title: Role of the junctional epithelium in periodontal innate defense and homeostasis.
abstract: OBJECTIVE
  The junctional epithelium provides the front-line defense against periodontal bacterial infection. The migration of neutrophils into the junctional epithelium might represent a protective reaction against bacterial infections. However, neutrophils penetrate into the junctional epithelium even under sterile conditions. In this study, we analyzed and compared the number of neutrophils and the cytokine expression related to neutrophil migration in the junctional epithelium in conventional and germ-free mice.
  
  
  METHODS
  Germ-free and conventional ICR mice were used at 12 wk of age. Frozen sections were used for the detection of Gr-1, macrophage inflammatory protein-2 (MIP-2/CXCL2) and proliferating cell nuclear antigen-positive cells in the two groups of mice. Laser capture microdissection and RT-PCR analysis were used to evaluate the expression of keratinocyte-derived chemokine (KC/CXCL1), MIP-2, interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) mRNAs in the two groups of mice.
  
  
  RESULTS
  Morphometric examination indicated an increase in the area of the junctional epithelium upon bacterial infection. Immunohistochemical studies also detected an increased number of neutrophils in the junctional epithelium upon bacterial infection. Higher up-regulation of KC and MIP-2 were detected in the junctional epithelium of conventional mice than in germ-free mice, whereas the expression of Il-1β and Tnfα mRNAs was not affected.
  
  
  CONCLUSIONS
  Junctional epithelium cells constitutively expressed several types of chemokines and cytokines and the expression of chemokines was augmented by bacterial infection. Therefore, the constitutive expression of cytokines in junctional epithelium might be related to the morphological and functional homeostasis of the junctional epithelium in addition to the defense against the bacterial infection.
authors.affiliation: Department of Oral Anatomy and Developmental Biology, Showa University School of Dentistry, Shinagawa-ku, Tokyo, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Tsukamoto
authors.forename: M
authors.initials: M
authors.lastname: Usui
authors.forename: G
authors.initials: G
authors.lastname: Yamamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Takagi
authors.forename: T
authors.initials: T
authors.lastname: Tachikawa
authors.forename: M
authors.initials: M
authors.lastname: Yamamoto
authors.forename: M
authors.initials: M
authors.lastname: Nakamura
mesh_terms: D000818:Animals; D054360:Chemokine CXCL1 / Q000096:biosynthesis / Q000235:genetics; D054426:Chemokine CXCL2 / Q000096:biosynthesis / Q000235:genetics; D016207:Cytokines / Q000096:biosynthesis* / Q000235:genetics; D004846:Epithelial Attachment / Q000276:immunology*; D005856:Germ-Free Life; D006706:Homeostasis / Q000276:immunology*; D054884:Host-Pathogen Interactions; D053583:Interleukin-1beta / Q000096:biosynthesis / Q000235:genetics; D061346:Laser Capture Microdissection; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009504:Neutrophils / Q000502:physiology; D010518:Periodontitis / Q000276:immunology*; D018809:Proliferating Cell Nuclear Antigen / Q000096:biosynthesis / Q000235:genetics; D019707:Receptors, Chemokine / Q000096:biosynthesis; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000235:genetics
chemical_list: D054360:Chemokine CXCL1; D054426:Chemokine CXCL2; D016207:Cytokines; C503133:Gr-1 protein, mouse; D053583:Interleukin-1beta; D018809:Proliferating Cell Nuclear Antigen; D019707:Receptors, Chemokine; D014409:Tumor Necrosis Factor-alpha