Monday, November 17, 2014

Does exposure of a developing, immature mouse lung to high levels of oxygen impact antiviral immunity?

From our esteemed  associate editor Dr. Rory Morty:

I would like to draw your attention to an interesting paper published last week in AJP-Lung “Articles in Press”. In their study titled “Neonatal hyperoxia leads topersistent alterations in NK cell responses to influenza A virus infection” (DOI: 10.1152/ajplung.00233.2014, published on 7th November 2014), Reilly et al. address the question of whether exposure  of a developing, immature mouse lung to high levels of oxygen would impact antiviral immunity in later life. There is currently much interest in the long-terms of exposure to hyperoxia, since exposure of immature, developing lungs to high levels of oxygen is a life-saving intervention in pre-term infants that have a limited gas-exchange capacity. Whether or not exposure of developing, immature lungs to high oxygen concentrations has an impact on lung function that extends into later life, and thus, may predispose prematurely born infants to respiratory disease and complications in later life, is currently a matter of much interest and investigation. The study by Reilly et al. makes some interesting inroads into this little-explored area of lung developmental biology. Focusing on natural killer (NK) cell dynamics and function, Reilly et al. report that in adult mice that had been exposed to 100% oxygen for 96 hours immediately after birth and then returned to room air, that number of gamma-interferon-positive and granzyme B-positive NK cells were elevated seven days after influenza virus exposure. Additionally, as early as day five post-influenza virus infection, fewer NK cells produced interleukin (IL)-22 in mice that had been exposed to an hyperoxic environment as neonates. Thus, early life exposure to a high-oxygen environment resulted in a persistent “skewing” of the NK cell population from a regulatory to a classical cytotoxic NK cell population. The authors went on to demonstrate, using bone-marrow transplantation studies, that neonatal oxygen supplementation influences both the inherent properties of hematopoietic cells as well dynamically developing extra-hematopoietic environments, in this case, the lung. These studies highlight the need to better understand how early-life oxygen exposure may disrupt both the pulmonary and extra-pulmonary systems, which have important functional consequences for lung health in later life. The entire Editorial team looks forward to receiving more manuscripts that experimentally address the question of how perturbed late lung development per se, as well as the strategies that we employ to correct this important pediatric intensive care problem, may predispose prematurely-born infants to respiratory and other diseases in later life.

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