Ontology highlight
ABSTRACT:
PROVIDER: PRJNA379509 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5351720.fastq.gz | Fastqsanger.gz | |||
| SRR5351730.fastq.gz | Fastqsanger.gz | |||
| SRR5351721.fastq.gz | Fastqsanger.gz | |||
| SRR5351731.fastq.gz | Fastqsanger.gz | |||
| SRR5351722.fastq.gz | Fastqsanger.gz |
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Project description:Gene expression profiling was performed on nasal scrape samples obtained from asthmatics and matched healthy controls, to identify markers associated with various asthma subtypes. Nasal scrape samples were collected from asthmatics and healthy controls and subjected to expression profiling using Affymetrix HG-U133Plus2.0 microarrays.
2015-10-23 | E-GEOD-41862 | biostudies-arrayexpress
Project description:Gene expression profiling was performed on nasal scrape samples obtained from asthmatics and matched healthy controls, to identify markers associated with various asthma subtypes.
2015-10-23 | GSE41862 | GEO
Project description:NSAID-exacerbated respiratory disease (N-ERD) represents a particularly severe endotype of chronic rhinosinusitis with nasal polyps (CRSwNP), which affects around 10-16% of CRSwNP patients. N-ERD is characterized by severe and refractory nasal polyposis, bronchial asthma and intolerance to non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin. Today, the pathogenesis of N-ERD remains incompletely understood and curative treatments are lacking. Using a global transcriptomic approach, we identified local changes between the mucosa of N-ERD nasal polyps and healthy control inferior turbinates. Nasal brushing samples were collected from inferior turbinates of healthy controls and nasal polyps of N-ERD patients under anterior rhinoscopy and stored at -80°C in RNAprotect until RNA isolation and RNAseq.
2020-06-30 | E-MTAB-7962 | biostudies-arrayexpress
Project description:Although the nose, as a gateway for organism-environment interactions, may have a key role in asthmatic exacerbation, the rhinobiome of exacerbated children with asthma was widely neglected to date. Deep nasopharyngeal swab specimens, nasal epithelial spheroid cultures (NAEsp), and blood samples of acute exacerbated wheezers (WH), asthmatics (AB), and healthy controls (HC) were used for culture (n=146), 16 S-rRNA gene amplicon sequencing (n=64), proteomic and cytokine analyses. Interestingly, Proteobacteria were over-represented in WH (WH to AB: p=0.005; WH to HC: p=0.021), whereas Firmicutes and Bacterioidetes were associated with AB. In contrast, Actinobacteria commonly colonized HCs (PermANOVA p=0.005). Moreover, Staphylococcaceae (p<0.05), Enterobacteriaceae (p<0.05), Burkholderiaceae (p<0.05), Xanthobacteraceae (p<0.05), and Sphingomonadaceae (p<0.05) were significantly more abundant in AB compared to WH and HC. The α‐diversity analyses demonstrated an increase of bacterial abundance levels in atopic AB and a decrease in WH samples. Microbiome profiles of atopic WH differed significantly from atopic AB. The NAEsp bacterial exposure with M. catarrhalis, S. aureus and H. influenzae experiments provided a disrupted epithelial cell integrity, a cytokine release and cohort specific proteomic differences especially for M. catarrhalis cultures. Our comprehensive dataset contributes to a deeper insight into the poorly understood plasticity of the nasal microbiota, and, in particular, may enforce our understanding in the pathogenesis of asthma exacerbation in childhood.
2021-05-27 | PXD024694 | Pride
Project description:<p>This first clinical study of the Human Microbiome Project (HMP) addresses whether individuals share a core human microbiome. It involves broad determination of the microbiota found in five anatomical sites: the oral cavity, skin, nasal cavity, gastrointestinal tract and vagina. This study will enroll approximately 300 healthy male and female adults, 18-40 years old, from two geographic regions of the US: Houston, TX and St. Louis, MO. The participation of healthy individuals will create a baseline for discovery of the core microbiota typically found in various areas of the human body. The information from this initial study can then be used to help assess the changes in the complement of microbiota found on or within diseased individuals.</p>
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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:Background: In asthma, airway epithelium remodeling can already be detected during childhood, and epithelial cells are more susceptible to virus and oxidative stress. Their exact role in natural history and severity of children allergic respiratory disease remains however surprisingly unexplored. Aim: To analyze dysfunctions of epithelium in dust mite allergic respiratory disease (rhinitis ± asthma) in children. Methods: Expression profilings of nasal epithelial cells collected by brushing were performed on Affymetrix Hugene 1.0 ST arrays. All allergic patients were sensitized to dust mite. 19 patients had an isolated allergic rhinitis (AR). 14 patients had AR associated with asthma. Patients were compared to 12 controls, their severity and control being assessed according to NAEPP and ARIA criteria. Infections by respiratory viruses were excluded by real-time PCR measurements. Results: 61 probes were able to distinguish allergic rhinitis children from healthy controls. A majority of these probes was under the control of Th2 cytokines, as evidenced by parallel experiments performed on primary cultures of nasal epithelial cells. In uncontrolled asthmatic patients, we observed not only an enhanced expression of these Th2-responsive transcripts, but also a down-regulation of interferon-responsive genes. Conclusion: Our study identifies a Th2 driven epithelial phenotype common to all dust mite allergic children. Besides, it suggests that epithelium is involved in the severity of the disease. Expression profiles observed in uncontrolled asthmatic patients suggest that severity of asthma is linked at the same time to atopy and to impaired viral response. Nasal epithelium gene expression profiling of dust mite allergic children with isolated rhinitis, rhinitis associated with asthma and controls. 38 samples classified in 4 categories : 14 isolated rhinitis (R), 6 rhinitis with uncontrolled asthma (UA), 7 rhinitis with controlled asthma (CA) and 11 healthy subjects (C )
2012-01-05 | E-GEOD-19187 | biostudies-arrayexpress
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
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