Vitamin A deficiency decreases and high dietary vitamin A increases disease severity in the mouse model of asthma.
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.
Schuster
Gertrud U
GU
Nutrition Department, U.S. Department of Agriculture Western Human Nutrition Research Center, University of California-Davis, 430 West Health Science Drive, Davis, CA 95616, USA. gschuster@ucdavis.edu
Kenyon
Nicholas J
NJ
Stephensen
Charles B
CB
D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000473:pathology; D001835:Body Weight / Q000187:drug effects; D016535:Bronchial Hyperreactivity / Q000139:chemically induced / Q000276:immunology / Q000473:pathology; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology / Q000276:immunology; D004032:Diet; D004195:Disease Models, Animal; D005260:Female; D007073:Immunoglobulin E / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D015847:Interleukin-4 / Q000032:analysis; D015848:Interleukin-5 / Q000032:analysis; D008099:Liver / Q000378:metabolism; D008168:Lung / Q000473:pathology; D008264:Macrophages / Q000276:immunology; D008297:Male; D051379:Mice; D010047:Ovalbumin / Q000276:immunology; D011657:Pulmonary Eosinophilia / Q000139:chemically induced* / Q000276:immunology / Q000473:pathology; D012130:Respiratory Hypersensitivity / Q000139:chemically induced* / Q000276:immunology / Q000473:pathology; D014801:Vitamin A / Q000008:administration & dosage / Q000378:metabolism / Q000633:toxicity*; D014802:Vitamin A Deficiency / Q000276:immunology*
D007074:Immunoglobulin G; D015848:Interleukin-5; D014801:Vitamin A; D015847:Interleukin-4; D007073:Immunoglobulin E; D010047:Ovalbumin