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Aim: Gram-negative anaerobic periodontal pathogens are well known for their ability to stimulate innate immune response once being recognized by special receptors of epithelial pocket lining. The aim of this study was to investigate the expression of toll-like receptor 4 (TLR4) and nuclear factor kappa-lightchain-enhancer of activated B cells (NF-κB) following exposure to Fusobacterium nucleatum. Materials and methods: Primary oral keratinocytes were collected from gingiva of Wistar Han rat and cultured to confluency. Then, the epithelial cells were stimulated with heat-killed F. nucleatum and 20 μg/mL Escherichia coli lipopolysaccharide (E. coli LPS). Expression of NF-κB was assayed by immunocytochemistry in addition to semi-quantitative reverse transcriptase (RT)-polymerase chain reaction (PCR), which was also used to determine transcription of TLR4 in comparison with unstimulated control. Results: Immunocytochemical analysis indicated that nuclear translocation of NF-κB was significantly increased (p < 0.05) in cultures stimulated with bacteria as compared with control. In addition, the expression of TLR4 and NF-κB in stimulated keratinocytes was also significantly increased (p < 0.05) 3and 2.5-fold respectively, in comparison with unstimulated cultures. Conclusion: Fusobacterium nucleatum potentially triggers NF-κB signaling pathway through activation of TLR4 in oral epithelial cells. Clinical significance: Recognition of early immune response against pathogenic periodontal bacteria would highlight new aspects in pathogenesis of periodontal diseases that could provide potential therapeutic opportunity for these conditions.

world journal of dentistry

Differential Expression of Toll-like Receptor 4 and Nuclear Factor κB of Primary Rat Oral Keratinocytes in Response to Stimulation with<i>Fusobacterium nucleatum</i>

Differential Expression of Toll-like Receptor 4 and Nuclear Factor κB of Primary Rat Oral Keratinocytes in Response to Stimulation withFusobacterium nucleatum