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Enterococcus faecalis Extracellular Vesicles Promote Apical Periodontitis.

R Y Ma1, Z L Deng1, Q Y Du1

  • 1Department of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Journal of Dental Research
|April 28, 2024
PubMed
Summary
This summary is machine-generated.

Enterococcus faecalis extracellular vesicles (EVs) drive apical periodontitis by promoting M1 macrophage polarization via NOD2/RIPK2 signaling. This study reveals bacterial EVs as virulence factors, clarifying their role in periapical tissue destruction.

Keywords:
NOD2RIPK2extracellular vesiclemacrophagepattern recognition receptorsubiquitination

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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.