Mice exposed to retinoid deficiency in utero exhibit bronchial hyperresponsiveness as adults

Individuals with asthma and COPD are subject to debilitating bronchospasm as a result of airways that are hyperresponsive to stimuli. Factors that lead to the development of airway hyperresponsiveness are not well characterized.

In this issue of the Journal of Clinical Investigation, Wellington Cardoso and colleagues at the Boston University School of Medicine reveal that mice born to mothers with retinoid deficiency during pregnancy are at increased risk of developing airway hyperesponsiveness. Prenatal retinoid deficiency promoted altered airway development and lung differentiation. Bronchial hyperresponsiveness and abnormal phenotypes persisted throughout the postnatal period regardless for vitamin A status in the adult.

These results suggest that retinoid signaling in the lung is important for proper airway development and prevention of inappropriate pulmonary inflammatory responses.