Premature babies who are exposed to excess amount of oxygen (hyporexia) are more prone to lack key lung cells and are more probable to experience severe respiratory viral infections in their later life, researchers say. A study was led by researchers from University of Rochester Medical Centre in New York concluded that babies born prematurely lack alveolar type II cells- these cells are responsible for producing pulmonary surfactant, an important compound for the developing lungs. The healthy infants have these cells in abundance.
When the lungs mature after birth, some of these cells may get reduced. But the lungs of premature babies take this process way too far. They reduce too many of the type II cells which ups their risk of vulnerability to influenza and other lungs-related diseases.
The study was published in the American Journal of Respiratory Cell and Molecular Biology, in which newborn rodents were exposed to surplus oxygen at time of birth. This caused their lungs to respond and develop similarly to those of premature babies. They ended up with much lesser type II cells as they reached adulthood.
Due to the absence of the type II cells, these mice responded worse when exposed to influenza virus as adults, and developed a much more severe disease than mice born in a traditional oxygen environment. The discovery may provide a potential explanation for preterm infants' added susceptibility to influenza and other lung diseases later in their lives, the researchers said.
"There's a direct correlation between the loss of these cells and an inferior response to lung disease, and we do know that there's something about that early oxygen-rich environment that causes a mouse to respond poorly to viral infection later in life," O'Reilly from the URMC said.
(With IANS Inputs)
