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Effect of carbon dioxide on neonatal mouse lung: a genomic approach

¹Department of Pediatrics, University of California San Diego, San Diego, California; and ²Department of Pediatrics, Section of Respiratory and Sleep Medicine, Albert Einstein College of Medicine and Children's Hospital at Montefiore, Bronx, New York

Submitted 23 August 2005 ; accepted in final form 25 July 2006

Despite the deleterious effects associated with elevated carbon dioxide (CO₂) or hypercapnia, it has been hypothesized that CO₂ can protect the lung from injury. However, the effects of chronic hypercapnia on the neonatal lung are unknown. Hence, we investigated the effect of chronic hypercapnia on neonatal mouse lung to identify genes that could potentially contribute to hypercapnia-mediated lung protection. Newborn mouse litters were exposed to 8% CO₂, 12% CO₂, or room air for 2 wk. Lungs were excised and analyzed for morphometric alterations. The alveolar walls of CO₂-exposed mice appeared thinner than those of controls. Analyses of gene expression differences by microarrays revealed that genes from a variety of functional categories were differentially expressed following hypercapnia treatment, including those encoding growth factors, chemokines, cytokines, and endopeptidases. In particular and of major interest, the expression level of genes encoding surfactant proteins A and D, as well as chloride channel calcium-activated 3, were significantly increased, but the expression of WNT1-inducible signaling pathway protein 2 was significantly decreased. The significant changes in gene expression occurred mostly at 8% CO₂, but only a few at 12% CO₂. Our results lead us to conclude that 1) there are a number of gene families that may contribute to hypercapnia-mediated lung protection; 2) the upregulation of surfactant proteins A and D may play a role as anti-inflammatory or antioxidant agents; and 3) the effects of CO₂ seem to depend on the level to which the lung is exposed.

hypercapnia; lung disease; gene expression; surfactant

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