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Oral commensal bacteria differentially modulate epithelial cell death.

Tyresia White1, Yelena Alimova2, Vanessa Tubero Euzebio Alves2

  • 1Division of Periodontics, College of Dentistry, University of Kentucky, 800 Rose St, Lexington, KY, 40536-7001, United States.

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|October 23, 2020
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Summary

Oral commensal bacteria, Streptococcus gordonii and Streptococcus sanguinis, induce oral epithelial cell (OEC) death, unlike pathogens. This suggests a role for OEC death in managing bacterial colonization and preventing inflammation.

Keywords:
ApoptosisOral commensal bacteriaOral epithelial cellsOral pathogenic bacteriaPyroptosis

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Area of Science:

  • Oral microbiology
  • Immunology
  • Cell biology

Background:

  • Epithelial cell death is a key innate defense mechanism at mucosal surfaces.
  • Cell death eliminates pathogens and regulates immune responses.
  • Oral epithelial cells (OECs) are the first line of defense in the oral cavity.

Purpose of the Study:

  • To investigate the differential effects of oral commensal and pathogenic bacteria on OEC death.
  • To test the hypothesis that OEC death is modulated differently by various oral bacteria.

Main Methods:

  • Assessed OEC death induced by specific oral bacteria (commensals: Sg, Ss, Vp; pathogens: Pg, Tf, Fn).
  • Utilized flow cytometry for apoptosis and necrosis detection (Annexin-V/PI staining).
  • Measured caspase-3/7 (apoptosis) and caspase-1 (pyroptosis) activities, and IL-1β/IL-8 protein levels.

Main Results:

  • Commensals Streptococcus gordonii (Sg) and Streptococcus sanguinis (Ss) significantly increased OEC apoptosis and necrosis.
  • Pathogen Porphyromonas gingivalis (Pg) induced lower levels of apoptosis; Veillonella parvula (Vp), Tannerella forsythia (Tf), and Fusobacterium nucleatum (Fn) had minimal impact.
  • Sg, Ss, and Pg activated caspase-3/7; Ss uniquely elevated caspase-1 activity and IL-1β levels.

Conclusions:

  • Oral commensal and pathogenic bacteria differentially induce OEC death pathways.
  • Sg and Ss exhibit stronger pro-apoptotic and pro-pyroptotic effects compared to tested pathogens.
  • Commensal-induced OEC death may be a physiological process to control bacterial load, and its dysbiosis may increase inflammation risk.