Nicotine involved in periodontal disease through influence on cytokine levels

Abstract

Periodontal disease, for which smoking is a known risk factor, is infectious, and is associated with oral biofilm. Cytokines mediate and regulate immune and inflammatory responses. Lipopolysaccharide produced by periodontopathic bacteria plays a role in the progression of periodontitis. The effect of nicotine on cytokine production in mice was evaluated in this study. Nicotine (10 or 200 μg mouse-1) was administered intraperitoneally to 4-week-old female BALB/c mice, once a day, for 49 days. Control mice received injections of phosphate-buffered saline. Blood was collected from all mice and serum IL-6, IL-10, tumor necrosis factor (TNF)-α and IFN-γ levels were measured by an enzyme-linked immunosorbent assay on the 42nd day. IL-6, IL-10 and IFN-γ levels in the nicotine-treated mice were higher than those in the control mice. However, no differences were found in TNF-α levels between nicotine-treated and control mice. Lipopolysaccharide (20 μg mouse-1) purified from Aggregatibacter actinomycetemcomitans (formerly Actinobacillus actinomycetemcomitans) Y4 was administered intraperitoneally on the 49th day. A rapid increase in TNF-α was observed in the control mice at 2 h after administration of lipopolysaccharide. In contrast, no increase was noted in the nicotine-treated groups. Significantly higher levels of IFN-γ were seen in the 200 μg nicotine-treated mice at 2 h after administration of lipopolysaccharide (P<0.05). The results showed that cytokine levels were influenced by nicotine in mice. © 2008 Federation of European Microbiological Societies.