E3de7f0d-aff3-4183-b9c2-2b308a9315ca - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001008767 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:This study included nasal gene expression data collected from nasal brushes of adolescents in PIAMA birth cohort.
| EGAS00001006240 | EGA
Project description:Nasal DNA methylation at three CpG sites predicts childhood allergic disease
| EGAD00010002263 | EGA
Project description:The link between upper and lower airways in patients with both asthma and allergic rhinitis is still poorly understood. As the biological complexity of these disorders can be captured by gene expression profiling we hypothesized that the clinical expression of rhinitis and/or asthma is related to differential gene expression between upper and lower airways epithelium. We used micro array to profile gene expression of primary nasal and bronchial epithelial cells from the same individuals and examining the impact of allergic rhinitis with and without concomitant allergic asthma on expression profiles. 17 subjects were included in a cross-sectional study (6 allergic asthma and allergic rhinitis; 5 allergic rhinitis; 6 healthy controls). RNA was extracted from isolated and cultured epithelial cells from bronchial brushes and nasal biopsies, and analyzed by microarray (Affymetrix U133+ PM Genechip Array).
2013-02-05 | E-GEOD-44037 | biostudies-arrayexpress
Project description:Rhinovirus infections are the most common cause of asthma exacerbations. The complex responses by the airway epithelium to rhinovirus can be captured by gene expression profiling. We hypothesized that the upper and lower airway epithelium exhibit differential responses to double-stranded RNA (dsRNA), and that this is modulated by the presence of asthma and allergic rhinitis. Identification of dsRNA-induced gene expression profiles by microarray of primary nasal and bronchial epithelial cells from the same individuals and examining the impact of allergic rhinitis with and without concomitant allergic asthma on expression profiles. 17 subjects were included in a cross-sectional study (6 allergic asthma and allergic rhinitis; 5 allergic rhinitis; 6 healthy controls). RNA was extracted from isolated and cultured epithelial cells that were stimulated with Poly(I:C) for 24 hours from bronchial brushes and nasal biopsies, and analyzed by microarray (Affymetrix U133+ PM Genechip Array).
2013-10-18 | E-GEOD-51392 | biostudies-arrayexpress
Project description:Genome wide DNA methylation profiling of nasal-epithelial swabs collected from vaping and non-vaping (within 6 months) adolescents from Denver, Aurora, and Pueblo, CO . The Illumina Infinium Human Methylation 850K beadchip profiling microarray was used to obtain DNA methylation profiles across approximately 868,000 CpGs. Samples included 11 swabs from adolescents who had vaped in the last 6 months, and 37 who had not.
2024-07-05 | GSE240130 | GEO
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: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: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
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:Objectives: To determine whether disease processes related to granulomatosis with polyangiitis (GPA) are reflected in gene expression profiles of nasal mucosa. Methods: Nasal brushings of the inferior turbinate were obtained from 32 patients with GPA (10 with active nasal disease, 13 with prior nasal disease, 9 with no history of nasal disease) and a composite comparator group with and without inflammatory nasal disease (12 healthy people, 15 with sarcoidosis, 8 with allergic rhinitis). Differential gene expression was assessed between subgroups of GPA and comparators. Results: 339 genes were differentially expressed between the GPA and comparator groups (absolute fold change > 1.5; false discovery rate < 0.05). Top canonical pathways upregulated in nasal brushings from patients with GPA include granulocyte adhesion and diapedesis (p=8.6 E-22), agranulocyte adhesion and diapedesis (p=1.3 E-14), interleukin 10 signaling (3.0 E-11), and TREM1 signaling (9.0 E-11). A set of genes differentially expressed in GPA independent of nasal disease activity status included genes related to epithelial barrier integrity (fibronectin 1, desmosomal proteins) and several matricellular proteins (e.g. osteonectin, osteopontin). Significant overlap of differentially expressed genes was observed between active and prior nasal disease GPA subgroups. Peripheral blood neutrophil and mononuclear gene expression levels associated with GPA were similarly altered in the nasal gene expression profiles of patients with active or prior nasal disease. Conclusions: Profiling the nasal transcriptome in GPA reveals gene expression signatures related to innate immunity, inflammatory cell chemotaxis, extracellular matrix composition, and epithelial barrier integrity. Airway-based expression profiling is feasible and informative in GPA.
2018-08-29 | GSE119136 | GEO