Journal
JOURNAL OF CLINICAL PERIODONTOLOGY
Volume 39, Issue 7, Pages 626-634Publisher
WILEY
DOI: 10.1111/j.1600-051X.2012.01894.x
Keywords
cigarette smoke extract; cotinine; Fc?-receptor; Fusobacterium nucleatum; lucigenin; neutrophil; nicotine; periodontitis; superoxide
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Funding
- IADR
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Aim To determine the effect of cigarette smoke extract, nicotine and cotinine on lucigenin-detectable neutrophil superoxide production. Materials & Methods Neutrophils from periodontally healthy individuals were treated with aqueous smoke extract, nicotine and cotinine, prior to stimulation or at the same time as stimulation with Fusobacterium nucleatum, IgG-opsonized Staphylococcus aureus and Escherichia coli Lipopolysaccharide (LPS). Superoxide generation was determined by lucigenin chemiluminescence. Results Smoke extract induced superoxide release from neutrophils (p <0.0001) in a dose-dependent manner. By contrast, superoxide generation by neutrophils in response to pathologically relevant stimuli was inhibited by pre-treatment with smoke extract (p <0.01). This inhibition did not require the continued presence of the extract. A similar reduction in stimulated superoxide production by smoke extract was detected when neutrophils were simultaneously exposed to the extract and stimuli. Nicotine and cotinine (010 mu g/ml) had no effect on superoxide release from unstimulated or stimulated neutrophils. Conclusions Stable water-soluble components of cigarette smoke directly induce superoxide generation by otherwise unstimulated neutrophils, but reduce superoxide responses of cells to pathologically relevant stimuli. These data suggest potential neutrophil-mediated mechanisms by which smoking may initiate and maintain oxidative stress at periodontally healthy sites and participate in disease progression, by reducing innate immune responses.
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