Camille N Banson
| Camille N Banson |
Camille N Banson,Xia Xia-Juan, Min Jiang, Erin C Mooney
Sinem E Sahingur
Periodontics, University of Pennsylvania, School of Dental Medicine
Introduction
The interaction between host immune cells and the oral microbiome, and subsequent crosstalk between innate signaling pathways play a critical role in determining periodontal disease outcome. Macrophages are one of the key cells responding to microbial insult in periodontitis pathogenesis. Quercetin, a plant-derived polyphenolic flavonoid, has been linked with health benefits in both humans and animals. We sought to determine the effect of Quercetin on TLR signaling, cytokine responses and NF-κB activity in human macrophages challenged with periodontal bacteria and TLR agonists.
Methods
The human monocytic leukemia cell line (THP-1; ATCC TiB-202) were treated with Quercetin (5µg/mL) for 2 hours prior to challenge with bacteria, P.gingivalis, and F.nucleatum and toll-like receptor agonists. The cells and supernatants were collected at predetermined time points to determine cytokine production and nuclear translocation of NF-κB using enzyme-linked immunoabsorbent assay and immunoflurosence staining and confocal imaging, respectively. Statistical analyses included analyses of variance with Tukey multiple comparisons and the p value was set <0.05.
Results
Quercetin treatment significantly reduced TNF and IL-6 production in human macrophages following challenge with bacteria and TLR agonists compared to the control cells treated with vehicle. Further analyses using immunofluorescence and confocal imaging revealed that Quercetin exerts its effect on inflammation through decreasing NF-κB nuclear translocation. Consistent with the proven clinical safety profile, Quercetin showed no effect on cell viability or structure.
Conclusion
Taken together, these data indicate that Quercetin regulates oral bacteria-induced inflammatory cytokine response through its effect on NF-κB signaling pathway.