GEO DataSets

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

(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 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) 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) Alveolar macrophages from never smokers and active smokers were isolated by bronchoalveolar lavage and gene expression was measured. Chronic cigarette smoke exposure, as occurs in smoker's lungs, leads to significant changes in gene expression. Of note, RNA was isolated immediately following bronchoscopy. Alveolar macrophage levels were >95%.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL5175

8 Samples

Download data: CEL

(Submitter supplied) Cigarette smoking is the leading cause of emphysema in the United States. Alveolar macrophages play a critical role in the inflammation-mediated remodeling of the lung parenchyma in emphysema. However, the exact gene pathways and the role of DNA methylation in moderating this pathological transformation are not known. In order to more exactly understand this process, we compared genome-wide expression and methylation signatures of alveolar macrophages isolated from heavy smokers with those isolated from non-smoking controls. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL5175

23 Samples

Download data: CEL

(Submitter supplied) Disparate Oxidant-related Gene Expression of Human Small Airway Epithelium Compared to Autologous Alveolar Macrophages in Response to the In Vivo Oxidant Stress of Cigarette Smoking The oxidant burden of cigarette smoking induces lung cell dysfunction, and play a significant role in the pathogenesis of lung disease. Two cell populations directly exposed to the oxidants in cigarette smoke are the small airway epithelium and alveolar macrophages. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

98 Samples

Download data: CEL, CHP

(Submitter supplied) Cigarette smoking is the leading cause of the respiratory diseases collectively known as chronic obstructive pulmonary disease (COPD). While the pathogenesis of COPD is complex, there is abundant evidence that alveolar macrophages (AM) play an important role. Based on the concept that COPD is a slow-progressing disorder likely involving multiple mediators released by AM activated by cigarette smoke, the present study focuses on the identification of previously unrecognized genes that may be linked to early events in the molecular pathogenesis of COPD, as opposed to factors associated with the presence of disease. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS1436

Platform:

GPL80

10 Samples

Download data: CEL, EXP

Anlaysis of alveolar macrophages of 5 phenotypically normal smokers who consume ~20 packs cigarettes/year. Smoking is the leading cause of respiratory diseases collectively known as chronic obstructive pulmonary disease (COPD). Provides insight into early events in molecular pathogenesis of COPD.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 2 stress sets

Platform:

GPL80

Series:

GSE3212

10 Samples

Download data: CEL, EXP

(Submitter supplied) HIV1+ smokers develop emphysema at an earlier age and with a higher incidence than HIV1- smokers. Based on the knowledge that human alveolar macrophages (AM) are capable of producing proteases that degrade extracellular matrix components, we hypothesized that upregulation of AM matrix metalloproteinases may be associated with the emphysema of HIV1+ smokers. To test this hypothesis, microarray analysis was used to screen which MMP genes were expressed by AM isolated by bronchoalveolar lavage (BAL) of HIV1+ smokers with early emphysema. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

11 Samples

Download data: CEL, CHP

(Submitter supplied) Lectins are proteins present on cell surfaces or as shed extracellular proteins that function in innate immune defense as phagocytic receptors to recognize specific bacterial cell wall components. Based on the knowledge that cigarette smoking is associated with increased risk of bacterial infection, we hypothesized that cigarette smoking may modulate the expression of lectin genes in the airway epithelium. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

87 Samples

Download data: CEL, CHP

(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) Increased small airway resistance and decreased lung elasticity contribute to the airflow limitation in chronic obstructive pulmonary disease (COPD). The lesion that corresponds to loss of lung elasticity is emphysema; the small airway obstruction is due to inflammatory narrowing and obliteration. Despite their convergence in altered physiology, different mechanisms contribute to these processes. The relationships between gene expression and these specific phenotypes may be more revealing than comparison with lung function. We measured the ratio of alveolar surface area to lung volume (SA/V) in lung tissue from 43 smokers. Two samples from 21 subjects, in which SA/V differed by > 49 cm2/mL were profiled to select genes whose expression correlated with SA/V. The level of expression of 181 transcripts was related to SA/V ( p< 0.05). The relationship between expression of these transcripts and SA/V was tested in the 22 remaining subjects as a replication. Thirty of the 181 genes remained significantly associated with SA/V (P<0.05) and the direction of association was the same in 164/181. Pathway and network analysis revealed enrichment of genes involved in protein ubiquitination, and western blotting showed altered expression of genes involved in protein ubiquitination in obstructed individuals. These data implicate modified protein ubiquitination and degradation as a potentially important pathway in the pathogenesis of emphysema. Raw data not available for this study

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL3991

42 Samples

Download data: TXT

(Submitter supplied) In a prior report, we observed two distinct lung microbiomes in healthy subjects that we termed “pneumotypes”: pneumotypeSPT, characterized by high bacterial load and supraglottic predominant taxa (SPT) such as the anaerobes Prevotella and Veillonella; and pneumotypeBPT, with low bacterial burden and background predominant taxa (BPT) found in the saline lavage and bronchoscope. Here, we determined the prevalence of these two contrasting lung microbiome types, in a multi-center study of healthy subjects. more...

Organism:

human lung metagenome

Type:

Other

Platform:

GPL21074

1 Sample

Download data: TXT

(Submitter supplied) Smoking is the second leading cause of preventable death in the United States. Cohort epidemiological studies have demonstrated that women are more vulnerable to cigarette-smoking induced diseases than their male counterparts, however, the molecular basis of these differences has been remained unknown to date. In this study, we explored if there were differences in the gene expression patterns between male and female smokers, and how these patterns might reflect different gender-specific responses to the stress of smoking.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6480

48 Samples

Download data: TXT

(Submitter supplied) Smoking-induced lung disease is one of the most prevalent forms of lung disease but also one of the more diverse. Based on the phenotypic diversity caused by the same environmental stress, we hypothesized that smoking may induce changes in lung cell expression of genes that, with specific variants, are causative of monogenic lung disease, i.e., not that smoking induces a phenocopy of a genetic disease, but smoking may subtly modify the expression of genes known to be associated with genetic disorders with distinct lung disease phenotypes. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

230 Samples

Download data: CEL, CHP