Commensal Bacteria Influence Innate Status Within Gingival Tissues: A Pilot Study

Mice, Inbred BALB C Reverse Transcriptase Polymerase Chain Reaction Gingiva Gene Expression Enzyme-Linked Immunosorbent Assay Pilot Projects Mice, SCID Host-Parasite Interactions Mice 03 medical and health sciences 0302 clinical medicine Animals Cytokines Germ-Free Life RNA, Messenger Cell Adhesion Molecules DNA Primers Interleukin-1
DOI: 10.1902/jop.2004.75.11.1486 Publication Date: 2005-02-17T16:00:08Z
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‐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.
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