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  • Title: Streptococcus cristatus modulates the Fusobacterium nucleatum-induced epithelial interleukin-8 response through the nuclear factor-kappa B pathway.
    Author: Zhang G, Chen R, Rudney JD.
    Journal: J Periodontal Res; 2011 Oct; 46(5):558-67. PubMed ID: 21521225.
    Abstract:
    BACKGROUND AND OBJECTIVE: We previously reported that the interleukin-8 (IL-8) response to Fusobacterum nucleatum was attenuated in the presence of Streptococcus cristatus. Here, we further examined the underlying mechanism(s) involved in the modulating effect of S. cristatus by looking specifically at its impact on the nuclear factor-kappa B (NF-κB) pathway under the toll-like receptor (TLR) signaling background. MATERIAL AND METHODS: OKF6/TERT-2 and KB cells were co-cultured with F. nucleatum and S. cristatus, either alone or in combination. Secretion of IL-8 protein was measured by ELISA. The nuclear translocation of NF-κB was evaluated by confocal microscopy, while DNA-binding activity was quantified using TransAM™ ELISA kits. Western blot analysis was performed to determine whether the anti-inflammatory effect of S. cristatus is related to the modulation of the NF-κB inhibitory protein IκB-α. RESULTS: Incubation with F. nucleatum significantly enhanced the nuclear translocation of NF-κB. Exposure to S. cristatus alone did not cause detectable NF-κB translocation and was able to inhibit the F. nucleatum-induced NF-κB nuclear translocation. The TransAM assay further confirmed that S. cristatus blocked the nuclear translocation of NF-κB in response to F. nucleatum stimulation. In contrast to the nearly complete degradation of IκB-α induced by F. nucleatum alone, the presence of S. cristatus stabilized IκB-α. Pre-incubation with TLR2 and TLR4 antibodies, however, did not affect the epithelial response to either species alone or in combination. CONCLUSION: The mechanism by which S. cristatus attenuates F. nucleatum-induced proinflammatory responses in oral epithelial cells appears to involve blockade of NF-κB nuclear translocation at the level of IκB-α degradation.
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