Regulation of visfatin by microbial and biomechanical signals in PDL cells
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This in vitro study was established to examine whether visfatin thought to be a link between periodontitis and obesity is produced by periodontal ligament (PDL) cells and, if so, whether its synthesis is modulated by microbial and/or biomechanical signals.
Materials and methods
PDL cells seeded on BioFlex® plates were exposed to the oral pathogen Fusobacterium nucleatum ATCC 25586 and/or subjected to biomechanical strain for up to 3 days. Gene expression of visfatin and toll-like receptors (TLR) 2 and 4 was analyzed by RT-PCR, visfatin protein synthesis by ELISA and immunocytochemistry, and NFκB nuclear translocation by immunofluorescence.
F. nucleatum upregulated the visfatin expression in a dose- and time-dependent fashion. Preincubation with neutralizing antibodies against TLR2 and TLR4 caused a significant inhibition of the F. nucleatum-upregulated visfatin expression at 1 day. F. nucleatum stimulated the NFκB nuclear translocation. Biomechanical loading reduced the stimulatory effects of F. nucleatum on visfatin expression at 1 and 3 days and also abrogated the F. nucleatum-induced NFκB nuclear translocation at 60 min. Biomechanical loading inhibited significantly the expression of TLR2 and TLR4 at 3 days. The regulatory effects of F. nucleatum and/or biomechanical loading on visfatin expression were also observed at protein level.
PDL cells produce visfatin, and this production is enhanced by F. nucleatum. Biomechanical loading seems to be protective against the effects of F. nucleatum on visfatin expression.
Visfatin produced by periodontal tissues could play a major role in the pathogenesis of periodontitis and the interactions with obesity and other systemic diseases.
KeywordsBiomechanics Tension Forces Fusobacterium nucleatum Visfatin Periodontal ligament
This study was supported by a grant from São Paulo Research Foundation (FAPESP: 2010/07771-4, 2011/13752-5), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES: 2385-11-2), the German Research Foundation (DFG: KFO208/TP4), and the Medical Faculty of the University of Bonn. We would like to thank Ms. Ramona Hömig, Dr. Susanne Reimann, and Prof. Werner Götz for their great support.
Conflict of interest
The authors declare that they have no conflict of interest.
- 17.Preshaw PM, Foster N, Taylor JJ (2007) Cross-susceptibility between periodontal disease and type 2 diabetes mellitus: an immunobiological perspective. Periodontol 2000 45:138-157Google Scholar