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Dual Action of Myricetin on Porphyromonas gingivalis and the Inflammatory Response of Host Cells: A Promising Therapeutic Molecule for Periodontal Diseases.

Grenier D, Chen H, Ben Lagha A, Fournier-Larente J, Morin MP - PLoS ONE (2015)

Bottom Line: Myricetin was found to attenuate the virulence of P. gingivalis by reducing the expression of genes coding for important virulence factors, including proteinases (rgpA, rgpB, and kgp) and adhesins (fimA, hagA, and hagB).In conclusion, our study brought clear evidence that the flavonol myricetin exhibits a dual action on the periodontopathogenic bacterium P. gingivalis and the inflammatory response of host cells.Therefore, myricetin holds promise as a therapeutic agent for the treatment/prevention of periodontitis.

View Article: PubMed Central - PubMed

Affiliation: Oral Ecology Research Group, Faculty of Dentistry, Université Laval, Quebec City, Quebec, Canada.

ABSTRACT
Periodontitis that affects the underlying structures of the periodontium, including the alveolar bone, is a multifactorial disease, whose etiology involves interactions between specific bacterial species of the subgingival biofilm and the host immune components. In the present study, we investigated the effects of myricetin, a flavonol largely distributed in fruits and vegetables, on growth and virulence properties of Porphyromonas gingivalis as well as on the P. gingivalis-induced inflammatory response in host cells. Minimal inhibitory concentration values of myricetin against P. gingivalis were in the range of 62.5 to 125 μg/ml. The iron-chelating activity of myricetin may contribute to the antibacterial activity of this flavonol. Myricetin was found to attenuate the virulence of P. gingivalis by reducing the expression of genes coding for important virulence factors, including proteinases (rgpA, rgpB, and kgp) and adhesins (fimA, hagA, and hagB). Myricetin dose-dependently prevented NF-κB activation in a monocyte model. Moreover, it inhibited the secretion of IL-6, IL-8 and MMP-3 by P. gingivalis-stimulated gingival fibroblasts. In conclusion, our study brought clear evidence that the flavonol myricetin exhibits a dual action on the periodontopathogenic bacterium P. gingivalis and the inflammatory response of host cells. Therefore, myricetin holds promise as a therapeutic agent for the treatment/prevention of periodontitis.

No MeSH data available.


Related in: MedlinePlus

Effect of myricetin on P. gingivalis-induced NF-κB activation using the U937-3xκB-LUC cell line model.Cells were treated for 30 min with myricetin prior to stimulation with P. gingivalis (ATCC 33277) at MOI of 100. A value of 100% was assigned to NF-κB activation induced by P. gingivalis. The commercial inhibitor BAY-11-7082 was used as positive inhibitory control. *, significant decrease at P < 0.05 compared to P. gingivalis-stimulated monocytes not treated with myricetin.
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pone.0131758.g003: Effect of myricetin on P. gingivalis-induced NF-κB activation using the U937-3xκB-LUC cell line model.Cells were treated for 30 min with myricetin prior to stimulation with P. gingivalis (ATCC 33277) at MOI of 100. A value of 100% was assigned to NF-κB activation induced by P. gingivalis. The commercial inhibitor BAY-11-7082 was used as positive inhibitory control. *, significant decrease at P < 0.05 compared to P. gingivalis-stimulated monocytes not treated with myricetin.

Mentions: To investigate the anti-inflammatory properties of myricetin, the U937-3xκB-LUC cell line transfected with a luciferase reporter gene was used to determine the effect of this flavonol on P. gingivalis-mediated activation of the NF-κB signaling pathway. Fig 3 shows that P. gingivalis induced NF-κB activation, while the commercial inhibitor (BAY-11-7082) completely prevented this activation. Myricetin dose-dependently inhibited the P. gingivalis-induced NF-κB activation. More specifically, myricetin at 16 and 32 μg/ml significantly decreased the NF-κB activation by 15.9% and 38.2%, respectively.


