title: Natural killer T cells mediate alveolar bone resorption and a systemic inflammatory response in response to oral infection of mice with Porphyromonas gingivalis.
abstract: OBJECTIVE
  T and B cells are known to be involved in the disease process of periodontitis. However, the role of natural killer T cells in the pathogenesis of periodontitis has not been clarified.
  
  
  METHODS
  To examine the role of these cells, C57BL/6J (wild-type), CD1d(-/-) and α-galactosylceramide (αGC)-stimulated wild-type mice were orally infected with Porphyromonas gingivalis strain W83.
  
  
  RESULTS
  Apart from CD1d(-/-) mice, the level of alveolar bone resorption was elevated by the infection and was further accelerated in αGC-stimulated mice. The infection induced elevated levels of serum amyloid A and P. gingivalis-specific IgG in the sera, although the degree of elevation was much smaller in the CD1d(-/-) mice. Infection-induced RANKL elevation was only observed in αGC-stimulated mice. Although the cytokines produced by splenocytes were mainly T-helper 1 type in wild-type mice, those in αGC-stimulated mice were predominantly T-helper 2 type. In the liver, the infection demonstrated no effect on the gene expression for interferon-γ, interleukin-4 and RANKL except αGC-stimulated mice in which the infection upregulated the gene expressions.
  
  
  CONCLUSIONS
  This study is the first to show that natural killer T cells upregulated systemic and local inflammatory responses induced by oral infection with P. gingivalis, thereby contributing to the progression of alveolar bone resorption.
authors.affiliation: Center for Transdisciplinary Research, Niigata University, Niigata, Japan; Division of Oral Science for Health Promotion, Laboratory of Periodontology and Immunology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Aoki-Nonaka
authors.forename: T
authors.initials: T
authors.lastname: Nakajima
authors.forename: S
authors.initials: S
authors.lastname: Miyauchi
authors.forename: H
authors.initials: H
authors.lastname: Miyazawa
authors.forename: H
authors.initials: H
authors.lastname: Yamada
authors.forename: H
authors.initials: H
authors.lastname: Domon
authors.forename: K
authors.initials: K
authors.lastname: Tabeta
authors.forename: K
authors.initials: K
authors.lastname: Yamazaki
mesh_terms: D016301:Alveolar Bone Loss / Q000276:immunology* / Q000382:microbiology; D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood; D055610:Antigens, CD1d / Q000276:immunology; D016866:Bacteroidaceae Infections / Q000276:immunology*; D005699:Galactosylceramides / Q000494:pharmacology; D007074:Immunoglobulin G / Q000097:blood; D007249:Inflammation / Q000276:immunology; D007371:Interferon-gamma / Q000032:analysis; D015847:Interleukin-4 / Q000032:analysis; D007694:Killer Cells, Natural / Q000276:immunology* / Q000382:microbiology; D008099:Liver / Q000276:immunology; D008297:Male; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D010518:Periodontitis / Q000276:immunology / Q000382:microbiology*; D016966:Porphyromonas gingivalis / Q000276:immunology*; D053245:RANK Ligand / Q000032:analysis / Q000187:drug effects; D000685:Serum Amyloid A Protein / Q000032:analysis; D013154:Spleen / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D000907:Antibodies, Bacterial; D055610:Antigens, CD1d; C584692:CD1d antigen, mouse; D005699:Galactosylceramides; D007074:Immunoglobulin G; D053245:RANK Ligand; D000685:Serum Amyloid A Protein; C505689:Tnfsf11 protein, mouse; C493154:alpha-galactosylceramide; D015847:Interleukin-4; D007371:Interferon-gamma
keywords: Porphyromonas gingivalis; inflammation; natural killer T cell; periodontal infection