GEO DataSets

(Submitter supplied) The toll-like receptors (TLRs) are important components of the respiratory epithelium host innate defense, enabling the airway surface to recognize and respond to a variety of insults in inhaled air. Based on the knowledge that smokers are more susceptible to pulmonary infection and the airway epithelium of smokers with chronic obstructive pulmonary disease (COPD) is characterized by bacterial colonization and acute exacerbation of airway infections, we assessed whether smoking alters the expression of TLRs in human small airway epithelium, the primary site of smoking-induced disease. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

169 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) To help define the genes associated with mucus synthesis and secretion in the human small airway epithelium, we hypothesized that comparison of the transcriptomes of the small airway epithelium of individuals that express high vs low levels of MUC5AC, a major secretory mucin and the major component of airway mucus, could be used as a probe to identify the genes related to human small airway mucus production / secretion. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

132 Samples

Download data: CEL, CHP, TXT

(Submitter supplied) Down-regulation of the Notch Differentiation Pathway in the Human Airway Epithelium in Normal Smokers and Smokers with Chronic Obstructive Lung Disease In cigarette smokers, the toxic components of smoke place the epithelium under the constant stress of a variety of mechanisms of injury, with consequent modulation of airway epithelial regeneration and disordered differentiation. Based on the underlying hypothesis that these airway epithelial changes must involve quantitative changes in genes involved with the regulation of differentiation, we assessed the expression of the Notch pathway, a signaling pathway known to play a fundamental role in the embryonic lung as a gatekeeper for differentiation, in the small airway epithelium of non-smokers, normal smokers, and smokers with COPD. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

20 Samples

Download data: CEL, CHP

(Submitter supplied) Upregulation of Expression of the Ubiquitin Carboxyl Terminal Hydrolase L1 Gene in Human Airway Epithelium of Cigarette Smokers The microarray data deposited here is from 39 HG-U133 Plus 2.0 GeneChips, from 12 normal non-smokers, 12 phenotypic normal smokers, 9 Early COPD and 6 COPD individuals, all small airways, all small airway. A subset of these samples have been already submitted under GEO Accession Number GSE 4498. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

39 Samples

Download data: CEL, CHP

(Submitter supplied) Modification of Gene Expression of the Small Airway Epithelium in Response to Cigarette Smoking The earliest morphologic evidence of changes in the airways associated with chronic cigarette smoking is in the small airways. To help understand how smoking modifies small airway structure and function, we developed a strategy using fiberoptic bronchoscopy and brushing to sample the human small airway (10th-12th order) bronchial epithelium to assess gene expression (HG-133 Plus 2.0 array) in phenotypically normal smokers (n=10, 33 ± 7 pack-yr) compared to matched non-smokers (n=12). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS2486

Platform:

GPL570

22 Samples

Download data: CEL, CHP

Analysis of small airway epithelial cells of phenotypically normal smokers. The earliest morphologic evidence of changes in the airways associated with chronic cigarette smoking is in the small airways. Results provide insight into how smoking modifies small airway structure and function.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 2 stress sets

Platform:

GPL570

Series:

GSE4498

22 Samples

Download data: CEL, CHP

(Submitter supplied) The Wnt pathway plays a central role in controlling differentiation of epithelial tissues; when Wnt is on, differentiation is suppressed, but when Wnt is off, differentiation is allowed to proceed. Based on this concept, we hypothesized that expression of key genes in the Wnt pathway are suppressed in the human airway epithelium under the stress of cigarette smoking, a stress associated with dysregulation of the differentiated state of the airway epithelium. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

127 Samples

Download data: CEL, CHP

(Submitter supplied) The earliest morphologic evidence of changes in the airways associated with chronic cigarette smoking is in the small airways. To help understand how smoking modifies small airway structure and function, we developed a strategy using fiberoptic bronchoscopy and brushing to sample the human small airway (10th-12th order) bronchial epithelium to assess gene expression (Affymetrix HG-U133A array) in phenotypically normal smokers (n=6, 24 ± 4 pack-yr) compared to matched non-smokers (n=5). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS1304

Platform:

GPL96

11 Samples

Download data

Analysis of phenotypically normal 10th to 12th order small airway bronchial epithelia from cigarette smokers. Cigarette smoking is the most common cause of chronic obstructive pulmonary disease (COPD). Results provide insight into the early pathogenesis of COPD.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 2 stress sets

Platform:

GPL96

Series:

GSE3320

11 Samples

Download data

(Submitter supplied) Cystatin A (gene: CSTA), is up-regulated in non-small-cell lung cancer (NSCLC) and dysplastic vs normal human bronchial epithelium. In the context that chronic obstructive pulmonary disease (COPD), a small airway epithelium (SAE) disorder, is independently associated with NSCLC (especially squamous cell carcinoma, SCC), but only occurs in a subset of smokers, we hypothesized that genetic variation, smoking and COPD modulate CSTA gene expression levels in SAE, with further up-regulation in SCC. more...

