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Ziegler-Heitbrock, L. ; Frankenberger, M. ; Heimbeck, I. ; Burggraf, D. ; Wjst, M. ; Häussinger, K.* ; Brightling, C.* ; Gupta, S.* ; Parr, D.* ; Subramanian, D.* ; Singh, D.* ; Kolsum, U.* ; Boschetto, P.* ; Potena, A.* ; Gorecka, D.* ; Nowinksi, A.* ; Barta, I.* ; Döme, B.* ; Strausz, J.* ; Greulich, T.* ; Vogelmeier, C.* ; Bals, R.* ; Hohlfeld, J.* ; Welte, T.* ; Venge, P.* ; Gut, I.* ; Boland, A.* ; Olaso, R.* ; Hager, J.* ; Hiemstra, P.* ; Rabe, K.F.* ; Unmüßig, M.* ; Müller-Quernheim, J.* ; Prasse, A.*

The EvA study: Aims and strategy.

Eur. Respir. J. 40, 823-829 (2012)

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The EvA study is an EU funded project (# 200506) under Frame Work Program 7 (FP7), which aims at defining new markers for COPD and its subtypes. The acronym is derived from emphysema versus airway disease, indicating that the project targets these two main phenotypes of the disease. The EvA study is based on the concept that emphysema and airway disease are governed by different pathophysiological processes and these are driven by different genes and a differential gene expression in the lung. To define these genes patients and non-COPD controls are recruited for clinical examination, lung function analysis and computed tomography of the lung. CT scans are used to define the phenotypes based on lung density and airway wall thickness. This is followed by bronchoscopy in order to obtain samples from the airways and the alveoli. These tissue samples along with blood samples are then subjected to genome-wide expression and association analysis and markers linked to the phenotypes are identified. The population of the EvA study is different from other COPD study populations, since patients with current oral glucocorticoid, antibiotics, exacerbations or current smoking are excluded, such that the signals detected in the molecular analysis are due to the distinct inflammatory process of emphysema and airway disease in COPD.

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