GEO DataSets

(Submitter supplied) Airway mucus obstruction triggers macrophage activation and MMP12-dependent emphysema

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

6 Samples

Download data: CEL

(Submitter supplied) Chronic obstructive pulmonary disease (COPD) is characterized by a progressive decline in lung function, caused by exposure to exogenous particles, mainly cigarette smoke (CS). COPD pathogenesis is initiated and perpetuated by an abnormal CS-induced inflammatory response of the lungs, involving both innate and adaptive immunity. Specifically, B cells organized in iBALT structures, as well as macrophages, accumulate in the lungs and contribute to CS-induced emphysema, but the mechanisms thereof remain unclear. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS5438

Platform:

GPL6885

12 Samples

Download data: TXT

Analysis of lung from cigarette smoke (CS)-treated C57BL/6N females at 4 and 6 months of age. Tobacco smoking is a major cause of chronic obstructive pulmonary disease (COPD). Results provide insight into the molecular mechanisms underlying cigarette smoke-induced COPD.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 age, 2 stress sets

Platform:

GPL6885

Series:

GSE52509

12 Samples

Download data

(Submitter supplied) Introduction: Sarcoidosis is a multisystem immuno-inflammatory disorder of unknown etiology that most commonly involves the lungs. We hypothesized that an unbiased approach to identify pathways activated in alveolar macrophages—a key immuno-inflammatory cell in the lung—can shed light on the pathogenesis of this complex disease. Methods: We recruited 15 patients with various stages of sarcoidosis and 12 healthy controls. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL571

27 Samples

Download data: CEL

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

Organism:

Mus musculus

Type:

Expression profiling by array

Platforms:

GPL6246 GPL11533

84 Samples

Download data: CEL

(Submitter supplied) Scnn1b-Tg mice overexpress the beta subunit of the epithelial sodium channel (Scnn1b) in airway Club cells. The general phenotype of these mice is described in three published manuscripts (Mall et al. 2004, Nature Medicine, 10(5):487-93; Mall et al. 2008, Am J Respir Crit Care Med. 177(7):730-42; Livraghi-Butrico et al. 2012, Physiol. Genomics 44(8):470-84; and Livraghi-Butrico et al. 2012, Mucosal Immunology 5(4):397-408). more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

24 Samples

Download data: CEL

(Submitter supplied) Scnn1b-Tg mice overexpress the beta subunit of the epithelial sodium channel (Scnn1b) in airway Club cells. The general phenotype of these mice is described in three published manuscripts (Mall et al. 2004, Nature Medicine, 10(5):487-93; Mall et al. 2008, Am J Respir Crit Care Med. 177(7):730-42; and Livraghi-Butrico et al. 2012, Physiol. Genomics 44(8):470-84. Briefly, overexpression of the Scnn1b transgene in airway Club cells leads to hyperabsorption of sodium from the airway surface liquid, dehydrated airway surface liquid and mucus, and reduced mucus clearance associated with accumulation of mucus plugs/plaques. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL11533

36 Samples

Download data: CEL

(Submitter supplied) Scnn1b-Tg mice overexpress the beta subunit of the epithelial sodium channel (Scnn1b) in airway Club cells. The general phenotype of these mice is described in three published manuscripts (Mall et al. 2004, Nature Medicine, 10(5):487-93; Mall et al. 2008, Am J Respir Crit Care Med. 177(7):730-42; Livraghi-Butrico et al. 2012, Physiol. Genomics 44(8):470-84; and Livraghi-Butrico et al. 2012, Mucosal Immunology 5(4):397-408). more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

24 Samples

Download data: CEL

(Submitter supplied) We have used microarrays to identify individual genes and pathways regulated by Gq/11 or G12/13 signalling in type II alveolar epithelial cells isolated from the lungs of knockout mice.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

12 Samples

Download data: CEL, CHP

(Submitter supplied) This series represents alveolar macrophages from a mouse model of emphysema, deletion of the integrin beta6 Keywords: parallel sample

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS1874

Platform:

GPL1792

15 Samples

Download data: TIFF

(Submitter supplied) This series represents isolated alveolar macrophages from human subjects. Keywords: parallel sample

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS1269

Platform:

GPL570

45 Samples

Download data: CEL

Analysis of alveolar macrophages of integrin beta-6 (Itgb6) deficient animals treated with doxycycline. Itgb6 mutants develop emphysema. Effect of TGFbeta transgene induction to suppress the effect of the Itgb6 mutation also examined.

