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A novel whole blood gene expression signature for asthma, dermatitis and rhinitis multimorbidity in BAMSE and INMA cohort

ABSTRACT: A novel whole blood gene expression signature for asthma, dermatitis and rhinitis multimorbidity in BAMSE and INMA cohort

PROVIDER: PRJNA594327 | ENA |

REPOSITORIES: ENA

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A novel whole blood gene expression signature for asthma, dermatitis and rhinitis multimorbidity in BAMSE cohort

Project description:A novel whole blood gene expression signature for asthma, dermatitis and rhinitis multimorbidity in BAMSE cohort

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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).

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Expression data from airway epithelial cells stimulated with Poly(I:C) from patients with asthma, rhinitis, and healthy controls

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2013-10-18 | E-GEOD-51392 | biostudies-arrayexpress

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Atopic Dermatitis RNA-seq cohort

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Mapping the Periostin splice isoforms in atopic dermatitis and an in vitro asthma model – A multi-platform analysis using mass spectrometry and RT-qPCR

Project description:Periostin is a matricellular protein known to be alternatively spliced to produce isoforms with a molecular weight of 78-91 kDa. In the extracellular matrix, periostin attach to cell surfaces and induce signaling via integrin-binding and participates in fibrillogenesis to organize collagen in the extracellular space. In the atopic diseases atopic dermatitis and asthma, periostin is known to participate in driving the disease-causing type 2 inflammation. The periostin isoforms expressed in these diseases and the implication of the alternative splicing events are unknown. Here we present two universal assays to map the expression of periostin isoforms on both the transcriptional (RT-qPCR) and translational (PRM-based mass spectrometry) level. We use these assays to study the splice profile of periostin in atopic dermatitis lesions from patients in active treatment vs. normal skin and in in vitro models of atopic dermatitis and asthma. All isoforms expect isoform 3 show decreased expression at the transcriptional level in AD lesions from patients treated with corticosteroids compared to normal skin. The isoforms display an elevated amount at the translational level indicating a delayed response in periostin level during treatment. Expression of the isoforms were upregulated in the in vitro models of atopic dermatitis and asthma at both the transcriptional and translational level with isoform 3 and 5 displaying the highest level of overexpression. Interestingly, the often overlooked isoform 9 and 10 behaved opposite to the other isoforms as they were equally or even less abundant in the disease models compared to the control, and they were identified in the normal skin samples but not in atopic dermatitis lesions. With the assays and findings presented in the publication connected to this dataset we can take further steps in mapping and understanding the role of periostin isoforms.

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