Organism:

Homo sapiens

Type:

Expression profiling by array; SNP genotyping by SNP array

Platforms:

GPL570 GPL6804

342 Samples

Download data: CEL, CHP, TXT

(Submitter supplied) The first changes associated with smoking are in the small airway epithelium (SAE). Given that smoking alters SAE gene expression, but only a fraction of smokers develop chronic obstructive pulmonary disease (COPD), we hypothesized that assessment of SAE genome-wide gene expression would permit biologic phenotyping of the smoking response, and that a subset of healthy smokers would have a “COPD-like” SAE transcriptome. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

171 Samples

Download data: CEL, CHP

(Submitter supplied) Rationale: Even after quitting smoking, the risk of the development of chronic obstructive pulmonary disease (COPD) and lung cancer remains significantly higher compared to never-smokers. Objectives: Based on the knowledge that COPD and most lung cancers start in the small airway epithelium (SAE), we hypothesized that smoking modulates miRNA expression in the SAE linked to the pathogenesis of smoking-induced airway disease, and that some of these changes persist after smoking cessation. more...

Organism:

synthetic construct; Homo sapiens

Type:

Non-coding RNA profiling by array

Platform:

GPL14613

29 Samples

Download data: CEL

(Submitter supplied) The apical junctional complex (AJC), composed of tight junctions and adherens junctions, is essential for maintaining epithelial barrier function. Since cigarette smoking and chronic obstructive pulmonary disease (COPD), the major smoking-induced disease, are both associated with increased lung epithelial permeability, we hypothesized that smoking alters the transcriptional program regulating AJC integrity in the small airway epithelium (SAE), the primary site of pathological changes in COPD. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

135 Samples

Download data: CEL, CHP

(Submitter supplied) Study Smoking and COPD are associated with decreased mucociliary clearance and healthy smokers have shorter cilia in the large airway than nonsmokers. Intraflagellar transport (IFT) is the process by which cilia are produced and maintained. We assessed expression of IFT-related genes in smokers and nonsmokers and evaluated cilia length in the large and small airway of nonsmokers, healthy smokers, and smokers with COPD. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

149 Samples

Download data: CEL, CHP

(Submitter supplied) Rhinovirus infections exacerbate chronic respiratory inflammatory diseases such as asthma and chronic obstructive pulmonary disease (COPD). Airway epithelial cells are the primary site of rhinovirus replication and responsible for initiating the host immune response to infection. Numerous studies have reported that the anti-viral innate immune response in asthma is deficient leading to the conclusion that epithelial innate immunity is a key determinant of disease severity during a rhinovirus induced exacerbation. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

120 Samples

Download data: CSV

(Submitter supplied) Despite overwhelming data that cigarette smoking causes chronic obstructive pulmonary disease (COPD), only a minority of chronic smokers are affected, strongly suggesting that genetic factors modify susceptibility to this disease. We hypothesized that there are individual variations in the response to cigarette smoking, with variability among smokers in expression levels of protective / susceptibility genes. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

54 Samples

Download data: CEL, CHP

(Submitter supplied) Background: When exposed to specific stimuli, macrophages exhibit distinct activation programs, M1 and M2 polarization, that define macrophage function as inflammatory/immune effectors or anti-inflammatory/tissue remodeling cells, respectively. Due to their position on the lung epithelial surface, alveolar macrophages (AM) directly interact with environmental stimuli such as cigarette smoke, the major risk factor for the development of chronic obstructive pulmonary disease (COPD). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

70 Samples

Download data: CEL, CHP

(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) Gamma-aminobutyric acid (GABA) is a multifunctional mediator that functions as a neurotransmitter in the central nervous system and a trophic factor during nervous system development, affecting proliferation, differentiation and cell death [1-3].GABA is synthesized from glutamate, catalyzed by GAD65 and GAD67, glutamic acid decarboxylase {Tillakaratne, Medina-Kauwe, et al. 1995 21 /id}{Owens & Kriegstein 2002 3 /id}{Watanabe, Maemura, et al. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

157 Samples

Download data: CEL, CHP