Methods: Gene and protein expressions in periodontal tissue constituent cells were analyzed with RT-PCR and Western blot analysis, respectively. The expressions of TLRs in LPS-induced periodontal tissue destruction model of rats with or without oral administration of bLF were evaluated by immunohistochemical staining.
Results: In periodontal ligament cells, LPS up-regulated TLR5 and TLR9 expression and the sensitivity of TLR5 and TLR9 to each ligands. LPS, then, increased TNF-a production. The up-regulation of TLR5 and TLR9 expressions by LPS stimulation were also observed in osteoblasts and cementoblasts. bLF inhibited LPS-induced degradation of IkBa and phospholyration of p65, resulting in suppressing induction of TLR5 and TLR9. Moreover, bLF reduced LPS-induced TNF-a production and the expression of TLR5 and TLR9 in vivo experimental animals.
Conclusions: In the pathogenesis of periodontitis, LPS plays a central role among several pathogenic factors through affecting crosstalk of TLRs. We demonstrated that bLF inhibits LPS-induced crosstalk of TLRs and production of TNF-a by suppressing NFkB activation. Taken all together, bLF could be used as an effective agent against the destruction of alveolar bone induced by pathogenic factors in periodontitis.