GEO DataSets

(Submitter supplied) The initial site of smoking-induced lung disease is the small airway epithelium, which is difficult and time consuming to sample by fiberoptic bronchoscopy. We developed a rapid, office-based procedure to obtain trachea epithelium without conscious sedation from healthy nonsmokers (n=26) and healthy smokers (n=19, 27 ± 15 pack-yr). Gene expression differences [fold-change >1.5, p< 0.01, Benjamini-Hochberg correction] were assessed with Affymetrix microarrays. 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) 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) 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

(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 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

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) 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) Nuclear factor erythroid 2-related factor 2 (NFE2L2, Nrf2) is an oxidant responsive transcription factor known to induce phase 2 detoxifying and antioxidant genes to protect cells from oxidative stress. Cigarette smoke, with its large oxidant content, is a major stressor to the small airway epithelium, the cells of which are vulnerable to oxidant damage and consequent malignant transformation. In this study, we assessed the role of cigarette smoke in activation of Nrf2 in the human small airway epithelium in vivo. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

83 Samples

Download data: CEL, CHP

(Submitter supplied) Smokers weigh less and have less body fat than non-smokers, and increased body fat and weight gain are observed following smoking cessation. To assess a possible molecular mechanism underlying the inverse association between smoking and body weight, we hypothesized that smoking may induce the expression of a fat depleting gene in the airway epithelium, the cell population that takes the brunt of the stress of cigarette smoke. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platforms:

GPL80 GPL570 GPL96

92 Samples

Download data: CEL, CHP

(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) 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

(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) The aldokatoreductases (AKRs) represent a gene superfamily that code for monomeric, soluble NAD(P)H-dependent oxidoreductases that mediate elimination reactions. AKR1B10, an AKR that functions to eliminate retinals, has been observed to be upregulated in squamous metaplasma and non small cell lung cancer, and has been suggested as a diagnostic marker specific to tobacco-related carcinogenesis. In the context of the link of smoking and lung cancer and the enhanced expression of AKR1B10 expression in lung cancer, we hypothesize that enhanced expression of AKR1B10 may be initiated in healthy smokers, prior to the development of any evidence of lung cancer. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

161 Samples

Download data: CEL, CHP

(Submitter supplied) RNA was obtained from histologically normal bronchial epithelium of never, former, and current smokers undergoing fiberoptic bronchoscopy. Statistical analysis of the gene expression data identified gene differentially expressed between current and never smokers and classified these genes as irreversible, slowly reversible, or rapidly reversible based on their behavior in former smokers Keywords: Disease state analysis

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL96

104 Samples

Download data: CEL

(Submitter supplied) The small airway epithelium (SAE), the first site of smoking-induced lung pathology, exhibits genome-wide changes in gene expression in response to cigarette smoking. Based on the increasing evidence that the epigenome can respond to external stimuli in a rapid manner, we assessed the SAE of smokers for genome-wide DNA methylation changes compared to nonsmokers, and whether changes in SAE DNA methylation were linked to the transcriptional output of these cells. more...

Organism:

Homo sapiens

Type:

Expression profiling by array; Methylation profiling by genome tiling array

Platforms:

GPL570 GPL16419

75 Samples

Download data: CEL, CHP, PAIR

(Submitter supplied) Smoking is the leading cause of lung cancer death, although only a small percentage of smokers develop the disease. Cigarette smoke exposure is known to cause a field of injury in cells throughout the respiratory tract, and while these airway epithelial cells are morphologically normal, they can undergo genetic alterations in response to cigarette smoke exposure. We used microarrays to analyze the gene expression of epithelial cells in the extrathoracic epithelium, specifically nasal and buccal epithelium, to see if these cells underwent similar genetic alterations in response to tobacco exposure as seen in bronchial epithelial cells as has been previously reported. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Datasets:

GDS3054 GDS3309

Platforms:

GPL96 GPL571

25 Samples

Download data: CEL, CHP, EXP

Analysis of nasal epithelia from cigarette smokers. Cigarette smoke creates a field of injury in epithelial cells lining the respiratory tract. Results extend the concept of a smoking-induced field of injury beyond intrathoracic (bronchial) epithelia to extrathoracic epithelia that line the nose.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 2 agent sets

Platform:

GPL571

Series:

GSE8987

15 Samples

Download data: CEL, CHP, EXP

Analysis of buccal epithelia from cigarette smokers. Cigarette smoke creates a field of injury in epithelial cells lining the respiratory tract. Results extend the concept of a smoking-induced field of injury beyond intrathoracic (bronchial) epithelia to extrathoracic epithelia that line the mouth.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 2 agent sets

Platform:

GPL96

Series:

GSE8987

10 Samples

Download data: CEL, CHP, EXP

(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