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ABSTRACT:
PROVIDER: PRJNA1143493 | ENA |
REPOSITORIES: ENA
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Project description:CD4+ cells and pediatric obesity-related asthma
| PRJNA947501 | ENA
Project description:To investigate the contribution of CD4+ T cells in pediatric obesity-related asthma.
2025-03-21 | GSE227915 | GEO
Project description:To investigate the contribution of CD4+ T cells in pediatric obesity-related asthma.
2025-04-09 | GSE274583 | GEO
Project description:Obesity is a risk factor for asthma severity and morbidity, displaying a distinct clinical phenotype that is less responsive to inhaled corticosteroids. CD4+ T-cells are central to the immunologic pathways of asthma and may contribute to the unique obese asthma phenotype. We sought to characterize the single cell CD4+ transcriptional profile among obese children with asthma compared to matched normal weight children with asthma.
2025-05-01 | GSE230024 | GEO
Project description: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 TGFM-NM-2, 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
2014-04-14 | E-GEOD-43705 | biostudies-arrayexpress
Project description: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.
2014-04-14 | GSE43705 | GEO
Project description:Different naïve or memory cell subpopulations (i.e., central memory/CM, effector memory/EM, or terminally differentiated effector memory/EMRA) are involved in asthma development, and they display variable levels of the CD26 (dipeptidyl peptidase 4/DPP4). The phenotype and/or severity of the disease could drive to a phenotypic shift in naïve/memory lymphocyte subsets. Therefore, the aim of our work was to evaluate the association of the phenotype and severity of asthma with the relative frequency of CD26-/lo, CD26int, and CD26hi subsets within CD4+ effector T cells (Teff), total CD4- lymphocytes, γδ-T cells, NK cells, and NKT cells. For that, flow cytometry analyses were performed in peripheral blood samples from healthy donors (N=30) and asthma patients (N=119) with different phenotypes/severities. To avoid a priori bias, we have performed a K-means clustering analysis including clinical and flow cytometry data, resulting in four groups, two of them with opposite inflammatory profiles (eosinophilic vs. neutrophilic). CD4-CD26hi cells were reduced in neutrophilic asthma, and negatively correlated with degree of systemic inflammation. Interestingly, the eosinophilic group displayed a general expansion of CD26-/lo lymphocyte subsets. The expansion of CD4+CD26-/lo Teff cells with a TEM/TEMRA phenotype was confirmed in asthma, especially in atopic patients. Further characterisation of this subset by LC MS/MS revealed upregulated levels of innate (e.g., MPO and RNASE2) and cytoskeleton/extracellular matrix (e.g., MMP9, ACTN1) proteins, which matches its terminally differentiated phenotype. Validation by immunofluorescence confirmed the presence of many of these proteins in CD4+ T cells, as well as an enrichment in “flower-like” nuclei and MMP9/RNASE2 levels in CD4+CD26-/lo Teff compared to CD4+ T lymphocytes. Therefore, there is an association between CD26 levels in different lymphocyte subsets and asthma phenotypes/severities. CD4+CD26-/loTEMRA cells expressing innate proteins specific to eosinophils/neutrophils could be relevant in sustaining long-term inflammation in adult allergic asthma.
2025-02-17 | PXD051222 | Pride
Project description:Genetic and Epigenetic Determinants of Pediatric Obesity-Associated Asthma
| PRJNA533156 | ENA
Project description:Genetic and Epigenetic Determinants of Pediatric Obesity-Associated Asthma
| PRJNA533157 | ENA
Project description:Purpose: Obesity is known to be a multifactorial condition that is highly heritable. There have been ~60 susceptibility loci identified, but they only account for a fraction of cases.. As copy number variations (CNVs) have been implicated in the etiology of a multitude of human disorders including obesity, here, we investigated the contribution of rare CNVs (<0.1% population frequency) in pediatric cases of obesity. Methods: We genotyped 67 pediatric patients presenting with obesity, including 22 with co-morbid developmental delay and prioritized rare CNVs at known associated loci, as well as, those impacting genes involved in energy homeostasis or related processes. Results: We identified clinically relevant or potentially clinically-relevant CNVs in 15% (10/67) of individuals. Of these, 4% (3/67) had 16p11.2 microdeletions encompassing the known obesity risk gene SH2B1. Notably, we identified two unrelated probands harboring different 6p22.2 microduplications encompassing SCGN, a potential novel candidate gene for obesity. Further, we identified other biologically relevant candidate genes for pediatric obesity including ARID5B, GPR39, PTPRN2, and HNF4G. Conclusion: We found previously reported candidate loci for obesity, and new ones, suggesting CNV analysis may assist in the diagnosis of pediatric obesity.
2018-07-12 | GSE101417 | GEO