EVA

Markers for emphysema versus airway disease in COPD

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 Obiettivo del progetto (Objective)

'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.'

Introduzione (Teaser)

Chronic obstructive pulmonary disease ranks high on the global mortality list. It is characterised by emphysema and airway disease, both of which lead to airway obstruction.

Descrizione progetto (Article)

Although most chronic obstructive pulmonary disease (COPD) patients have both emphysema and airway disease, in some cases only one of the features is present. The 'Markers for emphysema versus airway disease in COPD' (EVA) project aims to identify markers linked specifically to emphysema and airway disease at the DNA, RNA and protein levels. The EU-funded project is working on the hypothesis that the processes leading to these pathologies can be differentiated with regard to inflammatory response and genetic predisposition.

Participating clinical centres have to date recruited some 180 cases and 170 healthy controls. Computer tomography (CT) scans are being used to select patients with either emphysema or airway disease. Image analysis will further define emphysema based on density of the lung tissue, and airway disease based on thickness of the airway wall. By plotting airway wall area against lung density, patients can be identified as having emphysema only or airway disease only.

Material obtained from lungs and blood will be analysed for elements of gene expression. However, crucial analysis will be performed in a single batch at the end of the study, when all samples have been collected. At that point, DNA, RNA and protein data will be available for cases as well as controls. This will help EVA produce the results required to identify markers specifically associated with emphysema and airway disease sub-phenotypes.

As elements of the differential pathogenesis for the different disease processes in COPD, these markers will be extremely useful for diagnosing the sub-phenotypes. Such markers will also provide a basis for exploring targets for new therapeutic approaches to COPD. This will also afford greater opportunities to better manage the disease.