Proceedings of the American Thoracic Society
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The Proceedings of the American Thoracic Society 6:697-700 (2009)
© 2009 The American Thoracic Society
doi: 10.1513/pats.200907-076DP
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Airway Gene Expression in Chronic Obstructive Pulmonary Disease

Katrina Steiling1,2, Marc E. Lenburg2,3 and Avrum Spira1,2,3

1 The Pulmonary Center, Boston University Medical Campus; 2 Bioinformatics Program, Boston University; and 3 Department of Pathology and Laboratory Medicine, Boston University Medical Campus, Boston, Massachusetts

Correspondence and requests for reprints should be addressed to Katrina Steiling, M.D., The Pulmonary Center, Boston University Medical Center, 72 East Concord Street R-304, Boston, MA, 02118. E-mail: steiling{at}bu.edu

ABSTRACT

Although cigarette smoking is the major cause of chronic obstructive pulmonary disease (COPD), only a subset of smokers develops this disease. There is significant clinical, radiographic, and pathologic heterogeneity within smokers who develop COPD that likely reflects multiple molecular mechanisms of disease. It is possible that variations in the individual response to cigarette smoking form the basis for the distinct clinical and molecular phenotypes and variable natural history associated with COPD. Using the biologic premise of a molecular field of airway injury created by cigarette smoking, this response to tobacco exposure can be measured by molecular profiling of the airway epithelium. Noninvasive study of this field effect by profiling airway gene expression in patients with COPD holds important implications for our understanding of disease heterogeneity, early disease detection, and identification of novel disease-modifying therapies.

Key Words: airway gene expression • chronic obstructive pulmonary disease • bioinformatics




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