title: IL-8 and TNF-alpha from peripheral neutrophils and acute-phase proteins in periodontitis.
abstract: OBJECTIVE
  In other studies, we have found deviant functions in peripheral neutrophils in periodontitis. The aim here was to study (1) the release of cytokines, IL-8 and TNFalpha, from neutrophils in 15 treated periodontitis patients and pair-matched controls as well as (2) the effects of cigarette smoking.
  
  
  METHODS
  Cytokines released in the incubation medium from un-stimulated and Fcgamma-R-stimulated neutrophils and some acute-phase reactants were measured with ELISA.
  
  
  RESULTS
  Non-smoking patients had trends for lower TNFalpha release compared to non-smoking controls, while corresponding trends were rather similar for Il-8. Smoking had a moderate but inconsistent effect on the release of both cytokines. However, in patients, the ratio between stimulated/un-stimulated release of Il-8 was significantly lowered by smoking (p<0.03). The parameters of inflammation in plasma differed only slightly between patients and controls, indicating that periodontal disease in a quiet phase has a negligible systemic effect with the possible exception for a higher IL-8 level. In contrast, smoking had significant systemic effect on the neutrophil count and IgG levels.
  
  
  CONCLUSIONS
  Release of IL-8 and TNF-alpha from peripheral neutrophils and various parameters of inflammation in plasma seem to be affected more by cigarette smoking than periodontal disease.
authors.affiliation: Karolinska Institutet, Department of Odontology, Division of Periodontology, Huddinge, Sweden. margareta.fredriksson@ofa.ki.se
authors.forename: M
authors.initials: M
authors.lastname: Fredriksson
authors.forename: K
authors.initials: K
authors.lastname: Bergström
authors.forename: B
authors.initials: B
authors.lastname: Asman
mesh_terms: D000209:Acute-Phase Proteins / Q000032:analysis*; D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D016022:Case-Control Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D053590:Interleukin 1 Receptor Antagonist Protein; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood*; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000276:immunology*; D010518:Periodontitis / Q000097:blood*; D010865:Pilot Projects; D017452:Receptors, IgG / Q000097:blood; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood; D047888:Receptors, Tumor Necrosis Factor, Type I; D012795:Sialoglycoproteins / Q000097:blood; D012907:Smoking / Q000097:blood*; D018709:Statistics, Nonparametric; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis*
chemical_list: D000209:Acute-Phase Proteins; D015703:Antigens, CD; C507763:IL1RN protein, human; D007074:Immunoglobulin G; D053590:Interleukin 1 Receptor Antagonist Protein; D015850:Interleukin-6; D016209:Interleukin-8; D017452:Receptors, IgG; D017472:Receptors, Interleukin-1; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein