title: Artificial dental pulp exposure injury up-regulates antigen-presenting cell-related molecules in rat central nervous system.
abstract: BACKGROUND
  Bacterial infection and resulting inflammation of the dental pulp might not only trigger neuroimmune interactions in this tissue but also sensitize the central nervous system (CNS) such as the thalamus via nociceptive neurons. Thus, immunopathologic changes in the rat thalamus that take place after pulp inflammation were investigated.
  
  
  METHODS
  Pulp exposure was made in mandibular right first molars of 5-week-old Wistar rats. After 24 hours, the thalamus was retrieved and subjected to either immunohistochemistry for class II major histocompatibility complex (MHC) molecules and glial fibrillary acidic protein (GFAP) or mRNA expression analysis of antigen-presenting cell-related molecules and N-methyl-D-aspartate receptor 2D subunit (NR2D) by means of reverse transcription-polymerase chain reaction (RT-PCR) and real-time PCR.
  
  
  RESULTS
  At 24 hours after pulp exposure, the density of class II MHC molecule-expressing and GFAP-expressing cells was increased in the contralateral thalamus. Gene expression analysis revealed the up-regulation of class II MHC molecules, CD80, CD83, CD86, and NR2D in the contralateral thalamus, as compared with the ipsilateral thalamus.
  
  
  CONCLUSIONS
  These results suggest the signal of pulp inflammation induces neuronal activation in the CNS.
authors.affiliation: Pulp Biology and Endodontics, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan. tomoendo@tmd.ac.jp
authors.forename: Tomoatsu
authors.initials: T
authors.lastname: Kaneko
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Kaneko
authors.forename: Uraiwan
authors.initials: U
authors.lastname: Chokechanachaisakul
authors.forename: Jun
authors.initials: J
authors.lastname: Kawamura
authors.forename: Reika
authors.initials: R
authors.lastname: Kaneko
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Sunakawa
authors.forename: Takashi
authors.initials: T
authors.lastname: Okiji
authors.forename: Hideaki
authors.initials: H
authors.lastname: Suda
mesh_terms: D000818:Animals; D000938:Antigen-Presenting Cells / Q000166:cytology* / Q000276:immunology; D003789:Dental Pulp Exposure / Q000276:immunology* / Q000473:pathology; D005904:Glial Fibrillary Acidic Protein / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D000949:Histocompatibility Antigens Class II / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D008297:Male; D008334:Mandible; D008963:Molar; D015213:Neuroimmunomodulation / Q000502:physiology; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D013788:Thalamus / Q000166:cytology / Q000276:immunology / Q000378:metabolism*
chemical_list: D005904:Glial Fibrillary Acidic Protein; D000949:Histocompatibility Antigens Class II; C533282:N-methyl D-aspartate receptor subtype 2D, rat; D012333:RNA, Messenger; D016194:Receptors, N-Methyl-D-Aspartate