title: Nicotine-induced release of elastase and eicosanoids by human neutrophils.
abstract: We examined the direct effects of nicotine on a variety of neutrophil functions at concentrations achievable in lung and oral tissues from cigarette smoking. The results show dose-dependent suppression of chemotaxis and phagocytosis, and enhancement of degranulation and eicosanoid generation, but not superoxide production. Cell viability was not affected by the concentrations of nicotine used in these experiments, as shown by trypan blue dye exclusion and MTT assays. These results implicate nicotine as the ingredient in cigarette smoke responsible for inflammatory damage to lungs and oral tissues observed in cigarette smokers.
authors.affiliation: Department of Dentistry, University of Queensland, Mater Childrens Hospital, South Brisbane, Australia.
authors.forename: W K
authors.initials: WK
authors.lastname: Seow
authors.forename: Y H
authors.initials: YH
authors.lastname: Thong
authors.forename: R D
authors.initials: RD
authors.lastname: Nelson
authors.forename: G D
authors.initials: GD
authors.lastname: MacFarlane
authors.forename: M C
authors.initials: MC
authors.lastname: Herzberg
mesh_terms: D015550:Cell Degranulation / Q000187:drug effects; D002634:Chemotaxis, Leukocyte / Q000187:drug effects; D015777:Eicosanoids / Q000378:metabolism*; D006801:Humans; D009504:Neutrophils / Q000187:drug effects* / Q000378:metabolism*; D009538:Nicotine / Q000494:pharmacology*; D009994:Osmolar Concentration; D010196:Pancreatic Elastase / Q000378:metabolism*; D011453:Prostaglandins / Q000096:biosynthesis
chemical_list: D015777:Eicosanoids; D011453:Prostaglandins; D009538:Nicotine; D010196:Pancreatic Elastase