GEO DataSets

Analysis of airway smooth muscle cells (ASM) from mild asthmatics after a 2hr interleukin-17A (IL-17A) treatment. IL-17A orchestrates airway inflammation by cooperating with and inducing proinflammatory cytokines. Results provide insight into immediate-early/primary response gene targets of IL-17A.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 2 agent, 2 disease state sets

Platform:

GPL6244

Series:

GSE35643

12 Samples

Download data: CEL

(Submitter supplied) Interleukin (IL)-17 plays an important and protective role in host defence and has been demonstrated to orchestrate airway inflammation by cooperating with and inducing proinflammatory cytokines. Mircoarrays were used to identify immediate-early/ primary response IL-17A-dependent gene transcripts in primary human bronchial ASM cells from mild asthmatic and healthy individuals.

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS4803

Platform:

GPL6244

12 Samples

Download data: CEL

(Submitter supplied) Background: Increased proliferation of airway smooth muscle (ASM) cells leading to hyperplasia and increased ASM mass is one of the most characteristic features of airway remodelling in asthma. A bioactive lipid, sphingosine-1-phosphate (S1P), has been suggested to affect airway remodelling by stimulation of human ASM cell proliferation. Objective: To investigate the effect of S1P on signalling and regulation of gene expression in ASM cells from healthy and asthmatic individuals. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL5188

6 Samples

Download data

(Submitter supplied) Glucocorticoids (GCs) and protein kinase A (PKA)-activating agents (beta-adrenergic receptor agonists) are mainstream asthma therapies based on their ability to prevent or reverse excessive airway smooth muscle (ASM) constriction. Their abilities to regulate another important feature of asthma - excessive ASM growth are poorly understood. Recent studies have suggested that GCs render agents of inflammation such as interleukin 1beta and tumor necrosis factor alpha mitogenic to ASM, via suppression of (antimitogenic) induced cyclooxygenase-2-dependent PKA activity. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL96

54 Samples

Download data: CEL

(Submitter supplied) Purpose: Using RNA-sequencing, determine the effect of corticosteroids on human airway smooth muscle cells (ASM) exposed to Th1 and/or Th17 cytokines. Effects of cytokines and/or corticosteroids on gene expression was assessed. Methods: Pediatric human ASM (ages 0-21; n=4/treatment group) were serum starved for 48 h and then treated with 10 ng/mL TNFα, IFNγ, IL-17A, TNFα/IFNγ, or IFNγ/IL-17A in the presence of vehicle (0.01% DMSO) or 10 nM fluticasone propionate (FP). more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL20301 GPL18573

48 Samples

Download data: TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by array; Methylation profiling by array

Platforms:

GPL21145 GPL28226

548 Samples

Download data: IDAT

(Submitter supplied) We generated genome-wide methylation data from primary cultured airway smooth muscle cells (ASMCs) exposed to IL-13, IL-17, IL-13+IL-17, and vehicle. This data was generated in combination with genome-wide expression data from the same individuals.

Organism:

Homo sapiens

Type:

Methylation profiling by array

Platform:

GPL21145

280 Samples

Download data: CSV, IDAT

(Submitter supplied) We generated genome-wide expression data from primary cultured airway smooth muscle cells (ASMCs) exposed to IL-13, IL-17, IL-13+IL-17, and vehicle. This data was generated in combination with genome-wide methylation data from the same individuals.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL28226

268 Samples

Download data: CSV

(Submitter supplied) Rationale: Asthma is a chronic inflammatory airway disease. Children with severe asthma have lower levels of vitamin D than children with moderate asthma, and among children with severe asthma, airway smooth muscle (ASM) mass is inversely related to vitamin D levels. Beta2 agonists are a common asthma medication that act partly by targetting the ASM. We used RNA-Seq to characterize the human ASM transcriptome of fatal and asthma vs. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

53 Samples

Download data: DIFF, TXT

(Submitter supplied) CCAAT/Enhancer Binding Protein D (CEBPD) is a transcription factor that regulates genes involved in immune and inflammatory responses. Based on our previous observation that CEBPD expression increases in airway smooth muscle (ASM) with glucocorticoid exposure, we sought to better understand its role in the ASM transcriptomic response to glucocorticoids via knockdown experiments. Primary human airway smooth muscle (ASM) cells from four non-asthma donors were transfected with 25pmol of siRNA non-targeting control or siCEBPD SMARTpool using RNAiMax. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

31 Samples

Download data: TXT

(Submitter supplied) Rationale: Asthma is a chronic inflammatory airway disease. The most common medications used for its treatment are β2-agonists and glucocorticosteroids, and one of the primary tissues that these drugs target in the treatment of asthma is the airway smooth muscle. We used RNA-Seq to characterize the human airway smooth muscle (HASM) transcriptome at baseline and under three asthma treatment conditions. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

16 Samples

Download data: DIFF, TXT

(Submitter supplied) Asthmatics have elevated levels of IL-17A compared to healthy controls. IL-17A is likely to contribute to reduced corticosteroid sensitivity of human airway epithelium. Here, we aimed to investigate the mechanistic underpinnings of this reduced sensitivity in more detail. Differentiated primary human airway epithelial cells (hAECs) were exposed to IL-17A in the absence or presence of dexamethasone. Cells were then collected for RNA sequencing analysis or used for barrier function experiments. Mucus was collected for volume measurement and basal medium for cytokine analysis. 2861 genes were differentially expressed by IL-17A (Padj<0.05), of which the majority was not sensitive to dexamethasone (<50% inhibition). IL-17A did inhibit canonical corticosteroid genes, such as HSD11B2 and FKBP5 (p<0.05). Inflammatory and goblet cell metaplasia markers, cytokine secretion and mucus production were all induced by IL-17A, and these effects were not prevented by dexamethasone. Dexamethasone did reverse IL-17A-stimulated epithelial barrier disruption, and this was associated with gene expression changes related to cilia function and development. We conclude that IL-17A induces function-specific corticosteroid-insensitivity. Whereas inflammatory response genes and mucus production in primary hAECs in response to IL-17A were corticosteroid-insensitive, corticosteroids were able to reverse IL-17A-induced epithelial barrier disruption.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24676

16 Samples

Download data: TXT

(Submitter supplied) Identification and characterization of gene expression using Next Generation Sequencing (NGS) of mRNA sequence from bronchial epithelial cells (BEC) obtained from asthma patients with varying clinical disease severity

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

67 Samples

Download data: TXT

(Submitter supplied) Bronchial Epithelial Cells were isolated processed as described (Chu et al., 2002 and Zhao et al., 2011). The objective of the study was to identify differentially expressed genes between normal control (NC), mild-moderate asmathic (notSA) and severe asthmatic (SA) patients. For demographics data, contact Dr.Sally Wenzel (wenzelse@upmc.edu)

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6480

155 Samples

Download data: TXT

(Submitter supplied) Bronchial Epithelial Cells were isolated processed as described (Chu et al., 2002 and Zhao et al., 2011). The objective of the study was to identify differentially expressed genes between normal control (NC), mild-moderate asthmatic (MMA) and severe asthmatic (SA) patients.

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS5037

Platform:

GPL6480

108 Samples

Download data: TXT

Analysis of bronchial epithelial cells from patients with severe asthma. Results provide insight into the molecular mechanisms underlying the development of severe asthma.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 3 disease state, 2 gender sets

Platform:

GPL6480

Series:

GSE43696

108 Samples

Download data: TXT