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Neutrophil superoxide production in the presence of cigarette smoke extract, nicotine and cotinine
Author(s) -
Matthews John B.,
Chen FaMing,
Milward Michael R.,
Ling Martin R.,
Chapple Iain L. C.
Publication year - 2012
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/j.1600-051x.2012.01894.x
Subject(s) - superoxide , nicotine , cotinine , chemistry , lucigenin , pharmacology , lipopolysaccharide , oxidative stress , superoxide dismutase , immunology , medicine , biochemistry , enzyme
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 (0–10 μ 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.