BackgroundNeonates have dampened expression of pro-inflammatory cytokines and difficulty clearing pathogens. This makes them uniquely susceptible to infections, but the factors regulating neonatal-specific immune responses are poorly understood. Epigenetics, including histone modifications, can activate or silence gene transcription by modulating chromatin structure and stability without affecting the DNA sequence itself and are potentially modifiable. Histone modifications are known to regulate immune cell differentiation and function in adults but have not been well studied in neonates.ResultsTo elucidate the role of histone modifications in neonatal immune function, we performed chromatin immunoprecipitation on mononuclear cells from 45 healthy neonates (gestational ages 23–40 weeks). As gestation approached term, there was increased activating H3K4me3 on the pro-inflammatory IL1B, IL6, IL12B, and TNF cytokine promoters (p < 0.01) with no change in repressive H3K27me3, suggesting that these promoters in preterm neonates are less open and accessible to transcription factors than in term neonates. Chromatin immunoprecipitation with massively parallel DNA sequencing (ChIP-seq) was then performed to establish the H3K4me3, H3K9me3, H3K27me3, H3K4me1, H3K27ac, and H3K36me3 landscapes in neonatal and adult CD14+ monocytes. As development progressed from neonate to adult, monocytes lost the poised enhancer mark H3K4me1 and gained the activating mark H3K4me3, without a change in additional histone modifications. This decreased H3K4me3 abundance at immunologically important neonatal monocyte gene promoters, including CCR2, CD300C, ILF2, IL1B, and TNF was associated with reduced gene expression.ConclusionsThese results provide evidence that neonatal immune cells exist in an epigenetic state that is distinctly different from adults and that this state contributes to neonatal-specific immune responses that leaves them particularly vulnerable to infections.Electronic supplementary materialThe online version of this article (doi:10.1186/s13148-016-0265-7) contains supplementary material, which is available to authorized users.

Livestock ownership may influence anaemia through complex and possibly contradictory mechanisms. In this study, we aimed to determine the association of household livestock ownership with anaemia among women aged 15–49 years and children aged 6–59 months in Ghana and to examine the contribution of animal source foods (ASFs) to consumption patterns as a potential mechanism mediating this association. We analysed data on 4,441 women and 2,735 children from the 2014 Ghana Demographic and Health Survey and 16,772 households from the Ghana Living Standards Survey Round 6. Haemoglobin measurements were used to define anaemia (non‐pregnant women: <120 g/L; children: <110 g/L). Child‐ and household‐level ASF consumption data were collected from 24‐hour food group intake and food consumption and expenditure surveys, respectively. In multiple logistic regression models, household livestock ownership was associated with anaemia among children (OR, 95% CI: 1.5 [1.1, 2.0]), but not women (1.0 [0.83, 1.2]). Household ownership of chickens was associated with higher odds of anaemia among children (1.6 [1.2, 2.2]), but ownership of other animal species was not associated with anaemia among women or children. In path analyses, we observed no evidence of mediation of the association of household livestock ownership with child anaemia by ASF consumption. Ownership of livestock likely has limited importance for consumption of ASFs among young children in Ghana and may in fact place children at an increased risk of anaemia. Further research is needed to elucidate if and how pathogen exposure associated with livestock rearing may underlie this increased risk of anaemia.

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