Vitamin A deficiency decreases and high dietary vitamin A increases disease severity in the mouse model of asthma

Gertrud U. Schuster, Nicholas Kenyon, Charles B. Stephensen

Research output: Contribution to journalArticle

77 Scopus citations

Abstract

The Th1/Th2 paradigm has become an important issue in the pathogenesis of asthma, characterized by normal Th1 and elevated Th2 cytokine expression. Vitamin A deficiency (VAD) can produce a Th1 bias, whereas high-level dietary vitamin A can promote a Th2 bias. We used the OVA exposure mouse model to determine the contributions of vitamin A-deficient, control (4IU/g), and high-level vitamin A (250-IU/g) diets to the development of allergic airway inflammation and hyperresponsiveness. VAD reduced serum IgE and IgG1 responses, pulmonary eosinophilia, and the levels of IL-4 and IL-5 in bronchoalveolar lavage specimens, whereas the 250-IU/g diet increased serum IgE. Also, VAD blocked pulmonary hyperresponsiveness following methacholine challenge while the 250-IU/g diet exacerbated pulmonary hyperresponsiveness. In conclusion, VAD diminished and high-level dietary vitamin A enhanced the development of experimental asthma in this model system. These data suggest that excessive intake of vitamin A may increase the risk or severity of asthma in industrialized countries whereas vitamin A deficiency continues to increase mortality from infectious diseases in developing countries.

Original languageEnglish (US)
Pages (from-to)1834-1842
Number of pages9
JournalJournal of Immunology
Volume180
Issue number3
StatePublished - Feb 1 2008

ASJC Scopus subject areas

  • Immunology

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