Abstract
Reports indicate contradictory outcomes for anti-inflammatory functions of the α-tocopherol isoform of vitamin E in clinical studies of asthma and atherosclerosis. These seemingly disparate clinical results are consistent with novel unrecognized properties of isoforms of vitamin E reported in this study. We demonstrate that the isoform d-γ-tocopherol elevates inflammation in experimental asthma. Moreover, d-γ-tocopherol, at as little as 10% the concentration of d-α-tocopherol, ablates the anti-inflammatory benefit of the d-α-tocopherol isoform. A mechanism for these opposing immunoregulatory functions of purified tocopherols at physiological concentrations is not through modulation of expression of several cytokines, chemokines, or adhesion molecules, but is, at least in part, by regulation of endothelial cell signals during leukocyte recruitment. These opposing regulatory functions of vitamin E isoforms have impact on interpretations of vitamin E studies. In summary, our studies with purified tocopherol isoforms alter our understanding of vitamin E regulation of vascular function and asthma.
Footnotes
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↵1 These studies were supported by National Institutes of Health Grants R01 HL69428 (to J.M.C.-M.) and R01 AT004837 (to J.M.C.-M.) and by American Heart Association Grant 0855583G.
↵2 S.B. and H.A.-V. contributed equally and share first authorship.
↵3 Address correspondence and reprint requests to Dr. Joan M. Cook-Mills, Allergy-Immunology Division, Northwestern University Feinberg School of Medicine, McGaw-M304, 240 East Huron, Chicago, IL 60611. E-mail address: j-cook-mills{at}northwestern.edu
- Received November 3, 2008.
- Accepted January 29, 2009.
- Copyright © 2009 by The American Association of Immunologists, Inc.
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