Résumé
Idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD) both affect smokers over 60 years old and are characterized by early small airways abnormalities. Orientation toward IPF or COPD after tobacco exposure could be decided in airways through a differential épithelial dysfunction. Methods: bronchial biopsies from 5 newly diagnosed IPF and 5 COPD patients were cultured in ALI, some wells were exposed to cigarette smoke extract. At day 28, RNA was extracted an analyzed. Some wells were scratched to study repair speed. Thoracic CT were used to compare the airway wall thickness between pathologies. Results: airway wall thickness is the same between the IPF and the COPD patients. Transcriptomic studies reveal that exposure to cigarette smoke extract induces inflammatory response in the COPD bronchial epithelium whereas it induces upregulation of genes involved in epitheliomensenchymal transition and proliferation in the IPF group. Only 3 genes are induced by tobacco both in the IPF and the COPD group, showing very divergent responses to the exposure between the two pathologies. Scratch repair is significantly faster and is aberrant in the IPF group. Conclusion: early increased airway wall thickness, aberrant repair and changes in gene expression after exposure to cigarette smoke extract suggest that the bronchial epithelium in IPF could initiate the fibrotic processes, according to the concept of bronchiolization.