Skip to main content
ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #234036
Title: Effect of vitamin E and SNPs at cytokine genes on cytokine production in the elderly

Author
item BELISLE, SARAH - JM USDA HNRCA @ TUFTS
item LEKA, LYNETTE - JM USDA HNRCA @ TUFTS
item DELGADO-LISTA, JAVIER - UNIV REINA SOFIA/CIBEROBN
item Jacques, Paul
item Ordovas, Jose
item Meydani, Simin

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/15/2008
Publication Date: 4/22/2009
Citation: Belisle, S.E., Leka, L.S., Delgado-Lista, J., Jacques, P., Ordovas, J.M., Meydani, S. 2009. Effect of vitamin E and SNPs at cytokine genes on cytokine production in the elderly. Journal of Federation of American Societies for Experimental Biology. 23:110.2.2.

Interpretive Summary:

Technical Abstract: Vitamin E (E) impacts cytokine production, yet individual response to E supplementation varies. Studies show cytokine production is heritable. Common single nucleotide polymorphisms (SNPs) may explain differences in cytokine production between individuals. We hypothesize that differential response to immunomodulatory actions of E reflect genetic differences among individuals, including SNPs at cytokine genes, which modulate cytokine levels. We used data from an E intervention in the elderly to test our hypothesis. We observed the effect of E on TNF-alpha production depended on TNF-alpha -308G>A. Subjects with G/G genotype at TNF-alpha -308G>A who were supplemented with E had higher TNF-alpha compared to subjects with G/G genotype given placebo. In contrast, subjects with A/A or A/G genotype at TNF-alpha -308G>A supplemented with E had lower TNF-alpha compared to subjects with A allele given placebo. This suggests individual immune response to E is in part mediated by genetics. Since A allele at TNF-alpha -308G>A has been associated with higher TNF-alpha, our results may indicate that anti-inflammatory effect of E is specific to those genetically predisposed to higher inflammation. Studies on the mechanism driving the E and TNF-alpha -308G>A interaction, and its disease implications are needed. Support: NIA NIH grant 5R01-AG013975; USDA agreement 58-1950-7-707; a DSM Nutritional Products, Inc. scholarship. CIBEROBN is an initiative of ISCIII.