Abstract # 8054 Event # 125:

Scheduled for Saturday, August 26, 2017 03:30 PM-03:45 PM: (Grand Ballroom) Oral Presentation


MATERNAL AND EPIGENETIC PROGRAMMING OF INFLAMMATION

E. L. Kinnally1,2, S. J. Martinez2 and A. Vogel-Ciernia1
1One Shields Avenue, UC Davis, One Shields Avenue, DAVIS, CA 95616, USA, 2CNPRC
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Early life experiences are formative, and make lifelong contributions to health. We have previously observed that poor quality maternal care, or low maternal sensitivity (MS) enhances inflammation, a risk factor for cardiovascular and metabolic disease, at a very early developmental stage in rhesus macaques. We characterized the potential epigenomic factors involved with this relationship in 44 infant rhesus macaques. Whole genome DNA methylation patterns were quantified from whole blood DNA using restricted representation bisulfite sequencing (RRBS). Bioinformatics analysis shows that over 13.6% of covered CpG sites (1252/9203 that meet QC standards, at least 10X coverage) are significantly differentially methylated based on MS and inflammatory status (high vs. low; q-value < .0001). A significant number of these differences were shared by low MS infants and infants exhibiting high inflammation (Fisher’s Exact test = 20.4, p = 2.49E-254). Gene ontology analysis shows that while MS-Inflammation DMRs affect multiple pathways, genes in the adrenergic and inflammatory pathways were enriched. In enriched pathway genes, functional analysis suggests that methylation ratios in low MS infants are likely to promote inflammation and ADR insensitivity, especially pertaining to B-AR signaling, relative to high MS infants. Taken together, these data suggest that low MS may predicted higher inflammation in infants by reducing immune cell sensitivity to sympathetic innervation and enhancing inflammatory signaling.