HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Berdnikovs, S. Articles by Cook-Mills, J. M. Search for Related Content PubMed PubMed Citation Articles by Berdnikovs, S. Articles by Cook-Mills, J. M. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information Asthma Hazardous Substances DB VEGETABLE OIL

Isoforms of Vitamin E Have Opposing Immunoregulatory Functions during Inflammation by Regulating Leukocyte Recruitment¹

Allergy-Immunology Division, Northwestern University Feinberg School of Medicine, Chicago, IL 60611

Reports indicate contradictory outcomes for anti-inflammatory functions of the -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--tocopherol elevates inflammation in experimental asthma. Moreover, D--tocopherol, at as little as 10% the concentration of D--tocopherol, ablates the anti-inflammatory benefit of the D--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.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

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

⁴ Abbreviations used in this paper: TTP, -tocopherol transfer protein; BAL, bronchoalveolar lavage; CBA, cytokine bead assay; Penh, enhanced pause; PKC, protein kinase C.