Abstract

<b>Objective:</b> We aimed to investigate the role of nicotine as a cause of EBD and EMT in human bronchial epithelial cells (HBEC) and asthmatic bronchial epithelial cells (AHBEC). <b>Methods:</b> We used HBEC and AHBEC commercial cell line cultures for this study and treated with 6x10-6 mol/l nicotine. We evaluated nicotine treated (NT) and nicotine non-treated (NNT) HBEC and AHBEC at 24, 48 and 72 hours. We measured E-cadherin (E-cad), N-cadherin (N-cad), α-smooth muscle actin (α-SMA) with Western Blot and levels of thymic stromal lymphopoietin (TSLP), Wnt3a as well as transforming growth factor-β1 (TGF-β1) with ELISA in these cultures. <b>Results:</b> Comparison of NT with NNT HBEC showed lower N-cad levels at 24 hours (p=0.043); no significant difference was detected at 48 and 72 hours. N-cad was found to be higher in non-NT AHBEC versus HBEC at 24 hours (p=0.046). Moreover, comparison of NT HBEC with AHBEC showed that N-cad was higher in AHBEC at 24 hours (p=0.046). However, there was no significant difference between the groups at 48 and 72 hours (table 1). <b>Conclusion:</b> Detection of higher N-cad levels in AHBEC compared to HBEC without nicotine exposure as well as during the early stages of nicotin exposure may be a sign of tendency of asthmatic epitelial cells for EMT. This may result in worse prognosis with nicotine exposure in asthmatic.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.