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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 mRNA expression of fimA, hagA, and hagB (Panel A), and rgpA, rgpB, and kgp (Panel B) genes in P. gingivalis ATCC 33277.Bacteria were incubated (8 h; anaerobic condition) in the presence of myricetin (50 and 100 μg/ml). Data are expressed as means ± standard deviations. The expression was normalized to 16S rRNA. *, significantly different (P < 0.01) compared to untreated control.
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pone.0131758.g002: Effect of myricetin on mRNA expression of fimA, hagA, and hagB (Panel A), and rgpA, rgpB, and kgp (Panel B) genes in P. gingivalis ATCC 33277.Bacteria were incubated (8 h; anaerobic condition) in the presence of myricetin (50 and 100 μg/ml). Data are expressed as means ± standard deviations. The expression was normalized to 16S rRNA. *, significantly different (P < 0.01) compared to untreated control.

Mentions: We then investigated the effect of myricetin on the expression of several virulence factor genes by P. gingivalis, relative to the expression of 16S rRNA. With this purpose, an early exponential growth phase culture of P. gingivalis (ATCC 33277) was exposed for 8 h under anaerobic conditions to myricetin at two sub-MICs (50 and 100 μg/ml) prior to monitoring mRNA expression by quantitative RT-PCR. Fig 2A reports the data for three genes (fimA, hagA, hagB) involved in bacterial colonization. A significant (at P < 0.01) decrease in the expression of all genes was observed following exposure of P. gingivalis to myricetin at a concentration of 100 μg/ml, while at 50 μg/ml, only fimA and hagB were significantly decreased. More specifically, myricetin at 100 μg/ml caused a decrease of 81, 93, and 64% for fimA, hagA, and hagB, respectively. When exposed to myricetin, the expression of rgpA, rgpB, and kgp, three cysteine protease genes related to inactivation of host defense mechanisms, tissue destruction, and nutrient acquisition, was also significantly down-regulated. At 100 μg/ml, the expression of rgpA, rgpB, and kgp decreased by 68, 49, and 96%, respectively (Fig 2B).


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 mRNA expression of fimA, hagA, and hagB (Panel A), and rgpA, rgpB, and kgp (Panel B) genes in P. gingivalis ATCC 33277.Bacteria were incubated (8 h; anaerobic condition) in the presence of myricetin (50 and 100 μg/ml). Data are expressed as means ± standard deviations. The expression was normalized to 16S rRNA. *, significantly different (P < 0.01) compared to untreated control.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0131758.g002: Effect of myricetin on mRNA expression of fimA, hagA, and hagB (Panel A), and rgpA, rgpB, and kgp (Panel B) genes in P. gingivalis ATCC 33277.Bacteria were incubated (8 h; anaerobic condition) in the presence of myricetin (50 and 100 μg/ml). Data are expressed as means ± standard deviations. The expression was normalized to 16S rRNA. *, significantly different (P < 0.01) compared to untreated control.
Mentions: We then investigated the effect of myricetin on the expression of several virulence factor genes by P. gingivalis, relative to the expression of 16S rRNA. With this purpose, an early exponential growth phase culture of P. gingivalis (ATCC 33277) was exposed for 8 h under anaerobic conditions to myricetin at two sub-MICs (50 and 100 μg/ml) prior to monitoring mRNA expression by quantitative RT-PCR. Fig 2A reports the data for three genes (fimA, hagA, hagB) involved in bacterial colonization. A significant (at P < 0.01) decrease in the expression of all genes was observed following exposure of P. gingivalis to myricetin at a concentration of 100 μg/ml, while at 50 μg/ml, only fimA and hagB were significantly decreased. More specifically, myricetin at 100 μg/ml caused a decrease of 81, 93, and 64% for fimA, hagA, and hagB, respectively. When exposed to myricetin, the expression of rgpA, rgpB, and kgp, three cysteine protease genes related to inactivation of host defense mechanisms, tissue destruction, and nutrient acquisition, was also significantly down-regulated. At 100 μg/ml, the expression of rgpA, rgpB, and kgp decreased by 68, 49, and 96%, respectively (Fig 2B).

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