Nicotine involved in periodontal disease through influence on cytokine levels

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.