COPD is characterized by emphysema (destruction of the lung alveoli) and airway disease (inflammation and thickening of the bronchial wall) both of which lead to airway obstruction. These two features co-exist in most patients but some patients present with only emphysema (E) or only airway disease (A). The aim of the project is to identify markers specific to E and A of COPD. Our hypothesis is that the mechanisms leading to these pathologies are distinct with respect to the type of inflammatory response and in terms of genetic predisposition. The differential pathogenesis for emphysema (E) and inflammatory airway disease (A) entails that in the two forms of COPD are linked to different markers at the DNA, RNA and protein level. Using computer tomography (CT) scans for selection of patients with emphysema only and airway disease only, we will obtain material from lung (leukocytes, bronchial cells) and blood (leukocytes), and will analyse elements of gene expression (SNP array, transcriptome). Data analysis will be done for E versus A (EvA) and versus a control cohort leading to identification of markers linked specifically to either E or A. These markers will be elements involved in a differential pathogenesis for the different disease processes in COPD. They can be used for diagnostic approaches and as therapeutic targets.