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Effect of nicotine, cotinine and cigarette smoke extract on the neutrophil respiratory burst
Author(s) -
Matthews John B.,
Chen FaMing,
Milward Michael R.,
Wright Helen J.,
Carter Kevin,
McDonagh Anna,
Chapple Iain L.C.
Publication year - 2011
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.2010.01676.x
Subject(s) - respiratory burst , cotinine , periodontitis , nicotine , chemistry , reactive oxygen species , fusobacterium nucleatum , neutrophil extracellular traps , saliva , pharmacology , oxidative stress , porphyromonas gingivalis , immunology , microbiology and biotechnology , medicine , biochemistry , biology , inflammation
Matthews JB, Chen FM, Milward MR, Wright HJ, Carter K, McDonagh A, Chapple ILC. Effect of nicotine, cotinine and cigarette smoke extract on the neutrophil respiratory burst. J Clin Periodontol 2011; 38: 208–218. 38: 208–218. doi: 10.1111/j.1600‐051X.2010.01676.x Abstract Aims: To determine the effect of nicotine, cotinine and cigarette smoke extract (CSE) on the neutrophil respiratory burst and their effect on activation of the nuclear factor‐ κ B (NF κ B) pathway in oral epithelium. Materials and Methods: Neutrophils from periodontally healthy individuals were treated with nicotine, cotinine and CSE before stimulation with Fusobacterium nucleatum , IgG‐opsonized Staphylococcus aureus and Escherichia coli lipopolysaccharide. Total and extracellular reactive oxygen species (ROS) generation was determined by luminol/isoluminol chemiluminescence. Activation of NF κ B in oral epithelial cells was determined by immunocytochemistry. Results: Smoke extract alone caused increased neutrophil extracellular isoluminol‐dependent chemiluminescence, not detectable with luminol. However, pre‐treatment with smoke extract reduced both total and extracellular ROS generation in response to all stimuli. Nicotine and cotinine had no effect on the neutrophil respiratory burst. Smoke extract, nicotine and cotinine did not induce oral epithelial cell NF κ B activation. Conclusions: These data demonstrate that smoke extract reduces the ability of neutrophils to generate ROS after stimulation with F. nucleatum and IgG‐opsonized S. aureus but, at high concentrations, stimulates extracellular ROS generation. During periodontitis, cigarette smoking may differentially affect neutrophil function, generally preventing elimination of periodontal pathogens but, in heavy smokers, also stimulating ROS release and oxidative stress mediated tissue damage.