title: Lipopolysaccharide induces rapid loss of follicular dendritic cell-secreted protein in the junctional epithelium.
abstract: Oshiro A, Iseki S, Miyauchi M, Terashima T, Kawaguchi Y, Ikeda Y, Shinomura T. Lipopolysaccharide induces rapid loss of follicular dendritic cell-secreted protein in the junctional epithelium. J Periodont Res 2012; 47: 689-694. © 2012 John Wiley & Sons A/S Background and Objective:  We have previously reported that mRNA encoding follicular dendritic cell-secreted protein (FDC-SP) is expressed specifically in the junctional epithelium at the gingival crevice. Other tissues, such as tonsil, prostate gland and trachea, also express high levels of FDC-SP. These tissues participate in a range of functions closely related to innate immunity. Therefore, it is hypothesized that FDC-SP plays a crucial role in close association with the host defense system within the gingival crevice. Accordingly, the main aim of this study was to investigate the expression and localization of FDC-SP in and around the junctional epithelium and to observe the dynamic changes of FDC-SP in experimental inflammation.
  
  
  METHODS
  We examined, immunohistochemically, the expression of FDC-SP in the junctional epithelium using a specific antibody raised in rabbit after immunization with a synthetic peptide derived from the hydrophilic region of FDC-SP. Experimental inflammation was induced in the upper molars of Wistar rats by applying bacterial lipopolysaccharide (LPS; 5 mg/mL in sterile saline) for 1 h.
  
  
  RESULTS
  We confirmed that FDC-SP is present in the junctional epithelium in a pattern that is consistent with the expression of FDC-SP mRNA. Of special interest is that no FDC-SP was detectable in the junctional epithelium 3 h after transient topical treatment with LPS.
  
  
  CONCLUSIONS
  The presence of FDC-SP in the junctional epithelium and its loss after LPS treatment strongly support our hypothesis of FDC-SP playing a crucial role in close association with the host defense system within the gingival crevice.
authors.affiliation: Tissue Regeneration, Graduate School of Medical and Dental Science, Tokyo Medical and Dental University, Tokyo, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Oshiro
authors.forename: S
authors.initials: S
authors.lastname: Iseki
authors.forename: M
authors.initials: M
authors.lastname: Miyauchi
authors.forename: T
authors.initials: T
authors.lastname: Terashima
authors.forename: Y
authors.initials: Y
authors.lastname: Kawaguchi
authors.forename: Y
authors.initials: Y
authors.lastname: Ikeda
authors.forename: T
authors.initials: T
authors.lastname: Shinomura
mesh_terms: D000818:Animals; D000918:Antibody Specificity; D020566:Dendritic Cells, Follicular / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism*; D004846:Epithelial Attachment / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D005881:Gingiva / Q000276:immunology* / Q000378:metabolism; D005891:Gingivitis / Q000378:metabolism*; D006801:Humans; D008070:Lipopolysaccharides / Q000276:immunology* / Q000494:pharmacology; D008297:Male; D051379:Mice; D011506:Proteins / Q000276:immunology / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D011993:Recombinant Fusion Proteins / Q000378:metabolism
chemical_list: D008070:Lipopolysaccharides; D011506:Proteins; D011993:Recombinant Fusion Proteins