Enterococcus faecalis Inhibits Osteoblast Differentiation and Induces Chemokine Expression

Park, Ok-Jin; Kim, Jiseon; Yang, Jihyun; Yun, Cheol‐Heui; Han, Seung Hyun

doi:10.1016/j.joen.2015.04.025

Cited by 20 publications

(14 citation statements)

References 33 publications

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“…E. faecalis ATCC 29212 used in the present work was the standard strain chosen in many associated studies concerning the pathogenesis of refractory or persistent apical periodontitis (Park et al . 2015, Wang et al . 2016, Chow et al .…”

Section: Discussionmentioning

confidence: 99%

Enterococcus faecalis induces necroptosis in human osteoblastic MG63 cells through the RIPK3 / MLKL signalling pathway

et al. 2020

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AimTo explore the activation of necroptosis triggered by Enterococcus faecalis in human osteoblastic MG63 cells and provide new insights into the pathogenesis of refractory apical periodontitis.MethodologyThe viability of MG63 cells exposed to live E. faecalis was investigated using the cell counting kit‐8 assay. The relative expressions of specific markers for necroptosis, namely p‐RIPK3 and p‐MLKL, were determined by western blotting. Cells pretreated with necrosulfonamide and GSK’872, which are specific inhibitors for MLKL and RIPK3, respectively, were then subjected to lactate dehydrogenase (LDH) cytotoxicity assay, flow cytometry analysis and Hoechst 33342/PI double fluorescence staining. Lentiviral‐delivered short hairpin RNA (shRNA) targeting MLKL was employed to further confirm the activation of necroptosis in MG63 cells infected with E. faecalis. Transmission electron microscopy was additionally used to observe the morphological characteristics. Statistical analysis was conducted using Student’s t‐tests or one‐way ANOVA followed by the Student–Newman–Keuls test.ResultsThe infection with E. faecalis significantly inhibited the viability of MG63 cells in a multiplicity of infection‐ and infection time‐dependent manners (P < 0.05). In line with this, the expression levels of necroptosis‐related markers, p‐RIPK3 and p‐MLKL, were significantly increased postinfection (P < 0.05). Significant reductions in death rate were detected in the case of E. faecalis‐infected MG63 cells following pretreatment with the inhibitors of RIPK3 and MLKL (P < 0.01). Furthermore, silencing of MLKL by shRNA significantly decreased LDH release (P < 0.01) and resulted in less mitochondrial swelling and vacuole‐like changes, as well as reduced endoplasmic reticulum expansion.ConclusionsEnterococcus faecalis infection‐induced necroptosis of MG63 cells via the RIPK3/MLKL signalling pathway, which may exert a negative influence on the healing process of refractory apical periodontitis. This study may offer novel insights into the pathogenesis and potential therapeutic targets of refractory apical periodontitis.

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Section: Discussionmentioning

confidence: 99%

Enterococcus faecalis induces necroptosis in human osteoblastic MG63 cells through the RIPK3 / MLKL signalling pathway

et al. 2020

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“…Heat-killed Enterococcus faecalis can inhibit osteoblast mineralization and decrease the expression of Runx2, osterix, Ocn, and Col-1 ( Park et al, 2015 ). P. gingivalis can dose-dependently invade osteoblasts and inhibit their differentiation and mineralization by inhibiting the expression of Cbfa-1 and osterix ( Zhang et al, 2010 ).…”

Section: Discussionmentioning

confidence: 99%

The Pathogenic Effects of Fusobacterium nucleatum on the Proliferation, Osteogenic Differentiation, and Transcriptome of Osteoblasts

Gao

Sun

Yang

et al. 2020

Front. Cell Dev. Biol.

