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Responses of Human Neutrophils to Nicotine and/or Porphyromonas gingivalis
Author(s) -
AlShibani Nouf K.,
Labban Nawaf Y.,
Kowolik Michael J.,
Ruby John D.,
Windsor L. Jack
Publication year - 2011
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2011.100757
Subject(s) - porphyromonas gingivalis , nicotine , microbiology and biotechnology , chemistry , periodontitis , medicine , biology , dentistry
Background: Tobacco smoking is considered a major modifiable risk factor for periodontal disease. Nicotine is the addictive ingredient in tobacco and has been shown to affect multiple cellular processes. Neutrophils are the first line of host defense and are critical cells in the maintenance of periodontal health through their role in the control of bacteria, but they can also contribute to the progression of periodontal disease by the production and release of reactive oxygen species (ROS). Virulence factors from periodontal pathogens, such as Porphyromonas gingivalis ( Pg ), stimulate the respiratory burst of neutrophils. The objective of this study is to explore the oxidative activity of neutrophils when stimulated with Pg , nicotine, or both. Methods: Neutrophils were separated from buffy coats by the double dextran gradient method. The generation of ROS by neutrophils was determined using luminol‐dependent chemiluminescence assays. The reaction was followed for 90 minutes, and the neutrophil activation was recorded as the total integrated energy output. Results: The Pg and Pg plus nicotine groups had a significantly higher active and peak chemiluminescence than the nicotine group (all with P <0.0001). The Pg and Pg with nicotine groups were not significantly different ( P = 0.90). Conclusion: In the presence of Pg , the nicotine did not further enhance the ROS release by the neutrophils, suggesting that the bacteria induced the maximum ROS release in this model system.