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Microglia isolated from juvenile offspring of dams with allergic asthma exhibit methylation and transcriptional alterations to autism risk genes

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE94569 | GEO | 2017/12/20

SECONDARY ACCESSION(S): PRJNA371477

REPOSITORIES: GEO

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Microglia isolated from juvenile offspring of dams with allergic asthma exhibit methylation and transcriptional alterations to autism risk genes [WGBS]

Project description:Asthma is one of the most common chronic diseases among pregnant women, and symptoms often worsen during pregnancy. Dysregulation in immune responses during pregnancy, such as those that develop with chronic allergic asthma, increase the risk of a having a child with an Autism Spectrum Disorder (ASD). We recently developed a mouse model of maternal allergic asthma (MAA) that induces alterations in behavioral outcomes of the offspring including changes in sociability, repetitive and perseverative behaviors. Pregnancy is also a time when epigenetic changes help a static genome adapt to the maternal environment, and consequently activation of the maternal immune system may alter the regulation of gene expression in the developing fetal brain. Perinatal exposure to maternal asthma alters DNA methylation of immune-related genes in human infants, suggesting that maternal asthma has long-lasting effects on the offspring’s’ immune function. Here we used the genome-wide approaches of whole genome bisulfite sequencing to examine DNA methylation combined with RNA sequencing to examine gene expression in acutely isolated microglia from juvenile MAA offspring. Differential analysis revealed significant alterations in the epigenome of microglia from MAA compared to PBS treated control offspring and identified genes involved in controlling microglial sensitivity to the environment and shaping both synaptic and long-range neuronal connections in the developing brain. Genes with altered methylation and expression in MAA juvenile microglia significantly overlapped with those identified in adult cortex from offspring of a different maternal immune activation (polyIC) autism model and with a curated list of autism risk genes in human, supporting a role for microglia in the pathogenesis of ASD.

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Microglia isolated from juvenile offspring of dams with allergic asthma exhibit methylation and transcriptional alterations to autism risk genes [RNA-Seq]

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Microglia from offspring of dams with allergic asthma exhibit epigenomic alterations in genes dysregulated in autism.

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Microglia isolated from juvenile offspring of dams with allergic asthma exhibit methylation and transcriptional alterations to autism risk genes

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Project description:We performed a pooled GWAS and individual genotyping in 269 children with allergic respiratory diseases comparing allergic children with and without asthma. We used a modular approach to identify the most significant loci associated with asthma by combining silhouette statistics and physical distance method with cluster-adapted thresholding. We found 97% concordance between pooled GWAS and individual genotyping, with 36 out of 37 top-scoring SNPs significant at individual genotyping level. The most significant SNP is located inside the coding sequence of C5, an already identified asthma susceptibility gene, while the other loci regulate functions that are relevant to bronchial physiopathology, as immune- or inflammation-mediated mechanisms and airway smooth muscle contraction. Integration with gene expression data (from mouse experimental asthma model taken from GSE6858 and GSE1301) showed that almost half of the putative susceptibility genes are differentially expressed in experimental asthma mouse models. Affymetrix SNP arrays (Mapping 250K NspI and StyI) were performed according to the manufacturer's directions on pooled DNA extracted from peripheral blood samples.The design is a pooled-GWAS. DNA samples were assigned to the Asthma group if displaying symptoms of asthma, alone or associated to other allergic phenotypes, including rhinoconjunctivitis (RC), and assigned to the RC group if displaying rhinitis or rhinoconjunctivits alone or associated to other allergic phenotypes, excluding asthma. Each of the two groups was subdiveded into 4 independent groups of samples, each containing 31-36 individuals. Individual DNA samples were then added to their respective pools in equivalent molar amounts. Each pool was labeled and hybridized independently on three different arrays (3 technical replicates for each pool).

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