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Enzyme Prevents Lung Damage in Premature Infants

Enzyme Prevents Lung Damage in Premature Infants
Enzyme Prevents Lung Damage in Premature Infants


Duke Health News Duke Health News

DURHAM, N.C. -- An enzyme that protects the body from reactive
chemicals called free radicals is crucial in preventing the
inflammation that causes chronic lung disease in premature infants,
according to three new studies.

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. The damage triggers the infant's immune system,
which sends in a horde of white blood cells that scavenger damaged
tissue. But in premature infants, the white blood cells often stay in
the lungs too long causing even more damage. The persistent
inflammation also delays lung development and robs nutrients from other

"We want to understand how to modify this immune response
in a safe way that prevents inflammation but avoids infections and
allow normal lung development," Auten said. The key to stopping such
inflammation in infant lungs might be superoxide dismutase, he said.

enzyme may also encourage lung development, Auten and his colleagues
found. The transgenic mice with an extra copy of the superoxide
dismutase gene had better blood vessel growth in their lungs than
normal mice when exposed to a 95 percent oxygen environment for one

Inflammation caused by an overactive immune system is not
the only source of lung problems for premature infants. Their lungs
lack surfactant, a protein that lubricates the lung's surface cells and
help keep small air sacs, called alveoli, open and functioning. Most
premature babies also have too few alveoli, which prevents their lungs
from fully expanding and taking in enough air. Combined with the need
for supplemental oxygen or ventilation, these factors lead to
respiratory distress syndrome and chronic lung disease.

there is no good treatment to stop the cascade of injury in which
inflammation meant to heal becomes a biochemical attack on the body's
own tissue. Steroids can alleviate the inflammation, but the drugs can
slow brain and lung growth and impair immune function. The average
hospital stay for infants who develop chronic lung disease -- stiff,
scarred lungs -- is six months, according to the National Institutes of

Auten's co-authors include Mohamed Ahmed, M.D., fellow,
Duke University School of Medicine; Ganesh Konduri, M.D., associate
professor of pediatrics, Medical College of Wisconsin; Ann Lee, M.D.,
fellow, Medical College of Wisconsin; Neil Hogg, Ph.D., associate
professor of biophysics, Medical College of Wisconsin; and Rose Verber,
research technologist, Medical College of Wisconsin.

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