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Enterococcus faecalis OG1RF induces apoptosis in MG63 cells via caspase-3/-8/-9 without activation of caspase-1/GSDMD

Yang Li1, Cheng Wen1, Jialin Zhong1

  • 1Department of Endodontics, Affiliated Stomatology Hospital of Guangzhou Medical University, Guangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative Medicine, Guangzhou, China.

Oral Diseases
|August 9, 2021
PubMed
Abstract

Insights

Enterococcus faecalis OG1RF triggers apoptosis in osteoblast cells through caspase activation but does not induce pyroptosis. This finding is crucial for understanding persistent apical periodontitis.

Area of Science:

  • Cell Biology
  • Microbiology
  • Immunology

Background:

  • Regulated cell death is critical in persistent apical periodontitis pathogenesis.
  • Understanding cell death mechanisms in osteoblast-like cells during Enterococcus faecalis infection is essential.

Purpose of the Study:

  • To investigate the mechanisms of regulated cell death in MG63 cells infected with Enterococcus faecalis OG1RF.
  • To elucidate the roles of apoptosis and pyroptosis pathways.

Main Methods:

  • MG63 cells were infected with E. faecalis OG1RF.
  • Evaluated cell death using flow cytometry, TUNEL assay, and LDH release.
  • Measured caspase activity, IL-1β release, and protein expression (apoptosis-associated proteins, Gasdermin D).

Main Results:

  • E. faecalis OG1RF reduced mitochondrial membrane potential and increased apoptosis and LDH release.
  • Upregulated expression of caspase-3 and survivin, and activity of caspase-3/-8/-9.
  • Downregulated death receptor 6; caspase-1/Gasdermin D activity and IL-1β release were unaltered.

Conclusions:

  • E. faecalis OG1RF induces intrinsic and extrinsic apoptosis in MG63 cells via caspase-3/-8/-9 activation.
  • The pyroptotic pathway regulated by caspase-1/Gasdermin D was not activated.
Keywords:
Enterococcus faecalisapical periodontitisapoptosisosteoblastpyroptosis

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