Nasal DNA methylation at three CpG sites predicts childhood allergic disease
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ABSTRACT:
PROVIDER: EGAS00001005189 | EGA |
REPOSITORIES: EGA
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Project description:Nasal DNA methylation at three CpG sites predicts childhood allergic disease
| EGAD00010002263 | EGA
Project description:Analysis of nasal epithelial cells from adult patients with seasonal allergic rhinitis and from non allergic controls. Results provide insight into the molecular mechanisms associated with inflammatory responses in nasal mucosa. Total RNA was obtained from nasal epithelial cells of 7 seasonal allergic rhinitis patients and 5 non-allergic control subjects
2015-01-16 | E-GEOD-43523 | biostudies-arrayexpress
Project description:Analysis of nasal epithelial cells from adult patients with seasonal allergic rhinitis and from non allergic controls. Results provide insight into the molecular mechanisms associated with inflammatory responses in nasal mucosa.
2015-01-16 | GSE43523 | GEO
Project description:Purpose: Ipratropium bromide (IB) is able to ameliorate symptoms of allergic rhinitis (AR) by neuroimmunologic mechanism. We intended to explorer whether IB induced effect through modulating specific alteration of miRNA profiling or not. Methods: Nasal sRNAs (miRNAs) profiles of control mice and OVA-induced AR mice that were pre-treated with IB or normal saline before intranasal OVA challenge for 2 or 4 weeks were generated by high-throughput sequencing using Illumina Hiseq 2000.Raw data for sRNA (miRNA) profiles were processed to obtain corresponding clean data which were mapped to reference sequence(mm10) by TopHat(v2.0.9).The expression levels for these resulting mapped miRNAs were estimated by TPM (transcript per million),afterwards, the differentially expressed miRNAs were identified, and the candidate allergic-related miRNAs were further determined by RT-qPCR. Results: Using an optimized data analysis workflow,our data showed that in nasal mucosa of allergic mice with ipratropium bromide (IB) treatment 87 miRNAs are differentially expressed whereas in the nasal mucosa of non-allergic mice 113 miRNAs are differentially expressed, when compared with allergic mice treated with normal saline.IB treatment significantly up-regulated the levels of mmu-miR-124-3p/5p, -133b-5p, -133a-3p/5p, -384-3p, -181a-5p, -378a-5p, -3071-5p. RT-qPCR data further validated these miRNAs expression. Conclusions: Our study represents the detailed analysis of nasal mucosa miRNAs profiles of OVA-induced allergic mice treated with IB, generated by RNA-seq technology. Moreover, IB treatment orchestrated expression of allergic immune-related miRNAs of nasal mucosa in allergic mice, which may associate with ameliorated nasal allergic symptoms
2018-07-31 | GSE92975 | GEO
Project description:This study included nasal gene expression data collected from nasal brushes of adolescents in PIAMA birth cohort, which is used in the project Nasal DNA methylation at three CpG sites predicts childhood allergic disease. 186 samples were included in this analysis, and phenotypes (age and sex) were provided together with a gene expression count table. Gene expression was measured by the Illumina HiSeq2500 sequencer.
| EGAD00001008767 | EGA
Project description:Epigenetic alterations may represent new therapeutic targets and/or biomarkers of allergic rhinitis (AR). Our aim was to examine genome-wide epigenetic changes induced by controlled pollen exposure in the Environmental Exposure Unit (EEU). 38 AR-sufferers and 8 non-allergic controls were exposed to grass pollen for 3h on two consecutive days. We interrogated DNA methylation at baseline and 3h in peripheral blood mononuclear cells (PBMCs) using the Infinium Methylation 450K array. We corrected for demographics, cell composition, and multiple testing (Benjamini-Hochberg), and verified hits using bisulfite PCR-pyrosequencing and qPCR. To extend these findings to a clinically relevant tissue, we investigated DNA methylation and gene expression of mucin 4 (MUC4), in nasal brushings from a separate validation cohort exposed to birch pollen. In PBMCs of allergic rhinitis participants, 42 sites showed significant DNA methylation changes of 2% or greater. DNA methylation changes in tryptase gamma 1 (TPSG1), schlafen 12 (SLFN12) and MUC4 in response to exposure were validated by pyrosequencing. SLFN12 DNA methylation significantly correlated with symptoms (p<0.05), and baseline DNA methylation pattern was found to be predictive of symptom severity upon grass allergen exposure (p<0.05). Changes in MUC4 DNA methylation in nasal brushings in the validation cohort correlated with drop in peak nasal inspiratory flow (Spearman r = 0.314, p = 0.034), and MUC4 gene expression was significantly increased (p<0.0001). This study revealed novel and rapid epigenetic changes upon exposure in a controlled allergen challenge facility, identified baseline epigenetic status as a predictor of symptom severity.
2018-06-01 | GSE100386 | GEO
Project description:Allergic nasal polyposis is a chronic type 2 inflammatory condition of the upper respiratory tract. We characterize nasal polyps from 5 subjects using single-cell RNA-sequencing, identifying “allergic” tuft cells, characterized by increased expression of the prostaglandin synthetic pathway, in association with a PGE2-activated gene signature.
