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Published on: March 18, 2019
Enterococcus faecalis immunoregulates osteoclastogenesis of macrophages
Zhezhen Xu1, Zhongchun Tong1, Prasanna Neelakantan2
1Department of Operative Dentistry and Endodontics, Guanghua School of Stomatology, Hospital of Stomatology, Sun Yat-sen University, 56 Lingyuan Xi Road, Guangzhou 510055, Guangdong, China; Guangdong Province Key Laboratory of Stomatology, No. 74, 2nd Zhongshan Road, Guangzhou 510080, Guangdong, China.
Enterococcus faecalis infection does not kill cells but activates their immune functions. This bacterium surprisingly inhibits osteoclast differentiation, potentially impacting persistent apical periodontitis.
Area of Science:
- Oral biology
- Immunology
- Microbiology
Background:
- Persistent apical periodontitis (PAP) involves inflammation and bone loss.
- Enterococcus faecalis is a suspected cause of PAP, but mechanisms are unclear.
Purpose of the Study:
- Investigate E. faecalis 's effect on macrophage-like RAW264.7 cells.
- Examine its role in cell proliferation, inflammation, and osteoclast differentiation.
Main Methods:
- In vitro infection model using RAW264.7 cells and E. faecalis.
- Cell viability assays, electron microscopy, confocal microscopy, flow cytometry.
- Quantitative real-time PCR for gene expression analysis.
Main Results:
- E. faecalis infection did not cause cytotoxicity or apoptosis in RAW264.7 cells.
- Infection enhanced phagocytosis and inflammatory cytokine expression.
- Osteoclast differentiation and marker gene expression were significantly reduced.
Conclusions:
- E. faecalis activates macrophages but attenuates their differentiation into osteoclasts.
- This suggests a complex role in PAP pathogenesis beyond direct bone destruction.
