Title: | Maternal Vitamin D Deficiency Causes Sustained Impairment of Lung Structure and Function and Increases Susceptibility to Hyperoxia-induced Lung Injury in Infant Rats |
Author(s): | Mandell EW; Ryan S; Seedorf GJ; Gonzalez T; Smith BJ; Fleet JC; Abman SH; |
Address: | "Pediatric Heart Lung Center. Section of Neonatology, and. Section of Pulmonary Medicine, Department of Pediatrics, Children's Hospital Colorado and University of Colorado Anschutz Medical Center, Aurora, Colorado. Department of Bioengineering, College of Engineering and Applied Sciences, University of Colorado Denver, Anschutz Medical Campus, Aurora, Colorado; and. Department of Foods and Nutrition, and. Interdepartmental Nutrition Program, Purdue University, West Lafayette, Indiana" |
Journal Title: | Am J Respir Cell Mol Biol |
ISSN/ISBN: | 1535-4989 (Electronic) 1044-1549 (Print) 1044-1549 (Linking) |
Abstract: | "Vitamin D deficiency (VDD) during pregnancy is associated with increased respiratory morbidities and risk for chronic lung disease after preterm birth. However, the direct effects of maternal VDD on perinatal lung structure and function and whether maternal VDD increases the susceptibility of lung injury due to hyperoxia are uncertain. In the present study, we sought to determine whether maternal VDD is sufficient to impair lung structure and function and whether VDD increases the impact of hyperoxia on the developing rat lung. Four-week-old rats were fed VDD chow and housed in a room shielded from ultraviolet A/B light to achieve 25-hydroxyvitamin D concentrations <10 ng/ml at mating and throughout lactation. Lung structure was assessed at 2 weeks for radial alveolar count, mean linear intercept, pulmonary vessel density, and lung function (lung compliance and resistance). The effects of hyperoxia for 2 weeks after birth were assessed after exposure to fraction of inspired oxygen of 0.95. At 2 weeks, VDD offspring had decreased alveolar and vascular growth and abnormal airway reactivity and lung function. Impaired lung structure and function in VDD offspring were similar to those observed in control rats exposed to postnatal hyperoxia alone. Maternal VDD causes sustained abnormalities of distal lung growth, increases in airway hyperreactivity, and abnormal lung mechanics during infancy. These changes in VDD pups were as severe as those measured after exposure to postnatal hyperoxia alone. We speculate that antenatal disruption of vitamin D signaling increases the risk for late-childhood respiratory disease" |
Keywords: | "Animals Animals, Newborn Female Hyperoxia/*complications/metabolism Lung/metabolism/*physiopathology Lung Compliance/*physiology Lung Injury/*etiology/metabolism Pregnancy Rats Vitamin D/*analogs & derivatives/metabolism Vitamin D Deficiency/*complication;" |
Notes: | "MedlineMandell, Erica W Ryan, Sharon Seedorf, Gregory J Gonzalez, Tania Smith, Bradford J Fleet, James C Abman, Steven H eng K08 HL150222/HL/NHLBI NIH HHS/ R01 HL068702/HL/NHLBI NIH HHS/ R56 HL068702/HL/NHLBI NIH HHS/ Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't 2020/03/07 Am J Respir Cell Mol Biol. 2020 Jul; 63(1):79-91. doi: 10.1165/rcmb.2019-0295OC" |