4.7 Article

Apelin Enhances the Effects of Fusobacterium nucleatum on Periodontal Ligament Cells In Vitro

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Publisher

MDPI
DOI: 10.3390/ijms24054733

Keywords

apelin; APJ; periodontal ligament cells; Fusobacterium nucleatum; periodontitis; obesity

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This study aimed to investigate the effects of Fusobacterium nucleatum on periodontal ligament (PDL) cells, and the modulatory role of apelin, to better understand the relationship between periodontitis and obesity. F. nucleatum increased the expressions of COX2, CCL2, and MMP1 in a dose- and time-dependent manner. The combination of F. nucleatum and apelin resulted in the highest expression levels of various inflammatory and tissue turnover molecules. F. nucleatum downregulated the expression of apelin and its receptor APJ.
This study aimed to explore effects of Fusobacterium nucleatum with or without apelin on periodontal ligament (PDL) cells to better understand pathomechanistic links between periodontitis and obesity. First, the actions of F. nucleatum on COX2, CCL2, and MMP1 expressions were assessed. Subsequently, PDL cells were incubated with F. nucleatum in the presence and absence of apelin to study the modulatory effects of this adipokine on molecules related to inflammation and hard and soft tissue turnover. Regulation of apelin and its receptor (APJ) by F. nucleatum was also studied. F. nucleatum resulted in elevated COX2, CCL2, and MMP1 expressions in a dose- and time-dependent manner. Combination of F. nucleatum and apelin led to the highest (p < 0.05) expression levels of COX2, CCL2, CXCL8, TNF-alpha, and MMP1 at 48 h. The effects of F. nucleatum and/or apelin on CCL2 and MMP1 were MEK1/2- and partially NF-kappa B-dependent. The combined effects of F. nucleatum and apelin on CCL2 and MMP1 were also observed at protein level. Moreover, F. nucleatum downregulated (p < 0.05) the apelin and APJ expressions. In conclusion, obesity could contribute to periodontitis through apelin. The local production of apelin/APJ in PDL cells also suggests a role of these molecules in the pathogenesis of periodontitis.

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