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Gene expression profiles of T-lymphocytes are sensitive to the influence of heavy smoking

ABSTRACT: Cigarette smoke components have a proven negative influence on human health. Adverse metabolic effects have been observed in tissues and single cells. As T-lymphocytes get in contact with affected organs (e.g. lung) or cells (e.g.erythrocytes), as well as with smoke components and bioactive molecules, whose production is influenced by them, we compared the gene exression profiles in these cells of the adaptive immune system of three male heavy smokers and three male non-smokers We combined rapid immuno-precipitation and Affymetrix GeneChip® HG U133A2.0 microarray analysis to analyse the data set. 88 genes were found significantly (T-test) differentially expressed by a factor of 1.5-fold or larger between smokers and non-smokers. Using the gene function groups of the gene ontology consortium to categorize the functions of the differentially expressed genes the group termed “response to stimulus” was found most significantly affected by smoking. Our data indicate a prominent role of cytotoxic T-lymphocytes in response to smoking. Several genes that are typically found in these cells are found regulated although the ratio of cytotoxic and helper T-lymphocytes remained unchanged in smokers. Keywords: gene expression changes in T-lymphocytes in response to smoking

ORGANISM(S): Homo sapiens

PROVIDER: GSE4806 | GEO | 2006/12/31

SECONDARY ACCESSION(S): PRJNA95711

REPOSITORIES: GEO

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Project description:Although smoking-induced lung disease tends to be more common in the upper lobe, it is not known if this results from the skewed distribution of inhaled cigarette smoke or increased susceptibility of the upper lobes to these disorders. The distribution of inhaled cigarette smoke within the lung is complex, depending on lung pressure-volume relationships, gravity, individual smoking habits and the properties of the individual components of cigarette smoke. With the knowledge that the small airway epithelium is the earliest site of smoking-induced lung disease, and that the small airway epithelium is acutely sensitive to inhaled cigarette smoke with significant changes in the up- and down-regulation of hundreds of genes, we compared upper vs lower lobe gene expression in the small airway epithelium of the same cigarette smokers to determine if the gene expression patterns were similar or different. Active smokers (n=11) with early evidence of smoking-induced lung disease (normal spirometry but low diffusing capacity) underwent bronchoscopy and brushing of the small airway epithelium to compare upper vs lower lobe genome-wide gene expression assessed by microarray. Interestingly, cluster and principal component analysis demonstrated that, for each individual, the expression of the known small airway epithelium smoking-responsive genes were remarkably similar as upper vs lower lobe pairs, although, as expected, there were differences in the smoking-induced changes in gene expression from individual to individual. Thus, while there may be topographic differences in the distribution of cigarette smoke, sufficient smoke reaches the upper vs lower lobe small airway epithelium so that, within each smoker, the upper vs lower lobe gene expression are similar. These observations support the concept that the topographic differences in the occurrence of the smoking-induced lung diseases are likely secondary to topographic differences in the susceptibility of the upper vs lower lobes to cigarette smoke, not the topographic differences in distribution of inhaled cigarette smoke.

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Gene expression profiles of T-lymphocytes are sensitive to the influence of heavy smoking

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