Organism:

Mus musculus

Type:

Expression profiling by array, log ratio, 3 genotype/variation sets

Platform:

GPL1792

Series:

GSE2255

15 Samples

Download data: TIFF

Analysis of alveolar macrophages from 15 cigarette smokers, 15 non-smokers and 15 asthmatics. Results suggest that alveolar macrophage activation induced by smoking contributes to emphysema.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 3 agent sets

Platform:

GPL570

Series:

GSE2125

45 Samples

Download data: CEL

(Submitter supplied) The SWCNTs can induce airway hyper-responsiveness (AHR) and chronic obstructive pulmonary disease (COPD)-like changes in mice model. The SWCNTs can induce clusters of proteinases, chemokines/cytokines, and macrophage receptors triggered signaling, which might play critical roles in the SWCNTs-induced pathological changes, including chronic inflammation and tissues remodeling. We used microarrays to detail the global programme of gene expression underlying and identified distinct classes of up-regulated genes during this process.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

8 Samples

Download data: CEL

(Submitter supplied) Extravasation of monocytes into tissue and to the site of injury is a fundamental immunological process underlying a variety of innate inflammatory responses across multiple organ systems, which requires rapid responses via post translational modifications (PTM) of proteins. Specifically, methylation of protein by arginine methyltransferases (PRMTs) is an epigenetic PTM implicated in inflammatory responses. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

16 Samples

Download data: H5AD, MTX, TXT

(Submitter supplied) How LTβR-signalling drives chronic tissue damage particularly in the lung, which mechanisms regulate this process, and whether LTβR-blockade might be of therapeutic value has remained unclear. To study the mechanisms underlying LTβR-inhibition, a transcriptional analysis was performed on lung tissue from B6 mice exposed to cigarette smoke for 6 months and treated therapeutically with LTβR-Ig from 4 to 6 months compared to mice exposed to cigarette smoke for 6 months and treated with control Ig from 4 to 6 months and filtered air control. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

13 Samples

Download data: MTX, TXT

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

Organism:

Mus musculus

Type:

Methylation profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing

Platforms:

GPL13112 GPL19057

50 Samples

Download data

(Submitter supplied) Lung diseases, such as cystic fibrosis and COPD, are characterized by mucus obstruction and chronic airway inflammation, but their mechanistic link remains poorly understood. Here, we focused on the role of the mucostatic airway microenvironment on epigenetic reprogramming of airway macrophages (AM) and resulting transcriptomic and phenotypical changes. Using a muco-obstructive mouse model (Scnn1b-transgenic), we identified epigenetically controlled, differentially regulated pathways and transcription factors involved in inflammatory responses and macrophage polarization. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL13112

12 Samples

Download data: XLSX

(Submitter supplied) Lung diseases, such as cystic fibrosis and COPD, are characterized by mucus obstruction and chronic airway inflammation, but their mechanistic link remains poorly understood. Here, we focused on the role of the mucostatic airway microenvironment on epigenetic reprogramming of airway macrophages (AM) and resulting transcriptomic and phenotypical changes. Using a muco-obstructive mouse model (Scnn1b-transgenic), we identified epigenetically controlled, differentially regulated pathways and transcription factors involved in inflammatory responses and macrophage polarization. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

12 Samples

Download data: TXT, XLSX

(Submitter supplied) Lung diseases, such as cystic fibrosis and COPD, are characterized by mucus obstruction and chronic airway inflammation, but their mechanistic link remains poorly understood. Here, we focused on the role of the mucostatic airway microenvironment on epigenetic reprogramming of airway macrophages (AM) and resulting transcriptomic and phenotypical changes. Using a muco-obstructive mouse model (Scnn1b-transgenic), we identified epigenetically controlled, differentially regulated pathways and transcription factors involved in inflammatory responses and macrophage polarization. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL19057 GPL13112

12 Samples

Download data: TXT, XLSX