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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Methylation data from CD4+ cells at birth and 12 months from a cohort of children who were diagnosed with IgE food allergy to either egg milk or peanut at 12 months (n=12) and healthy controls (n=12).

ABSTRACT: Mononuclear cells were collected from 24 infants at birth (n=12) and resampled at 12 months (n=12) and cells were either activated with anti-CD3 (0.5 ug/mL) + IL2(20U) or rested in media alone for 24 hours. CD4+ cells were purified and DNA was harvested and bisulphite converted for methylation analysis on illumina HM450K array. This is a pooled design. Each sample is bisulphite converted gDNA pooled in equimolar amounts from n=2 individuals. There are 6 allergic pools and 6 non allergic pools. Each pool is sampled at two time points, birth and 12 months, and either treated or untreated at each time point.

ORGANISM(S): Homo sapiens

SUBMITTER: David Martino

PROVIDER: E-GEOD-34639 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Methylation data from CD4+ cells at birth and 12 months from a cohort of children who were diagnosed with IgE food allergy to either egg milk or peanut at 12 months (n=12) and healthy controls (n=12).

Project description:DNA methylation data derived from total CD4+ T-cells from a cohort of paediatric food allergy. There are 12 food allergic samples (6 activated and matched control), 12 non-allergic samples (6 activated and matched control) collected at birth and resample at 12-months, total 48 samples. Mononuclear cells were either activated with anti-CD3 (0.5 ug/mL) + IL2(20U) or rested in media alone for 24 hours. CD4+ cells were purified and DNA was harvested and bisulphite converted for methylation analysis on illumina HM450K array.

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miRNA analysis after three months on GH treatment and contribute to explain the growth response after 12 months.

Project description:Context: There is growing evidence on the role of epigenetic regulation of growth, and miRNAs potentially play a role. Objective: To identify changes in circulating miRNAs following GH treatment in subjects with isolated idiopathic GH deficiency (IIGHD) after the first 3 months on treatment, and verify whether these early changes can predict growth response. Methods: The expression profiles of 384 miRNAs were analyzed in serum in 10 prepubertal patients with IIGHD (5 M,5 F) at two time points before starting GH treatment (t-3, t0), and at 3 months on treatment (t+3). MiRNAs with a fold change (FC) >±1.5 at t+3 were considered as differentially expressed. In silico analysis of target genes and pathways led to a validation step on 8 miRNAs in 25 patients. Clinical and biochemical parameters were collected at baseline, 6 and 12 months. Simple linear regression analysis and multiple stepwise linear regression models were used to explain the growth response. Results: 16 miRNAs were up-regulated and 2 down-regulated at t+3 months. MiR-199a-5p (p=0.020), miR-335-5p (p=0.001), and miR-494-3p (p=0.026) were confirmed to be up-regulated at t+3. Changes were independent of peak GH values at testing, and levels stabilized after 12 months. The predicted growth response at 12 months was considerably improved compared with models using the common clinical and biochemical parameters. Conclusion: miR-199a-5p, miR-335-5p, and miR-494-3p changed after 3 months on GH treatment and likely reflected both the degree of GH deficiency and the sensitivity to treatment. Furthermore, they were of considerable importance to predict growth response.

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