Introduction: Studies in children with asthma have revealed that reduced levels of vitamin D are associated with reduced lung function, airway remodelling and poor asthma control. The aim of this study was to determine if Vitamin D deficiency alters lung function resulting in airway hyperresponsiveness (AHR) and/or causes alterations in ASM mass.

Methods: A physiologically relevant mouse model of Vitamin D deficiency was developed by raising BALB/c mice on Vitamin D-defi cient or -replete diet. Studies were carried out on offspring from defi cient and replete mice of both sexes at 8 weeks of age. Lung function and thoracic gas volume (TGV) were measured by the forced oscillation technique (FOT) and plethysmography, respectively. AHR was assessed by measuring lung function responses to increasing doses of inhaled methacholine. Formalin-fi xed lungs embedded in paraffi n were cut into 5 μm thick sections. Sections were stained with Masson’s Trichrome for ASM measurement.

Results: Vitamin D-defi cient females had a smaller TGV compared to replete controls (P < 0.05). At 20 cm H2O transrespiratory pressure, Vitamin D-deficient mice had a smaller lung volume compared to controls (females, P = 0.024; males, P = 0.028). There were no signifi cant differences in airway resistance, however tissue damping was higher for vitamin D-defi cient mice (females, P = 0.03; males, P = 0.006). The dose of methacholine required to cause a doubling in airway resistance was lower in female Vitamin D-deficient mice. ASM mass was not signifi cantly altered.

Conclusions: Vitamin D defi ciency can lead to alterations in lung function and an increased sensitivity to bronchoconstricting agents but does not alter ASM mass.