title: Impact of smoking on inflammation: overview of molecular mechanisms.
abstract: BACKGROUND
  Inflammation is a critical component of normal tissue repair, as well as being fundamental to the body's defense against infection. Environmental factors, such as smoking, have been reported to modify the host response and hence modify inflammation progression, severity and outcome. Therefore, a comprehensive understanding of the molecular mechanisms by which smoking affects inflammation is vital for preventive and therapeutic strategies on a clinical level.
  
  
  OBJECTIVE
  The purpose of the present article is to review the potential biological mechanisms by which smoking affects inflammation, emphasizing recent developments.
  
  
  RESULTS
  Smoking is reported to effect a number of biological mediators of inflammation through its effect on immune-inflammatory cells, leading to an immunosuppressant state. Recent evidence strongly suggests that the molecular mechanisms behind the modulation of inflammation by smoking mainly involve the nuclear factor-kappa B (NF-kB) family, through the activation of both an inhibitor of IkB kinase (IKK)-dependent and -independent pathway. In addition to NF-kB activation, a number of transcriptional factors including GATA, PAX5 and Smad 3/4, have also been implicated.
  
  
  CONCLUSIONS
  Multiple mechanisms may be responsible for the association of smoking and inflammation, and the identification of potential therapeutic targets should guide future research.
authors.affiliation: Department of Periodontology and Research Group in Oral Ecology, Faculty of Dentistry, Laval University, Quebec City, Canada.
authors.forename: R B
authors.initials: RB
authors.lastname: Gonçalves
authors.forename: R D
authors.initials: RD
authors.lastname: Coletta
authors.forename: K G
authors.initials: KG
authors.lastname: Silvério
authors.forename: L
authors.initials: L
authors.lastname: Benevides
authors.forename: M Z
authors.initials: MZ
authors.lastname: Casati
authors.forename: J S
authors.initials: JS
authors.lastname: da Silva
authors.forename: F H
authors.initials: FH
authors.lastname: Nociti
mesh_terms: D000818:Animals; D016207:Cytokines / Q000378:metabolism; D004249:DNA Damage; D005260:Female; D006801:Humans; D051550:I-kappa B Kinase / Q000378:metabolism; D007249:Inflammation / Q000209:etiology*; D008297:Male; D051379:Mice; D008954:Models, Biological; D016328:NF-kappa B / Q000378:metabolism; D009538:Nicotine / Q000378:metabolism; D010510:Periodontal Diseases / Q000378:metabolism; D011950:Receptors, Cholinergic / Q000378:metabolism; D012907:Smoking / Q000009:adverse effects*
chemical_list: D016207:Cytokines; D016328:NF-kappa B; D011950:Receptors, Cholinergic; D009538:Nicotine; D051550:I-kappa B Kinase