Submitted to: Journal of Immunology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/16/2007
Publication Date: 2/1/2008
Citation: Schuster, G.U., Kenyon, N.J., Stephensen, C.B. 2008. Vitamin A deficiency decreases and high dietary vitamin A increases disease severity in the mouse model of asthma. Journal of Immunology, 180:1834-1842.
Interpretive Summary: Asthma is increasing in prevalence in the US, apparently due to changes in the environment that have ocurred over the past few decades. Such changes include decreased burden of infectious diseases and increased exposure to allergens and perhaps environmental pollutants, such as ozone. Changes in diet may also affect the risk of asthma. This study demonstrates that high-level dietary vitamin A increases while vitamin A deficiency decreases the severity of asthma in a mouse model. These data suggest that level of intake of some nutrients during infancey and early childhood may affect the risk of asthma
Technical Abstract: The Th1/ Th2 paradigm has become an important issue in the pathogenesis of asthma, characterized by normal Th-1 and elevated Th-2 cytokine expression, resulting in a Th2 predominance. Vitamin A deficiency (VAD) produces a significant Th1 bias, while high-level dietary vitamin A supplementation promotes a Th2 bias. We used the ovalbumin exposure mouse model to determine the contributions of a vitamin A deficient (VAD), control (4IU/ g), and high-level vitamin A (250 IU/g) diets to the development of allergic airway inflammation and hyper-responsiveness. VAD reduced serum IgE and DNP-specific IgG1 responses, recruitment of eosinophils into the lung, and the level of IL-4 and IL-5 in bronchoalveolar lavage (BAL) specimens, while the250 IU/g diet increased serum IgE. Also, VAD blocked pulmonary hyper-responsiveness following methacholine challenge while the 250 IU/g diet exacerbated pulmonary hyper-responsiveness. In conclusion, VAD diminishes and high-level dietary vitamin A enhances the development of experimental asthma in this model system.