title: Expression of Toll-like receptor 2 and 4 in inflamed pulp in severe combined immunodeficiency mice.
abstract: BACKGROUND
  Toll-like receptors (TLRs) are important receptors mediating innate immune responses because they detect factors released from bacterial cell wall components during inflammatory reactions. However, the role of TLRs in dental pulp, which is bounded by hard tissues, is poorly understood. The purpose of this study was to investigate the relationship between the innate immune system and the defense of pulp tissue by using immunodeficient mice that lack an adaptive immune response
  
  
  METHODS
  Mice with severe combined immunodeficiency (SCID) were used as a model because they lack an adaptive immune response. The expression of TLR-2 and TLR-4 in experimentally inflamed pulps in SCID mice was measured by quantitative real-time polymerase chain reaction and immunohistochemistry. Total RNA was isolated from pulp tissues at 0 to 24 hours after bacterial dentinal infection. Anti-TLR-2, anti-TLR-4 cells, anti-CD64, and antinestin cells were detected with labeled streptavidin-biotin methods.
  
  
  RESULTS
  TLR-2 messenger RNA was detected at 3 hours after bacterial infection and then gradually increased from 9 to 24 hours. Numerous TLR-2- and CD64-positive cells detected on macrophages and dendritic-like cells, and TLR-4- and CD64-positive macrophages were detected in the early stage of pulpitis.
  
  
  CONCLUSIONS
  These results suggest that the expression of TLR-2 and TLR-4 may be triggered by bacterial infection in irreversible pulpitis without a need for an adaptive immune response. Those signals may relate to pulpal responses to bacterial infection.
authors: Department of Oral Medicine, Division of Endodontics, Kanagawa Dental College, Yokosuka, Japan.
authors: Noriko
authors: N
authors: Mutoh
authors: Hirotaka
authors: H
authors: Watabe
authors: Keiko
authors: K
authors: Chieda
authors: Nobuyuki
authors: N
authors: Tani-Ishii
mesh_terms: D000818:Animals; D003713:Dendritic Cells / Q000378:metabolism; D003731:Dental Caries / Q000276:immunology; D005260:Female; D007113:Immunity, Innate / Q000502:physiology*; D007124:Immunoenzyme Techniques; D007381:Intermediate Filament Proteins / Q000096:biosynthesis; D008264:Macrophages / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D016513:Mice, SCID; D009419:Nerve Tissue Proteins / Q000096:biosynthesis; D064231:Nestin; D009504:Neutrophils / Q000378:metabolism; D009804:Odontoblasts / Q000378:metabolism; D016133:Polymerase Chain Reaction; D011671:Pulpitis / Q000276:immunology* / Q000378:metabolism* / Q000382:microbiology; D012333:RNA, Messenger / Q000032:analysis; D051195:Toll-Like Receptor 2 / Q000096:biosynthesis*; D051197:Toll-Like Receptor 4 / Q000096:biosynthesis*
chemical_list: D007381:Intermediate Filament Proteins; D009419:Nerve Tissue Proteins; C577485:Nes protein, mouse; D064231:Nestin; D012333:RNA, Messenger; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4