title: The r40-kDa outer membrane protein human monoclonal antibody protects against Porphyromonas gingivalis-induced bone loss in rats.
abstract: BACKGROUND
  Porphyromonas gingivalis has been implicated as an important pathogen in the development of adult periodontitis, and its colonization of subgingival sites is critical in the pathogenic process. We recently reported the construction and characterization of human immunoglobulin G isotype clones, which were specifically reactive with recombinant (r) 40-kDa outer membrane protein (OMP) of P. gingivalis. The aim of this study was to investigate the efficacy of human monoclonal antibody (hMAb) against r40-kDa OMP of P. gingivalis to the protection alveolar bone loss by P. gingivalis in rats.
  
  
  METHODS
  The role of 40-kDa OMP in the adherence of P. gingivalis to human gingival epithelial cells (HGECs) was examined by preincubating with r40-kDa OMP hMAb before adding the HGECs. Moreover, we used a rat model to examine the effect of the anti-r40-kDa OMP hMAb in alveolar bone loss by oral infection. Forty-six days after the last infection, the periodontal bone level was assessed morphometrically on defleshed rat jaws.
  
  
  RESULTS
  The adherence to HGECs was reduced by 84% compared to adherence levels without the antibody. P. gingivalis could not be detected from rats in a P. gingivalis-non-infected group and a group that was administered the anti-r40-kDa OMP hMAb. The bone loss in P. gingivalis-infected animals that were administered the anti-r40-kDa OMP hMAb was significantly lower than that of P. gingivalis-infected rats.
  
  
  CONCLUSIONS
  Our results suggest that transchromosomic mouse-derived hMAb against r40-kDa OMP of P. gingivalis protects against periodontal bone loss. This newly constructed anti-r40-kDa OMP hMAb was used to protect against periodontal diseases caused by P. gingivalis infection.
authors.affiliation: Division of Microbiology, Department of Infection Control, Kanagawa Dental College, Kanagawa, Japan.
authors.forename: Nobushiro
authors.initials: N
authors.lastname: Hamada
authors.forename: Kiyoko
authors.initials: K
authors.lastname: Watanabe
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Tahara
authors.forename: Kumiko
authors.initials: K
authors.lastname: Nakazawa
authors.forename: Isao
authors.initials: I
authors.lastname: Ishida
authors.forename: Yasuko
authors.initials: Y
authors.lastname: Shibata
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Kobayashi
authors.forename: Hiromasa
authors.initials: H
authors.lastname: Yoshie
authors.forename: Yoshimitsu
authors.initials: Y
authors.lastname: Abiko
authors.forename: Toshio
authors.initials: T
authors.lastname: Umemoto
mesh_terms: D016301:Alveolar Bone Loss / Q000276:immunology / Q000382:microbiology / Q000517:prevention & control*; D000818:Animals; D000907:Antibodies, Bacterial / Q000276:immunology* / Q000627:therapeutic use; D000911:Antibodies, Monoclonal / Q000276:immunology* / Q000627:therapeutic use; D001425:Bacterial Outer Membrane Proteins / Q000276:immunology*; D016866:Bacteroidaceae Infections / Q000150:complications*; D002478:Cells, Cultured; D004195:Disease Models, Animal; D004847:Epithelial Cells / Q000276:immunology / Q000382:microbiology; D005881:Gingiva / Q000166:cytology; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology / Q000627:therapeutic use; D007132:Immunoglobulin Isotypes; D008297:Male; D010518:Periodontitis / Q000276:immunology / Q000382:microbiology; D016966:Porphyromonas gingivalis / Q000276:immunology* / Q000472:pathogenicity; D051381:Rats; D017208:Rats, Wistar; D011994:Recombinant Proteins; D018709:Statistics, Nonparametric
chemical_list: D000907:Antibodies, Bacterial; D000911:Antibodies, Monoclonal; D001425:Bacterial Outer Membrane Proteins; D007074:Immunoglobulin G; D007132:Immunoglobulin Isotypes; D011994:Recombinant Proteins