The most familiar symptoms of acid reflux include heartburn and acid regurgitation, but in some patients, acid reflux harms more than the gastrointestinal tract -- it also injures the respiratory tract. Acid aspiration into the lungs damages the epithelial barrier and initiates acute inflammation, resulting in asthma exacerbation, chronic cough, and in the most severe cases, acute respiratory distress syndrome (ARDS), a life-threatening condition. Current management involves supportive therapies: airway maintenance, supplemental oxygen, and fluid therapy.
Because treatment of acid-induced lung injury is lacking, investigators are examining how the body heals itself from such insults in the hopes of harnessing the same mechanisms for improved medical therapies. Recently, the cellular inflammatory regulators COX-2 and LXA4 have been identified in the resolution of acid-induced lung injury in a mouse model. To determine further how COX-2 and LXA4 work at the cellular/molecular level, Dr. Bruce Levy and colleagues are exploring the resolution of acid-induced injury of the epithelial barrier of the lungs.
Using a cell culture system that replicates the air-cell interface of the lungs, Dr. Levy's group applied acid directly to the surface of the cell layer, inducing injury and death of the top layer of cells, which were shed within 2 hours. Remarkably, the layer was mostly restored within 6 hours. But how did this restoration occur?
By 2 hours following injury, the researchers found increased expression of COX-2 and the LXA4 receptor (ALX), which relied, in part, on COX-2 derived products, such as prostaglandin E2. LXA4, known to aid r
Contact: Audra Cox
American Journal of Pathology