneumonia, septic shock, trauma, or inhaling chemicals.
The receptor identified by UVa doctors 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, UVa doctors 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.
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