Nicotine Induces the Production of IL-1β and IL-8 via the α7 nAChR/NF-κB Pathway in Human Periodontal Ligament Cells: an in Vitro Study

Background/Aims: Tobacco smoking is a major risk factor for the occurrence and progression of periodontitis. We previously demonstrated that nicotine could induce the expression of alpha 7 nicotinic acetylcholine receptors (alpha 7 nAChR) in human and rat periodontal tissues. To further examine the signal pathways mediated by alpha 7 nAChR in periodontal ligament (PDL) cells, we investigated whether nicotine affects interleukin-1 beta (IL-1 beta) and interleukin-8 (IL-8) via the alpha 7 nAChR/NF-kappa B pathway in human PDL cells. Methods: Human PDL cells were pre-incubated with alpha-bungarotoxin (alpha-BTX) or pyrrolidine dithiocarbamate (PDTC), then cultured with nicotine. Then, we used western blotting, a dual-luciferase reporter, real-time quantitative PCR and an enzyme linked immunoassay to assess expression of the NF-kappa B p65 subunit, NF-kappa B activity and production of IL-1 beta and IL-8 in human PDL cells. Results: Compared with the control group, nicotine could significantly induce production of IL-1 beta and IL-8 in human PDL cells and cause the similar effects on the expression of the NF-kappa B p65 subunit and NF-kappa B activity. Conclusion: This study demonstrates that nicotine could induce production of IL-1 beta and IL-8 via the alpha 7 nAChR/NF-kappa B pathway in human PDL cells, providing data for a better understanding of the relationships among smoking, nicotine, and periodontitis. Copyright (C) 2014 S. Karger AG, Basel