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Inhibition of Enterococcus faecalis Growth and Biofilm Formation by Molecule Targeting Cyclic di-AMP Synthetase

Lulu Chen1, Xin Li2, Xuedong Zhou3

  • 1State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, PR China; Department of Pediatric Dentistry, West China Hospital of Stomatology, Sichuan University, Chengdu, PR China.

Journal of Endodontics
|July 29, 2018
PubMed
Abstract

Insights

The small molecule ST056083 inhibits Enterococcus faecalis DNA integrity scanning protein (DisA) activity. This inhibition reduces bacterial growth, biofilm formation, and exopolysaccharide synthesis, offering potential therapeutic strategies.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Drug Discovery

Background:

  • Enterococcus faecalis is a key pathogen in oral diseases and endodontic treatment failures due to its robust biofilm formation.
  • Cyclic di-AMP (c-di-AMP) is a vital second messenger regulating essential cellular processes, including biofilm development in bacteria.
  • ST056083 is identified as a small molecule inhibitor targeting the c-di-AMP synthetase, DNA integrity scanning protein (DisA), in vitro.

Purpose of the Study:

  • To investigate the inhibitory effects of ST056083 on E. faecalis DisA activity.
  • To assess the impact of ST056083 on E. faecalis bacterial growth and biofilm formation.
  • To elucidate the mechanism by which ST056083 affects bacterial physiology.

Main Methods:

  • In vitro expression and purification of E. faecalis DisA.
  • Evaluation of ST056083's inhibitory effect on DisA activity using biochemical assays.
  • Assessment of bacterial growth, biofilm quantification, exopolysaccharide synthesis, and microscopic analysis (SEM, 3D confocal microscopy).

Main Results:

  • ST056083 effectively inhibits the biological activity of purified E. faecalis DisA.
  • The compound significantly reduces E. faecalis growth and biofilm formation.
  • ST056083 treatment leads to decreased exopolysaccharide synthesis in E. faecalis.

Conclusions:

  • The study confirms ST056083 as an inhibitor of E. faecalis DisA, impacting bacterial growth and virulence.
  • Findings contribute to understanding the role of c-di-AMP signaling in E. faecalis physiology.
  • This research provides a foundation for developing ST056083 as a potential therapeutic agent against E. faecalis infections.
Keywords:
BiofilmEnterococcus faecalisST056083cyclic di-AMP

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