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Series GSE10006 Query DataSets for GSE10006
Status Public on Dec 19, 2008
Title Decreased Expression of Intelectin 1 in The Human Airway Epithelium of Smokers Compared to Nonsmokers
Organism Homo sapiens
Experiment type Expression profiling by array
Summary 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. Affymetrix HG U133 Plus 2.0 microarrays were used to survey expression of lectin genes in large (3rd to 4th order bronchi) airway epithelium from 9 normal nonsmokers and 20 phenotypic normal smokers and small (10th to 12th order bronchi) airway epithelium from 13 normal nonsmokers and 20 phenotypic normal smokers. From the 72 lectin genes that were surveyed, there were no changes (>2-fold change, p<0.05) in gene expression in either large or small airway epithelium among normal smokers compared to nonsmokers except for a striking down regulation in both large and small airway epithelium of normal smokers of intelectin 1, a recently described lectin that participates in the innate immune response by recognizing and binding to galactofuranosyl residues in the cell walls of bacteria (large airway epithelium, p<0.003; small airway epithelium, p<0.002). TaqMan RT-PCR confirmed the observation that intelectin 1 was down-regulated in both large (p<0.05) and small airway epithelium (p<0.02) of normal smokers compared to normal nonsmokers. Immunohistochemistry assessment of biopsies of the large airway epithelium of normal nonsmokers demonstrated intelectin 1 was expressed in secretory cells, with qualitatively decreased expression in biopsies from normal smokers. Western analysis confirmed the decreased expression of intelectin 1 in airway epithelium of normal smokers compared to normal nonsmokers (p<0.02). Finally, compared to normal nonsmokers, intelectin 1 expression was decreased in small airway epithelium of smokers with early COPD (n= 13, p<0.001) and smokers with established COPD (n= 14, p<0.001), in a fashion similar to that of normal smokers. In the context that intelectin 1 is an epithelial molecule that likely plays a role in defense against bacteria, the down regulation of expression of intelectin 1 in response to cigarette smoking may contribute to the increase in susceptibility to infections observed in smokers, including those with COPD.
Keywords: COPD
 
Overall design Comparison of gene expression in airway epithelial cells of normal non-smokers, phenotypic normal smokers, smokers with early COPD, and smokers with COPD.
 
Contributor(s) Carolan B, Harvey B, De BP, Vanni H, Crystal RG
Citation(s) 18832735
Submission date Dec 21, 2007
Last update date Mar 25, 2019
Contact name Yael Strulovici-Barel
E-mail(s) yas2003@med.cornell.edu
Organization name Weill Cornell Medical College
Department Department of Genetic Medicine
Lab Crystal
Street address 1300 York Avenue
City New York
State/province NY
ZIP/Postal code 10021
Country USA
 
Platforms (1)
GPL570 [HG-U133_Plus_2] Affymetrix Human Genome U133 Plus 2.0 Array
Samples (87)
GSM252799 large airways, non-smoker 002
GSM252800 large airways, non-smoker 004
GSM252801 large airways, non-smoker 005
Relations
BioProject PRJNA108189

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE10006_RAW.tar 1.8 Gb (http)(custom) TAR (of CEL, CHP)
Processed data included within Sample table

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