Cigarette smoking is the main risk factor for for Chronic Obstructive Pulmonary Disease (COPD), yet only a subset of smokers develops COPD, therefore in order to obtain a deeper understanding of the first processes responsible of the disease, Lorenza Franciosi set up the acute smoking model in young susceptible and non-susceptible individuals, COPD patients and controls. Her data show that already at young age, subjects with a positive family history of COPD respond differently to cigarette smoke than those with a negative family history. Particularly SerpinB3 and Uteroglobin were found to be proteins that may play a role in the onset of COPD.
The scope of the thesis of Franciosi was to identify potential biomarkers for COPD via a proteomic approach.
In order to identify the first processes involved in the onset of COPD, she aimed to compare not only confirmed (older) COPD patients with healthy controls, but also younger subjects susceptible or non-susceptible to develop the disease, based on their family history.
After assessing the feasibility of our proteomic approach in the investigation in Epithelial Lining Fluid (ELF), Francioso firstly compared the differential proteomic profiles in COPD patients and healthy controls. The proteins that resulted as statistically significantly different between these groups were subsequently investigated via other approaches, namely immunohistochemistry and ELISA.
A comparative study of ELF from COPD patients and healthy controls using chemical stable isotope labeling (iTRAQ®-8Plex) showed that the levels of four proteins differed significantly between ELF from COPD patients and healthy controls. These proteins are directly involved in two of the key processes responsible for the onset and development COPD, namely inflammation and oxidative stress.
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