Dual Action of Myricetin on Porphyromonas gingivalis and the Inflammatory Response of Host Cells: A Promising Therapeutic Molecule for Periodontal Diseases.

Grenier D, Chen H, Ben Lagha A, Fournier-Larente J, Morin MP - PLoS ONE (2015)

Effect of myricetin on P. gingivalis-induced NF-κB activation using the U937-3xκB-LUC cell line model.Cells were treated for 30 min with myricetin prior to stimulation with P. gingivalis (ATCC 33277) at MOI of 100. A value of 100% was assigned to NF-κB activation induced by P. gingivalis. The commercial inhibitor BAY-11-7082 was used as positive inhibitory control. *, significant decrease at P < 0.05 compared to P. gingivalis-stimulated monocytes not treated with myricetin.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4487256&req=5

pone.0131758.g003: Effect of myricetin on P. gingivalis-induced NF-κB activation using the U937-3xκB-LUC cell line model.Cells were treated for 30 min with myricetin prior to stimulation with P. gingivalis (ATCC 33277) at MOI of 100. A value of 100% was assigned to NF-κB activation induced by P. gingivalis. The commercial inhibitor BAY-11-7082 was used as positive inhibitory control. *, significant decrease at P < 0.05 compared to P. gingivalis-stimulated monocytes not treated with myricetin.
Mentions: To investigate the anti-inflammatory properties of myricetin, the U937-3xκB-LUC cell line transfected with a luciferase reporter gene was used to determine the effect of this flavonol on P. gingivalis-mediated activation of the NF-κB signaling pathway. Fig 3 shows that P. gingivalis induced NF-κB activation, while the commercial inhibitor (BAY-11-7082) completely prevented this activation. Myricetin dose-dependently inhibited the P. gingivalis-induced NF-κB activation. More specifically, myricetin at 16 and 32 μg/ml significantly decreased the NF-κB activation by 15.9% and 38.2%, respectively.

Bottom Line: Myricetin was found to attenuate the virulence of P. gingivalis by reducing the expression of genes coding for important virulence factors, including proteinases (rgpA, rgpB, and kgp) and adhesins (fimA, hagA, and hagB).In conclusion, our study brought clear evidence that the flavonol myricetin exhibits a dual action on the periodontopathogenic bacterium P. gingivalis and the inflammatory response of host cells.Therefore, myricetin holds promise as a therapeutic agent for the treatment/prevention of periodontitis.

View Article: PubMed Central - PubMed

Affiliation: Oral Ecology Research Group, Faculty of Dentistry, Université Laval, Quebec City, Quebec, Canada.

ABSTRACT
Periodontitis that affects the underlying structures of the periodontium, including the alveolar bone, is a multifactorial disease, whose etiology involves interactions between specific bacterial species of the subgingival biofilm and the host immune components. In the present study, we investigated the effects of myricetin, a flavonol largely distributed in fruits and vegetables, on growth and virulence properties of Porphyromonas gingivalis as well as on the P. gingivalis-induced inflammatory response in host cells. Minimal inhibitory concentration values of myricetin against P. gingivalis were in the range of 62.5 to 125 μg/ml. The iron-chelating activity of myricetin may contribute to the antibacterial activity of this flavonol. Myricetin was found to attenuate the virulence of P. gingivalis by reducing the expression of genes coding for important virulence factors, including proteinases (rgpA, rgpB, and kgp) and adhesins (fimA, hagA, and hagB). Myricetin dose-dependently prevented NF-κB activation in a monocyte model. Moreover, it inhibited the secretion of IL-6, IL-8 and MMP-3 by P. gingivalis-stimulated gingival fibroblasts. In conclusion, our study brought clear evidence that the flavonol myricetin exhibits a dual action on the periodontopathogenic bacterium P. gingivalis and the inflammatory response of host cells. Therefore, myricetin holds promise as a therapeutic agent for the treatment/prevention of periodontitis.

No MeSH data available.


Related in: MedlinePlus