Enterococcus faecalis Extracellular Vesicles Promote Apical Periodontitis

Area of Science:

• Microbiology
• Immunology
• Oral Pathology

Background:

• Enterococcus faecalis is a key pathogen in chronic apical periodontitis.
• The precise mechanisms of E. faecalis-induced periapical tissue damage remain incompletely understood.
• Bacterial extracellular vesicles (EVs) are emerging as critical mediators of microbial pathogenesis.

Purpose of the Study:

• To investigate the role of E. faecalis-derived EVs in the pathogenesis of apical periodontitis.
• To elucidate the underlying molecular mechanisms by which E. faecalis EVs influence host immune responses.
• To explore the potential of EVs as virulence factors of E. faecalis.

Main Methods:

• Induction of apical periodontitis in mice using E. faecalis EVs.
• Assessment of periapical bone destruction and macrophage infiltration via immunofluorescence.
• In vitro studies on macrophage polarization and EV internalization.
• Mechanistic investigation involving NOD2 and RIPK2 signaling pathways.

Main Results:

• E. faecalis EVs induced significant inflammatory bone destruction in periapical lesions.
• EVs promoted M1 macrophage polarization and infiltration into apical lesions.
• Macrophage M1 polarization was mediated by the NOD2/RIPK2 signaling pathway.
• NOD2 expression and RIPK2 ubiquitination were upregulated by E. faecalis EVs.

Conclusions:

• E. faecalis EVs act as virulence factors contributing to apical periodontitis.
• EVs promote M1 macrophage polarization through the NOD2/RIPK2 signaling cascade.
• This study provides novel insights into the pathogenesis of apical periodontitis driven by bacterial EVs.