Lung injury is a common cause of death among patients with pneumonia, sepsis or trauma and in those who have had lung transplants. The damage often occurs suddenly and can cause life-threatening breathing problems and rapid lung failure.
There are no effective treatments. Patients usually are put on ventilators to give their lungs a chance to heal, but there is little else doctors can do but wait and hope for the best.
Now, researchers at Washington University School of Medicine in St. Louis report they have identified a gene that limits damage to the lung during acute stress from illness, trauma or transplant. Defects in the bcl3 gene likely leave some patients more vulnerable to lung injury, they say.
The scientists also have demonstrated that this critical gene, which is active in bone marrow cells, can prevent lung injury in mice. The research is published in the Journal of Clinical Investigation.
The new discovery lays the groundwork for developing therapies to reduce complications of pneumonia, trauma and lung transplants, which affect many thousands of people annually in the United States.
"Acute lung injury is a very serious problem," says senior author Andrew Gelman, PhD, assistant professor of surgery and of pathology and immunology. "Patients' lungs fill with fluid, they can't breathe, and sadly there are no drugs available to reverse the condition."
The real culprits underlying acute lung injury are infection-fighting white blood cells called neutrophils. When the body makes too many neutrophils, however, they begin to attack healthy tissue, causing even more damage and sometimes even death.
"In mice, we found that the bcl3 gene essentially controls how many neutrophils the body produces under acute stress in the lung," Gelman says.
The same gene exists in people. Mutations in bcl3 have long been associated with the development of leukemia and lymphoma. Only recently
|Contact: Caroline Arbanas|
Washington University School of Medicine