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National Institute of Environmental Health Sciences

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Your Environment. Your Health.

Publication Detail

Title: Maternal micronutrient supplementation suppresses T cell chemokine receptor expression and function in F1 mice.

Authors: Delaney, Colin; Hoeltzel, Mark; Garg, Sanjay K; Warner, Roscoe; Johnson, Kent; Yung, Raymond

Published In J Nutr, (2012 Jul)

Abstract: Prenatal environmental exposures play a critical role in determining late-life chronic disease susceptibility. However, the mechanisms linking the in utero environment and disease development in the offspring are poorly understood. Recent investigations have confirmed a central pathogenic role of T cell chemokine receptors, particularly C-C chemokine receptor (CCR) 2 and CCR5, in chronic inflammatory conditions. This study was designed to determine the effect of a synthetic prenatal micronutrient supplementation (MS) diet rich in methionine pathway metabolites on the T cell chemokine system in F1 C57Bl/6 mice. Female mice were fed either an MS or control diet 3 wk prior to mating, during pregnancy, and lactation. At 4 wk of age, F1 mice were killed for experiments or were fed the standard NIH-31 diet and allowed to age. Food consumption, maternal weight gain, and litter size were similar in dams fed the control and MS diets. However, the F1 offspring of dams fed the MS diet were smaller in size (P < 0.001). T cells from the MS F1 offspring had global hypermethylation compared with control F1 offspring (P < 0.005), corresponding to lower T cell chemokine receptor expression [CCR2 (P < 0.001), CCR5 (P < 0.001), and C-x-C chemokine receptor 3 (P < 0.01)] and cytokine expression [TNFα (P < 0.05), IL-2 (P < 0.001), and IL-4 (P < 0.01)]. Reduced T cell chemokine receptor gene expression in MS F1 mice was associated with decreased chemotaxis in vitro to C-C chemokine ligand (CCL) 2 and C-X-C chemokine ligand 10 (P < 0.01) and in vivo to CCL2 (P < 0.01). Taken together, the results suggest that epigenetic alteration through prenatal diet manipulation reduces the response to proinflammatory signals in mice.

PubMed ID: 22649261 Exiting the NIEHS site

MeSH Terms: Animals; Chemotaxis/drug effects; Cytokines/genetics; Cytokines/metabolism; DNA Methylation/drug effects; Diet; Dietary Supplements; Epigenesis, Genetic; Female; Gene Expression/drug effects*; Growth/drug effects*; Growth/genetics; Inflammation/genetics; Inflammation/metabolism; Inflammation/prevention & control*; Methionine/metabolism; Mice; Mice, Inbred C57BL; Micronutrients/pharmacology*; Pregnancy; Prenatal Care; Prenatal Nutritional Physiological Phenomena/drug effects*; Prenatal Nutritional Physiological Phenomena/immunology; Receptors, Antigen, T-Cell/antagonists & inhibitors; Receptors, Antigen, T-Cell/genetics; Receptors, Antigen, T-Cell/metabolism*; Receptors, Chemokine/antagonists & inhibitors; Receptors, Chemokine/genetics; Receptors, Chemokine/metabolism*; Signal Transduction/drug effects

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