title: Influence of nicotine and cotinine on epithelial colonization by periodontopathogens.
abstract: BACKGROUND
  Since smoking is an established risk factor for the development of periodontitis, the present study investigated whether nicotine and cotinine can make epithelial cells more prone to colonization by periodontopathogens.
  
  
  METHODS
  Primary epithelial cell mono-layers were inoculated with nicotine and cotinine prior to adhesion experiments with Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis. The number of bacteria associated with cells inoculated or not with nicotine or cotinine were assessed by an indirect culture viability assay. The same experimental set-up was used for assessing HeLa cells exposed to cigarette smoke extract (CSE).
  
  
  RESULTS
  Primary epithelial cells inoculated with concentrations of nicotine and cotinine, found in smokers and non smokers, did not show significant differences (P>0.05) in colonization susceptibility to A. actinomycetemcomitans. When these concentrations were increased to 1 mg/ml, a significant (P<0.05) and species-specific effect of the colonization susceptibility of epithelial cells was observed: It increased for A. actinomycetemcomitans, while it decreased for P. gingivalis. For both species the effects were more pronounced for nicotine, although this was not statistically significant. The change in colonization susceptibility did not result from alterations of the bacterial viability due to nicotine or cotinine. Treatment of HeLa cells with CSE also led to a species-specific variation in colonization tendency; i.e., increased for A. actinomycetemcomitans (P<0.05), but not for P. gingivalis.
  
  
  CONCLUSIONS
  The susceptibility of epithelial cells to become colonized by either A. actinomycetemcomitans or P. gingivalis could be altered by nicotine, cotinine, or CSE in a time-dependent, species-specific manner. Whether these findings that support the hypothesis of an increased patient susceptibility for bacterial adhesion to epithelial cells in smokers are clinically relevant remains to be proven.
authors.affiliation: Department of Periodontology, Catholic University Leuven, Leuven, Belgium.
authors.forename: Wim
authors.initials: W
authors.lastname: Teughels
authors.forename: Johan
authors.initials: J
authors.lastname: Van Eldere
authors.forename: Daniel
authors.initials: D
authors.lastname: van Steenberghe
authors.forename: Jean-Jaques
authors.initials: JJ
authors.lastname: Cassiman
authors.forename: Paula
authors.initials: P
authors.lastname: Fives-Taylor
authors.forename: Marc
authors.initials: M
authors.lastname: Quirynen
mesh_terms: D016976:Aggregatibacter actinomycetemcomitans / Q000472:pathogenicity; D000704:Analysis of Variance; D001422:Bacterial Adhesion / Q000187:drug effects*; D002478:Cells, Cultured; D015169:Colony Count, Microbial; D003367:Cotinine / Q000633:toxicity*; D004847:Epithelial Cells / Q000187:drug effects / Q000382:microbiology*; D005888:Gingival Pocket / Q000382:microbiology* / Q000473:pathology; D006367:HeLa Cells / Q000382:microbiology; D006801:Humans; D009538:Nicotine / Q000633:toxicity*; D018722:Nicotinic Agonists / Q000633:toxicity*; D016966:Porphyromonas gingivalis / Q000472:pathogenicity; D014028:Tobacco Smoke Pollution / Q000009:adverse effects
chemical_list: D018722:Nicotinic Agonists; D014028:Tobacco Smoke Pollution; D009538:Nicotine; D003367:Cotinine