The findings could lead to improved treatments to alleviate such inflammation, preserving the lungs of premature infants, said Richard Auten, M.D., a neonatalogist and associate professor of pediatrics at Duke University Medical Center. Auten and colleagues from the Medical College of Wisconsin reported their findings in three presentations on May 2 and 3, 2004, at the Pediatric Academic Societies' annual meeting in San Francisco. The research was sponsored by the American Lung Association and the National Institutes of Health.
In studies with mice, the researchers previously found that infant animals with an extra copy of the gene for the crucial enzyme, called superoxide dismutase, were better able to defend themselves against oxygen-free radicals. Oxygen-free radicals are highly reactive forms of oxygen that can readily combine with and damage proteins and other molecules in body tissues such as the lungs. Superoxide dismutase reacts with oxygen-free radicals, converting them into harmless byproducts.
The free radicals that attack lung cells are produced by white blood cells enlisted by the infant's immune system, and are not only a result of the oxygenated air breathed in by babies, according to experiments in lung cells conducted by Auten and his colleagues. This damage to lung cells can be partly prevented by turning on the gene which produces superoxide dismutase, the researchers found.
The fragile lungs of premature babies cannot take in enough air to support life, but supplemental oxygen or ventilation can damage delicate, underdeveloped lung tissue, causing inflammation and respiratory distress. Even exposure to normal room air may overwhelm the lungs of a premature infant, Auten said.
Contact: Becky Oskin
Duke University Medical Center