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Nutritional Immunology

Polymorphisms at Cytokine Genes May Determine the Effect of Vitamin E on Cytokine Production in the Elderly^1–3,

⁴ Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111; ⁵ Lipids and Atherosclerosis Research Unit, Reina Sofía University Hospital, University of Cordoba, Instituto Maimonides de Investigacion Biomedica de Cordoba, CIBER Fisiopatologia de la Obesidad y Nutricion Instituto de Salud Carlos III, Córdoba 14004, Spain; and ⁶ Department of Pathology, Sackler Graduate School of Biochemical Sciences, Tufts University, Boston, MA 02111

Vitamin E has been shown to affect cytokine production. However, individual response to vitamin E supplementation varies. Previous studies indicate that cytokine production is heritable and common single nucleotide polymorphisms (SNP) may explain differences in cytokine production between individuals. We hypothesize that the differential response to the immunomodulatory actions of vitamin E reflects genetic differences among individuals, including SNP at cytokine genes that modulate cytokine production. We used data from a double-blind, placebo-controlled 1-y vitamin E (182 mg d,l--tocopherol) intervention study in elderly men and women (mean age 83 y) to test this hypothesis (vitamin E, n = 47; placebo, n = 63). We found that the effect of vitamin E on tumor necrosis factor (TNF)- production in whole blood stimulated for 24 h with lipopolysaccharide (1.0 mg/L) is dependent on TNF -308G > A. Participants with the A/A and A/G genotypes at TNF -308G > A who were treated with vitamin E had lower TNF production than those with the A allele treated with placebo. These observations suggest that individual immune responses to vitamin E supplementation are in part mediated by genetic factors. Because the A allele at TNF has been previously associated with higher TNF levels in whole blood and isolated immune cells, our observations suggest that the antiinflammatory effect of vitamin E is specific to those genetically predisposed to higher inflammation. Further studies are needed to determine the biological mechanism driving the interaction between vitamin E treatment and TNF -308G > A and its implications for disease resistance.

^* To whom correspondence should be addressed. E-mail: simin.meydani{at}tufts.edu.

Manuscript received 1 July 2009. Initial review completed 8 July 2009. Revision accepted 31 July 2009.

Published online 26 August 2009.