title: Commensal bacteria influence innate status within gingival tissues: a pilot study.
abstract: BACKGROUND
  The objective of this study was to determine the contribution of commensal bacteria to the innate defense status of gingival tissue by examining the expression of innate host defense mediators in germ-free and conventionally reared groups in both BALBc/ByJ and SCID C.B17 mice.
  
  
  METHODS
  Semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) was utilized to determine the constitutive levels within each gingival tissue set (N = 5) for: E-selectin, P-selectin, interleukin-(IL)-8 homologue, tumor necrosis factor-alpha, IL-1beta, intercellular adhesion molecule-(ICAM)-1, ICAM-2, and vascular adhesion molecule-(VCAM)-1. In addition, IL-1beta protein content was determined by enzyme-linked immunosorbent assay (ELISA).
  
  
  RESULTS
  Gingival samples revealed that only IL-1beta mRNA expression among all mediators examined was significantly reduced in conventionally reared mice (P<0.01) compared to germ-free mice. In contrast, IL-1beta protein levels were significantly (P <0.001) higher in conventionally reared mice compared to germ-free animals. Conventionally reared and germ-free SCID C.B17 mice revealed a similar pattern in regard to reduced IL-1beta mRNA and significantly increased IL-1beta protein (P<0.0001).
  
  
  CONCLUSIONS
  Commensal microbial colonization influences innate host defense mediator expression of IL-1beta at both the mRNA and protein levels in healthy periodontal tissue in mice.
authors.affiliation: United States Army Dental Corps and Department of Periodontics and Oral Biology, University of Washington, School of Dentistry, Seattle, WA, USA.
authors.forename: Douglas R
authors.initials: DR
authors.lastname: Dixon
authors.forename: Robert A
authors.initials: RA
authors.lastname: Reife
authors.forename: John J
authors.initials: JJ
authors.lastname: Cebra
authors.forename: Richard P
authors.initials: RP
authors.lastname: Darveau
mesh_terms: D000818:Animals; D015815:Cell Adhesion Molecules / Q000032:analysis / Q000235:genetics; D016207:Cytokines / Q000032:analysis / Q000235:genetics; D017931:DNA Primers; D004797:Enzyme-Linked Immunosorbent Assay; D015870:Gene Expression / Q000276:immunology; D005856:Germ-Free Life / Q000235:genetics / Q000276:immunology; D005881:Gingiva / Q000276:immunology* / Q000382:microbiology; D006790:Host-Parasite Interactions / Q000235:genetics / Q000276:immunology*; D007375:Interleukin-1 / Q000032:analysis* / Q000235:genetics; D051379:Mice; D008807:Mice, Inbred BALB C / Q000276:immunology; D016513:Mice, SCID / Q000276:immunology; D010865:Pilot Projects; D012333:RNA, Messenger; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D015815:Cell Adhesion Molecules; D016207:Cytokines; D017931:DNA Primers; D007375:Interleukin-1; D012333:RNA, Messenger