2022-05-31 | GSE202100 | GEO
Project description:Chronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by persistent symptoms associated to the development of nasal polyps. To this day, the molecular mechanisms involved are still not well defined. However, it has been suggested that a sustained inflammation as allergy is involved in its onset. In this pilot study, we aimed to look into the effect of the allergic status of the patient and in their underlying mechanisms. To achieve this, we recruited 22 patients with CRSwNP and classified them in non-allergic and allergic using ImmunoCAP ISAC molecular diagnosis. Plasma samples were analyzed using liquid chromatography coupled to mass spectrometry (LC-MS). Subsequently, the identified changed metabolites from plasma that were commercially available were then analyzed by targeted analysis in some nasal polyps. Additionally, nasal polyp and mucosa tissue samples were examined for eosinophils and neutrophils. We found that 9 out of the 22 patients were sensitized to some aeroallergens (named as allergic). The other 13 patients had no sensitizations (non-allergic). Regarding metabolomics, we found that bilirubin, cortisol, lysophosphatidylcholines (LPCs) 16:0, 18:0 and 20:4 and lysophosphatidylinositol (LPI) 20:4, metabolites that are usually related to a sustained allergic inflammation, were unexpectedly increased in the plasma of non-allergic patients with CRSwNP compared to allergic patients with CRSwNP. LPC 16:0, LPC 18:0 and LPI 20:4 metabolites followed the same trend in the nasal polyp as they did in plasma. Comparison of nasal polyps with nasal mucosa tissue showed a significant increase in eosinophils (p < 0.001) and neutrophils (p < 0.01) in allergic patients with CRSwNP. There were also more eosinophils in the polyps of non-allergic patients with CRSwNP than in their nasal mucosa (p <0.01). The polyps from non-allergic patients with CRSwNP had less eosinophils than the polyps of allergic patients with CRSwNP (p < 0.05). Our data suggests that there is a systemic inflammatory response associated to CRSwNP in the absence of allergy, which could be accountable for the nasal polyp development. Allergic patients with CRSwNP presented a higher number of eosinophils located in nasal polyps suggesting that eosinophilia might be connected to the development of nasal polyps in these patients.
2021-03-17 | ST001734 | MetabolomicsWorkbench
Project description:Chronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by persistent symptoms associated to the development of nasal polyps. To this day, the molecular mechanisms involved are still not well defined. However, it has been suggested that a sustained inflammation as allergy is involved in its onset. In this pilot study, we aimed to look into the effect of the allergic status of the patient and in their underlying mechanisms. To achieve this, we recruited 22 patients with CRSwNP and classified them in non-allergic and allergic using ImmunoCAP ISAC molecular diagnosis. Plasma samples were analyzed using liquid chromatography coupled to mass spectrometry (LC-MS). Subsequently, the identified changed metabolites from plasma that were commercially available were then analyzed by targeted analysis in some nasal polyps. Additionally, nasal polyp and mucosa tissue samples were examined for eosinophils and neutrophils. We found that 9 out of the 22 patients were sensitized to some aeroallergens (named as allergic). The other 13 patients had no sensitizations (non-allergic). Regarding metabolomics, we found that bilirubin, cortisol, lysophosphatidylcholines (LPCs) 16:0, 18:0 and 20:4 and lysophosphatidylinositol (LPI) 20:4, metabolites that are usually related to a sustained allergic inflammation, were unexpectedly increased in the plasma of non-allergic patients with CRSwNP compared to allergic patients with CRSwNP. LPC 16:0, LPC 18:0 and LPI 20:4 metabolites followed the same trend in the nasal polyp as they did in plasma. Comparison of nasal polyps with nasal mucosa tissue showed a significant increase in eosinophils (p < 0.001) and neutrophils (p < 0.01) in allergic patients with CRSwNP. There were also more eosinophils in the polyps of non-allergic patients with CRSwNP than in their nasal mucosa (p <0.01). The polyps from non-allergic patients with CRSwNP had less eosinophils than the polyps of allergic patients with CRSwNP (p < 0.05). Our data suggests that there is a systemic inflammatory response associated to CRSwNP in the absence of allergy, which could be accountable for the nasal polyp development. Allergic patients with CRSwNP presented a higher number of eosinophils located in nasal polyps suggesting that eosinophilia might be connected to the development of nasal polyps in these patients.
2021-03-17 | ST001733 | MetabolomicsWorkbench
Project description:Background: Nasal epithelia are emerging as a proxy measure of gene expression of the airway epithelium in asthma. We hypothesized that epigenetic marks regulate gene expression of the nasal epithelia and consequently may provide a novel target for allergic asthma. Methods: We compared genomic DNA methylation patterns and gene expression in African American children with persistent atopic asthma [N=36] versus healthy controls [N=36]. Results were validated in an independent population of asthmatics [N=30]. Results: We identified 186 genes with significant methylation changes, either as regions (differentially methylated regions [DMRs]) or single CpGs (differentially methylated probes [DMPs]) after adjustment for age, gender, race/ethnicity, batch effects, inflation, and multiple comparisons (false discovery rate-adjusted q<0.05). Genes differentially methylated include those with established roles in asthma and atopy, components of the extracellular matrix, genes related to immunity, cell adhesion, epigenetic regulation, and airway obstruction. The methylation changes are large (median 9.5%, range: 2.6-29.5% methylation change) and similar in magnitude to those observed in malignancies. Hypo- and hyper-methylated genes were associated with increased and decreased gene expression respectively (P<2.8x10-6 for DMRs and P<7.8x10-10 for DMPs). Quantitative analysis of methylation-expression relationships in 53 differentially expressed genes demonstrated that 32 (60%) have significant (q<0.05) methylation-expression relationships within 5kb of the gene. 10 loci selected based on the relevance to asthma, magnitude of methylation change, and asthma specific methylation-expression relationships were validated in an independent cohort of children with asthma. Conclusions: Our findings that epigenetic marks in respiratory epithelia are associated with allergic asthma in inner-city children provide new targets for biomarker development, and novel approaches to understanding disease pathogenesis. case control design with nasal epithelial cells from 36 atopic asthmatic and 36 nonatopic nonasthmatic children from the inner city
2015-11-01 | E-GEOD-65163 | biostudies-arrayexpress