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Interaction of vitamin E isoforms on asthma and allergic airway disease
  1. Joan Cook-Mills1,
  2. Tebeb Gebretsadik2,
  3. Hiam Abdala-Valencia1,
  4. Jeremy Green1,
  5. Emma K Larkin2,
  6. William D Dupont2,
  7. Xiao Ou Shu2,
  8. Myron Gross3,
  9. Chunxue Bai4,
  10. Yu-Tang Gao5,
  11. Terryl J Hartman6,
  12. Christian Rosas-Salazar2,
  13. Tina Hartert2
  1. 1 Northwestern University, Chicago, Illinois, USA
  2. 2 Vanderbilt University Medical Center, Nashville, Tennessee, USA
  3. 3 Department of Laboratory Medicine and Pathology, School of Public Health, University of Minnesota, Minneapolis, Minnesota, USA
  4. 4 Zhongshan Hospital, Fudan University, Shanghai, People's Republic of China
  5. 5 Department of Epidemiology, Shanghai Cancer Institute, Shanghai, People's Republic of China
  6. 6 Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia, USA
  1. Correspondence to Dr Joan Cook-Mills, Northwestern University Feinberg School of Medicine, 240 E. Huron, McGaw M304, Chicago, IL 60611, USA; j-cook-mills{at}northwestern.edu

Abstract

Prospective epidemiological studies, observational cross-sectional studies and some randomised prevention trials have demonstrated inconsistent findings of the impact of vitamin E on asthma risk. The goals of this study were to explore whether this differing association of vitamin E on asthma risk is due to an interaction of vitamin E isoforms. To address this question, in a population-based asthma incidence study we assessed the interaction between the plasma concentrations of vitamin E isoforms α-tocopherol and γ-tocopherol on asthma risk. Second, to understand the mechanisms of any interaction of these isoforms, we conducted experimental supplementation of α-tocopherol and γ-tocopherol isoforms in mice on the outcome of allergic airway inflammation. We found that in the highest γ-tocopherol tertile, low levels of α-tocopherol were associated with increased asthma risk, while highest tertile α-tocopherol levels trended to be protective. Similarly, in a mouse model of asthma, diet supplementation with α-tocopherol decreased lung inflammation in response to house dust mite (HDM) challenge. In contrast, diet supplementation with γ-tocopherol increased lung inflammation in response to HDM. These human and animal studies provide evidence for the competing effects of the vitamin E isoforms, in physiological concentrations, on asthma and allergic airway disease.

  • Allergic lung disease
  • Asthma
  • Asthma Epidemiology
  • Asthma Mechanisms

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