SESSION TITLE: COPD: Etiology
SESSION TYPE: Original Investigation Poster
PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM
PURPOSE: To determined the role and signaling of CFTR in modulating cigarette smoke (CS)-induced COPD development.
METHODS: The COPD mouse model was established by cigarette smoke exposure and LPS. The STS intervention was given via atomization inhalation. Lung functions were assessed by using Buxco lung function measurement system. The Proinflammatory cytokines IL-6 and KC in BALF were assayed with ELISA. The lung tissue was subjected to H&E staining. Furthermore, the level of CFTR was determined by Western Blotting. 16HBE cells were used to evaluate the effects of STS on signaling change caused by cigarette smoke exposure (CSE). CSE was used to treat 16HBE cells with or without STS. The IL-6 and IL-8 level in cell culture medium were measured. The levels of CFTR, phosphorylated ERK1/2 and nucleic Nrf2 were determined. Then the effects of CFTR inhibitor inh-172 or ERK1/2 inhibitor PD98059 on Nrf2 nuclear translocation and IL-6 secretion, and the effects of small interfering RNA of Nrf2 (siNrf2) and Nrf2 agonist TBHQ on IL-6 secretion were assessed in CSE treated 16HBE cells.