Rhinovirus and cigarette smoke extract stimulation of interleukin-8 in human bronchial epithelial cells

Abstract

Background: Cigarette smoke(CS) and rhinovirus(RV)infections contribute tothe exacerbation of asthma and COPD. The manifestations of RV-and CS-induced pathologies are the result of virus- and CS-induced mediators of inflammation. Infection with RV induces release of interleukin(IL)-8 in epithelial cell.Purpose of this study was to examne the effects of a water-soluble cigarette smoke extract(CSE) &/or RV infection on release from human bronchial epithelial cells(HBEC) of IL-8. Materials and Methods: We compared the ability of RV-infected &/or CSE-stimulated HBEC, BEAS-2B cells, to produce the IL-8 with controls. We infected BEAS-2B cells with RV14 &/or CES. We harvest the supernatants from RV/CSE stimiulated BEAS-2B cells and the controls at 2hr, 4hr, 12hr, 48hr from inoculation time. We measured the concentration of IL-8 by ELISA kit from supernatant and analyzed mRNA transcript semiquantitatively by RT-PCR. Results: BEAS-2B cells produced small amounts of IL-8 that accumulated slowly with time in culture. RV and CSE were potent stimulators of IL-8 proteins production by BEAS-2B cells. There was an additive effect if the both agents were present, especially in CES and RV combination. Conclusion: RV infection and components of cigarette smoke elicit inflammatory responses in bronchial epithelial cells. RV and CSE could be more harmful to respiratory tract in combination.