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Introduction Chronic obstructive pulmonary disease (COPD) is associated with structural changes notably of the respiratory epithelium. Epithelial-to-mesenchymal transition (EMT), which is mainly induced by TGF-β, has been recently suggested in vitro in the airway epithelium in COPD. The objective is to address aberrant differentiation and EMT in the airway epithelium in COPD. Materials and methods Lung samples from 28 patients undergoing surgery for a solitary nodule or transplantation were collected for primary broncho-epithelial cultures in air-liquid interface (ALI-HBEC). ALI-HBEC were assayed for expression of epithelial (zonula occludens-1 and E-cadherin) and mesenchymal (vimentin) proteins by immunohistochemistry (IHC) and western-blot. The production of TGF-β1 was evaluated by ELISA. Results ALI-HBEC from COPD patients showed a significant increase in vimentin expression in IHC (p= 0.006, severe COPD (40 to 58% of positive area) versus controls (0 to 21%)) and western blot. In contrast, epithelial makers (E-cadherin and ZO-1) were both decreased (p=0.01 and p=0.03 respectively, mild or moderate COPD versus controls. In addition, increased vimentin expression was correlated to FEV1 (r=-0.56, p=0.03) in the COPD population and increased ZO-1 expression correlated also with FEV1 (r=0.46, p= 0.017). Vimentin, Ecadherin and ZO-1 correlated all with the Tiffeneau index (r=-0.48, p=0.09; r=0.487, p=0.09; r=0.519, p=0.006). TGF-β1 release was not significantly different between the groups. Discussion We show that the bronchial epithelium from COPD patients display after in vitro reconstitution, increased vimentin expression and decreased epithelial differentiation. These results suggest that the epithelium from COPD patients retains aberrant programming related to EMT, and that this could be independent from TGF-β.
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Gohy, S., Detry, B., Bouzin, C., Fregimilika, C., & Pilette, C. (2013). Increased vimentin expression in human primary bronchial epithelium reconstituted in vitro from patients with chronic obstructive pulmonary disease. ERS, Barcelona. https://hdl.handle.net/2078.5/200140