title: Loss of claudin-1 in lipopolysaccharide-treated periodontal epithelium.
abstract: OBJECTIVE
  The epithelial barrier is a critical component of innate immunity and provides protection against microbial invasion. Claudin-1, a tight junction protein, is known to contribute to the epithelial cell barrier. An experimentally induced rat periodontal disease model was used to study the effects of lipopolysaccharide (LPS) on the expression of tight junction-associated molecule genes in the junctional epithelium.
  
  
  METHODS
  LPS was applied for 8 wk in the gingival sulcus, and junctional epithelium was collected by laser-capture microdissection and subjected to microarray analysis.
  
  
  RESULTS
  Microarray analysis identified that expression of the claudin-1 gene was decreased in the epithelium by chronic LPS challenge. Immunohistochemical analysis confirmed the expression of claudin-1 protein in junctional epithelium and that 8 wk of chronic LPS topical application significantly reduced claudin-1 expression. The effect of LPS on claudin-1 protein expression was validated using a porcine junctional epithelial cell culture Transwell model. The epithelial barrier, as measured using transmembrane resistance, was significantly reduced after 3 wk of LPS challenge and this was associated with a decreased level of expression of claudin-1 protein.
  
  
  CONCLUSIONS
  These results confirm that the initiation of experimental periodontal disease is associated with reduction in the expression of claudin-1 gene and protein. This decreased level of a critical tight junction protein may result in the disruption of barrier function and may play an important role in the initiation of periodontal disease.
authors.affiliation: Department of Periodontal Medicine, Division of Frontier Medical Science, Hiroshima University Graduate School of Biomedical Sciences, Minami-ku, Hiroshima, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Fujita
authors.forename: J D
authors.initials: JD
authors.lastname: Firth
authors.forename: M
authors.initials: M
authors.lastname: Kittaka
authors.forename: D
authors.initials: D
authors.lastname: Ekuni
authors.forename: H
authors.initials: H
authors.lastname: Kurihara
authors.forename: E E
authors.initials: EE
authors.lastname: Putnins
mesh_terms: D000818:Animals; D018929:Cell Culture Techniques; D062445:Claudin-1; D004195:Disease Models, Animal; D004846:Epithelial Attachment / Q000187:drug effects* / Q000473:pathology; D004926:Escherichia coli; D007150:Immunohistochemistry; D061346:Laser Capture Microdissection; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D008565:Membrane Proteins / Q000187:drug effects* / Q000235:genetics; D046228:Microarray Analysis; D010518:Periodontitis / Q000382:microbiology / Q000473:pathology; D010519:Periodontium / Q000187:drug effects* / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D012697:Serine Endopeptidases / Q000494:pharmacology; D013305:Streptomyces griseus / Q000201:enzymology; D013552:Swine; D019108:Tight Junctions / Q000187:drug effects*
chemical_list: D062445:Claudin-1; C568114:Cldn1 protein, rat; D008070:Lipopolysaccharides; D008565:Membrane Proteins; D012697:Serine Endopeptidases