Publication Date
11-25-2024
Journal
BMC Pulmonary Medicine
DOI
10.1186/s12890-024-03391-1
PMID
39587520
PMCID
PMC11587781
PubMedCentral® Posted Date
11-25-2024
PubMedCentral® Full Text Version
Post-print
Published Open-Access
yes
Keywords
Animals, Hyperoxia, Animals, Newborn, Mice, Acute Lung Injury, Vitamin D, Mice, Inbred C57BL, Cytokines, Lung, Disease Models, Animal, Pulmonary Edema, Female, Dose-Response Relationship, Drug, Hyperoxia, Acute lung injury, HALI, Vitamin D, Preterm neonate, Inflammatory cytokines, Airway responsiveness
Abstract
BACKGROUND: Prolonged exposure to hyperoxia can lead to hyperoxic acute lung injury (HALI) in preterm neonates. Vitamin D (VitD) stimulates lung maturation and acts as an anti-inflammatory agent. Our objective was to determine if VitD provides a dose-dependent protective effect against HALI by reducing inflammatory cytokine expression and improving alveolarization and lung function in neonatal mice.
METHODS: C57BL/6 mouse neonates were randomized and placed in room air or hyperoxic (85% O
RESULTS: Neonatal mice treated with VitD in hyperoxic conditions had improved weight gain, reduced pulmonary edema and increased alveolar surface area compared to untreated pups in hyperoxia. No significant changes in cytokine expression were observed between untreated and VitD neonates. While changes in surfactant protein mRNA expression were impacted by hyperoxia and VitD administration, no significant changes in alveolar type II cell percentages were observed. At 3 weeks, mice in hyperoxia treated with VitD had greater lung compliance, diminished airway reactivity and improved weight gain.
CONCLUSIONS: High dose VitD significantly limited harmful effects of HALI. These results suggest that supplementation of VitD to neonatal mice during hyperoxia exposure provides both short-term and long-term protective benefits against HALI.