Dataset Information

Peripheral blood mononuclear cells HELP-tagging cytosine methylation data (Albert Einstein College of Medicine)

ABSTRACT: Obesity-associated asthma is recognized as a distinct entity with non-atopic T-helper 1 polarized systemic inflammation. DNA methylation is linked with T helper cell maturation and is associated with inflammatory patterns in asthma and obesity. However, it is unknown whether pathologic dysregulation of DNA methylation patterns occurs in obesity-associated asthma. Using HELP-tagging, we studied epigenome wide DNA methylation in peripheral blood mononuclear cells in 8 urban minority obese asthmatic pre-adolescent children and compared it to methylation in groups of 8 children with asthma alone, obesity alone and healthy controls. Ingenuity Pathway Analysis was used to identify biological pathways that were differentially targeted by methylation dysregulation. We found that obese asthmatics had distinct epigenome wide methylation patterns associated with decreased promoter methylation of a subset of genes, including RANTES, IL-12R and TBX21 and increased promoter methylation of CD23, a low affinity receptor for IgE and of TGFβ, inhibitor of Th cell activation. T cell signaling and macrophage activation were the two primary pathways that were selectively hypomethylated in obese asthmatics. These methylation patterns suggest that methylation is associated with non-atopic inflammation observed in obese asthmatic children compared to children with asthma alone and obesity alone. Our findings suggest a role of DNA methylation in the observed inflammatory patterns in pediatric obesity-associated asthma in minorities. 32 HpaII test

ORGANISM(S): Homo sapiens

SUBMITTER: Deepa Rastogi John Greally Masako Suzuki

PROVIDER: E-GEOD-43705 | ArrayExpress | 2014-04-14

SECONDARY ACCESSION(S): SRP018119GSE43705PRJNA187088

REPOSITORIES: GEO, ArrayExpress, ENA

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Dataset's files

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			Action	DRS
	E-GEOD-43705.idf.txt	Idf
	E-GEOD-43705.processed.1.zip	Processed
	E-GEOD-43705.processed.2.zip	Processed
	E-GEOD-43705.sdrf.txt	Txt

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Publications

Differential epigenome-wide DNA methylation patterns in childhood obesity-associated asthma.

Rastogi Deepa D Suzuki Masako M Greally John M JM

Scientific reports 20130101

While DNA methylation plays a role in T-helper (Th) cell maturation, its potential dysregulation in the non-atopic Th1-polarized systemic inflammation observed in obesity-associated asthma is unknown. We studied DNA methylation epigenome-wide in peripheral blood mononuclear cells (PBMCs) from 8 obese asthmatic pre-adolescent children and compared it to methylation in PBMCs from 8 children with asthma alone, obesity alone and healthy controls. Differentially methylated loci implicated certain bio ...[more]

PMID: 23857381

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Project description:OBJECTIVES:Pediatric asthma is heterogeneous with phenotypes that reflect differing underlying inflammation and pathophysiology. Little is known about the national prevalence of certain obesity- and allergy-related asthma phenotypes or associated characteristics. We therefore assessed the national prevalence, risk factors, and caregiver-reported severity of four asthma phenotypes: not-allergic-not-obese, allergic-not-obese, obese-not-allergic, and allergic-and-obese. METHODS:We analyzed data from the 2007-2008 National Survey of Children's Health (NSCH) of 10-17 year-olds with caregiver-reported asthma. We described sociodemographic and health risk factors of each phenotype and then applied logistic and ordinal regression models to identify associated risk factors and level of severity of the phenotypes. RESULTS:Among 4427 children with asthma in this NSCH cohort, the association between race and phenotype was statistically significant (p < 0.0001); white children with asthma were most likely to have allergic-not-obese asthma while black and Hispanic children with asthma were most likely to have the obese-nonallergic phenotype (p < 0.001). Attention-deficit disorder/attention-deficit hyperactivity disorder was more likely to be present in allergic-not-obese children (odds ratio (OR) 1.50, confidence interval (CI) 1.14-1.98, p = 0.004). The phenotype with the highest risk for more severe compared to mild asthma was the obese-and-allergic asthma phenotype (OR 3.34, CI 2.23-5.01, p < 0.001). CONCLUSIONS:Allergic-not-obese asthma comprised half of our studied asthma phenotypes, while obesity-related asthma (with or without allergic components) comprised one-fifth of asthma phenotypes in this cohort representative of the US population. Children with both obese and allergic asthma are most likely to have severe asthma. Future management of childhood asthma might consider more tailoring of treatment and management plans based upon different childhood asthma phenotypes.