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As one of the most common oral diseases, periodontitis is closely correlated with tooth loss in middle-aged and elderly people. Fusobacterium nucleatum ( F. nucleatum ) contributes to periodontitis, but the evidence in alveolar bone loss is still unclear. In this study, cytological experiments and transcriptome analyses were performed to characterize the biological process abnormalities and the molecular changes of F. nucleatum -stimulated osteoblasts. F. nucleatum could inhibit cell proliferation, promote cell apoptosis, and elevate pro-inflammatory cytokine production of osteoblasts, and it also inhibited osteoblast differentiation and mineralized nodule formation and decreased the expression of osteogenetic genes and proteins. Whole-transcriptome analyses identified a total of 235 transcripts that were differentially expressed in all six time points, most of which were inflammation-related genes. The genes, Ccl2 , Ccl20 , Csf1 , Cx3cl1 , Cxcl1 , Cxcl3 , Il6 , Birc3 , Map3k8 , Nos2 , Nfkb2 , Tnfrsf1b , and Vcam1 , played core roles in a PPI network, and interacted closely with other ones in the infection. In addition, 133 osteogenesis-related differential expression genes (DEGs) were time-serially dynamically changed in a short time-series expression miner (STEM) analysis, which were enriched in multiple cancer-related pathways. The core dynamic DEGs ( Mnda , Cyp1b1 , Comp , Phex , Mmp3 , Tnfrsf1b , Fbln5 , and Nfkb2 ) had been reported to be closely related to the development and metastasis in tumor and cancer progress. This study is the first to evaluate the long-term interaction of F. nucleatum on osteoblasts, which might increase the risk of cell carcinogenesis of normal osteoblasts, and provides new insight into the pathogenesis of bacterial-induced bone destruction.

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“…sehingga osteoklas yang dihasilkan tinggi dan kerusakan tulang pun menjadi lebih besar. 12,13 Hasil penelitian ekspresi NFATc-1 dan osteokalsin ini menunjukkan bahwa bakteri E.faecalis menyebabkan kerusakan pada tulang periapikal gigi, hal ini sesuai dengan penelitian Wang et al, (2015) yang menyebutkan bahwa E.faecalis berkontribusi pada resorpsi tulang dalam periodontitis apikalis melalui peningkatan osteoklastogenesis dengan menaikkan regulasi ekspresi dari marker spesifik osteoklas, salah satunya adalah NFATc-1. 14…”

Section: Hasil Dan Diskusiunclassified

EKSPRESI Nuclear Factor of Activated T cells c-1 (NFATc-1) DAN OSTEOKALSIN PADA KERUSAKAN TULANG PERIAPIKAL AKIBAT INDUKSI BAKTERI Enterococcus faecalis

Hadi

Roelianto

Subiyanto

et al. 2019

CDJ

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Background. The main etiology of endodontic treatment failure is caused by bacteries that stay in the root canal. E.faecalis is a bactery that is found as an etiology of endodontic treatment failure. Cell wall of this bacteria is containing Lipoteichoic acid (LTA). LTA can penetrate into the periradicular tissue, act as endotoxin in host and cause periradicular inflammation then lead to bone destruction. Bone destruction occurs due to the inflammation process that is mediated by immune system. The important cell in the process of bone destruction is osteoclast. Bone destruction is marked by the form of osteoclast that is called osteoclastogenesis. NFATc-1 and osteocalcin play important things in osteoclastogenesis. Purpose. The aim of this study is to know about the expression of NFATc-1 and osteocalcin during the periapical bone destruction due to induction of E.faecalis. Method. This study used laboratory experimental with the post test only control group design. A total of 54 male rats were randomly divided into 2 main groups, which each main group had 3 subgroups. Group A (control) : every tooth was induced only by sterile BHIb. Group A had 3 subgroups (A Control day 3, 10, and 21), group B : every tooth was induced by 10 μl BHI-b E.faecalis ATCC212(106 CFU), it was contained 3 sub groups (B day 3,10, and 21). The animals were sacrificed based on their days scheduled group and prepared for histological examination of periapical bone, then we did the immunohistochemistry followed by calculation on the light microscope. Result. The analysis revealed that the expression of NFATc-1 and osteoclast increased significantly in group B when E.faecalis was induced. Conclusion. From this study we know that the expression of NFATc-1 and osteocalcin are increasing during the periapical bone destruction that induced by E.faecalis.

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Enterococcus faecalis Inhibits Osteoblast Differentiation and Induces Chemokine Expression

Cited by 20 publications

References 33 publications

Enterococcus faecalis induces necroptosis in human osteoblastic MG63 cells through the RIPK3 / MLKL signalling pathway

Enterococcus faecalis induces necroptosis in human osteoblastic MG63 cells through the RIPK3 / MLKL signalling pathway

The Pathogenic Effects of Fusobacterium nucleatum on the Proliferation, Osteogenic Differentiation, and Transcriptome of Osteoblasts

EKSPRESI Nuclear Factor of Activated T cells c-1 (NFATc-1) DAN OSTEOKALSIN PADA KERUSAKAN TULANG PERIAPIKAL AKIBAT INDUKSI BAKTERI Enterococcus faecalis

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