Mapping and Characterization of Alveolar Cells During Smoking and Chronic Obstructive Disease

Chronic obstructive pulmonary diseases (COPD) have a major public health impact, as evidenced by the 250 million patients affected by these diseases and the 50% 5-year mortality for severe stages of chronic obstructive pulmonary disease (COPD). One pathophysiological mechanism of COPD and emphysema is a depletion of alveolar progenitor cells inducing a loss of alveolar-reparation capacities after an aggression. The genesis of these alterations and the mechanisms involved remain unknown. Alveolar type 2 cells (AT2) are the alveolar epithelial progenitor cells. AT2 proliferate and differentiate into alveolar type 1 cells (AT1) which form the alveolar-capillary barrier, along with endothelial cells, through which respiratory gas exchanges take place. The proliferation and differentiation of AT2 into AT1 are under the control of mesenchymal cells and endothelial cells located in close proximity. Together these cells form the alveolar stem cell niche. The characteristics and interactions of the different cell populations have been well described during lung growth, in the normal adult lung or during pulmonary fibrosis; however, participants are poorly described during smoking exposure and chronic obstructive diseases.

• Fibroblast proliferation capacity [Срок оценки: through study completion, an average of 3 years]
• Differentiation into myofibroblasts [Срок оценки: through study completion, an average of 3 years]
• Fibroblast migration capacity [Срок оценки: through study completion, an average of 3 years]
• Modulated signaling pathways in isolated fibroblasts between groups [Срок оценки: through study completion, an average of 3 years]
• Modulated signaling pathways in endothelial cells between groups [Срок оценки: through study completion, an average of 3 years]
• Evaluation of cytokines in fibroblasts supernatant [Срок оценки: through study completion, an average of 3 years]
• Tumor progression [Срок оценки: through study completion, an average of 3 years]
• Identification of different cell types on total lung [Срок оценки: through study completion, an average of 3 years]
• Severity of pulmonary emphysema, [Срок оценки: At inclusion, every year, up to 5 years after surgery]
• Type of pulmonary emphysema [Срок оценки: At inclusion, every year, up to 5 years after surgery]
• Research of pulmonary biomarkers [Срок оценки: through study completion, an average of 3 years]
• Identification of biomarkers in the pre and postoperative circulating blood [Срок оценки: through study completion, an average of 3 years]