title: Ability of oral bacteria to induce tissue-destructive molecules from human neutrophils.
abstract: OBJECTIVE
  The induction of tissue-destructive molecules from neutrophils by periodontopathic bacteria has been suggested as one of the mechanisms of periodontal destruction. The aim of this study was to determine whether the ability to stimulate neutrophils is an authentic characteristic of periodontopathic bacteria.
  
  
  METHODS
  We evaluated, along with phagocytosis, the production of reactive oxygen species (ROS), matrix metalloproteinase-8 (MMP-8), and interleukin-1beta by neutrophils in response to non-periodontopathic Streptococcus sanguinis and periodontopathic bacteria Fusobacterium nucleatum and Treponema denticola, in the absence or presence of antibodies. Phagocytosis, the death of neutrophils, and intracellular ROS production were measured by flow cytometry and the concentrations of MMP-8 and interleukin-1beta secreted into medium were determined by enzyme-linked immunosorbent assay.
  
  
  RESULTS
  S. sanguinis and F. nucleatum induced greater production of ROS, MMP-8, and interleukin-1beta than did T. denticola. The levels of tissue-destructive molecules produced by neutrophils had a positive correlation with phagocytosis. Opsonization of bacteria with antibodies significantly increased phagocytosis and ROS production and release, thus increasing both bacterial clearance and potential tissue damage.
  
  
  CONCLUSIONS
  The ability of oral bacteria to induce tissue-destructive molecules from neutrophils is not an inherent characteristic of periodontopathic bacteria, which would provide a new insight into the role of neutrophils in periodontal destruction.
authors.affiliation: Programs of Oromaxillofacial Infection & Immunity and BK21 CLS, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, Korea.
authors.forename: J
authors.initials: J
authors.lastname: Shin
authors.forename: S
authors.initials: S
authors.lastname: Ji
authors.forename: Y
authors.initials: Y
authors.lastname: Choi
mesh_terms: D000704:Analysis of Variance; D000907:Antibodies, Bacterial / Q000276:immunology; D016923:Cell Death; D002478:Cells, Cultured; D016967:Fusobacterium nucleatum / Q000502:physiology*; D006801:Humans; D053583:Interleukin-1beta / Q000096:biosynthesis; D020784:Matrix Metalloproteinase 8 / Q000096:biosynthesis; D018375:Neutrophil Activation; D009504:Neutrophils / Q000378:metabolism* / Q000382:microbiology*; D010587:Phagocytosis; D017382:Reactive Oxygen Species / Q000378:metabolism; D013298:Streptococcus sanguis / Q000502:physiology*; D048373:Treponema denticola / Q000502:physiology*
chemical_list: D000907:Antibodies, Bacterial; D053583:Interleukin-1beta; D017382:Reactive Oxygen Species; D020784:Matrix Metalloproteinase 8