Premium
Commensal Bacteria Influence Innate Status Within Gingival Tissues: A Pilot Study
Author(s) -
Dixon Douglas R.,
Reife Robert A.,
Cebra John J.,
Darveau Richard P.
Publication year - 2004
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2004.75.11.1486
Subject(s) - biology , germ , innate immune system , tumor necrosis factor alpha , messenger rna , immunology , microbiology and biotechnology , biochemistry , gene , immune system
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‐α, IL‐1β, intercellular adhesion molecule‐(ICAM)‐1, ICAM‐2, and vascular adhesion molecule‐(VCAM)‐1. In addition, IL‐1β protein content was determined by enzyme‐linked immunosorbent assay (ELISA). Results: Gingival samples revealed that only IL‐1β mRNA expression among all mediators examined was significantly reduced in conventionally reared mice ( P <0.01) compared to germ‐free mice. In contrast, IL‐1β 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‐1β mRNA and significantly increased IL‐1β protein ( P <0.0001). Conclusion: Commensal microbial colonization influences innate host defense mediator expression of IL‐1β at both the mRNA and protein levels in healthy periodontal tissue in mice. J Periodontol 2004;75:1486‐1492 .