title: Oral infection with Porphyromonas gingivalis and systemic cytokine profile in C57BL/6.KOR-ApoE shl mice.
abstract: OBJECTIVE
  Periodontal infection affects atherosclerotic diseases, such as coronary heart diseases. Mouse models have revealed that oral infection with Porphyromonas gingivalis induces changes in inflammatory- and lipid metabolism-related gene expression, regardless of the development of atherosclerotic lesions. However, the serum protein expression profile in the oral infection model has not been investigated. The present study aimed to analyse the effect of oral infection with P. gingivalis on the expression levels of multiple cytokines in the serum in apolipoprotein E-deficient mice by using a cytokine antibody array.
  
  
  METHODS
  C57BL/6.KOR-Apoe(shl) mice were orally infected with P. gingivalis five times at 3 day intervals and were then killed. Splenocytes were isolated and analysed for proliferative activity and immunoglobulin G (IgG) production in response to in vitro restimulation with P. gingivalis. The expression levels of various cytokines in the sera were analysed using a mouse antibody array glass chip.
  
  
  RESULTS
  Splenocytes from P. gingivalis-infected mice demonstrated significantly greater proliferation and IgG production in response to P. gingivalis compared with those from sham-infected mice. Antibody array analysis revealed the selective upregulation of matrix metalloproteinase 3, intercellular adhesion molecule 1, insulin-like growth factor binding protein 2 and chemokine (C-X-C motif) ligand 7 and the downregulation of interleukin-17, tumor necrosis factor-α and L-selectin.
  
  
  CONCLUSIONS
  These data demonstrate that oral infection with P. gingivalis induces alterations in systemic cytokine production. These cytokines could play roles in the development not only of periodontitis but also of atherosclerosis.
authors.affiliation: Center for Transdisciplinary Researh, Niigata University, Niigata, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Miyauchi
authors.forename: T
authors.initials: T
authors.lastname: Maekawa
authors.forename: Y
authors.initials: Y
authors.lastname: Aoki
authors.forename: H
authors.initials: H
authors.lastname: Miyazawa
authors.forename: K
authors.initials: K
authors.lastname: Tabeta
authors.forename: T
authors.initials: T
authors.lastname: Nakajima
authors.forename: K
authors.initials: K
authors.lastname: Yamazaki
mesh_terms: D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood; D001057:Apolipoproteins E / Q000235:genetics; D016866:Bacteroidaceae Infections / Q000276:immunology*; D049109:Cell Proliferation; D019743:Chemokines, CXC / Q000097:blood; D016207:Cytokines / Q000097:blood*; D004195:Disease Models, Animal; D007074:Immunoglobulin G / Q000097:blood; D018971:Insulin-Like Growth Factor Binding Protein 2 / Q000097:blood; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D020381:Interleukin-17 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D019041:L-Selectin / Q000097:blood; D008297:Male; D019278:Matrix Metalloproteinase 3 / Q000097:blood; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D009059:Mouth Diseases / Q000276:immunology / Q000382:microbiology*; D016966:Porphyromonas gingivalis / Q000276:immunology*; D013154:Spleen / Q000166:cytology / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D000907:Antibodies, Bacterial; D001057:Apolipoproteins E; D019743:Chemokines, CXC; C446301:Cxcl7 protein, mouse; D016207:Cytokines; C090509:Icam1 protein, mouse; D007074:Immunoglobulin G; D018971:Insulin-Like Growth Factor Binding Protein 2; D020381:Interleukin-17; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D019041:L-Selectin; D019278:Matrix Metalloproteinase 3; C511769:Mmp3 protein, mouse