Fsr quorum sensing system modulates the temporal development of Enterococcus faecalis biofilm matrix

• Published in: Molecular oral microbiology Vol. 37; no. 1; pp. 22 - 30
• Main Authors: Ali, Islam A. A., Lévesque, Celine M., Neelakantan, Prasanna
• Format: Journal Article
• Language: English
• Published: Denmark Wiley Subscription Services, Inc 01-02-2022
• Subjects: Antimicrobial resistance; bacteria; Bacterial Proteins - genetics; Bacterial Proteins - metabolism; Biofilms; Cell interactions; Chemical communication; Deactivation; Dental roots; Dentistry; Deposition; Enterococcus faecalis; Enterococcus faecalis - genetics; extracellular polymeric substance; Extracellular Polymeric Substance Matrix - metabolism; Gelatinase; gelatinases; Gelatinases - genetics; Gelatinases - metabolism; Gene Expression Regulation, Bacterial; Heart valves; Hospitals; Inactivation; Mutants; Nosocomial infection; Nucleic acids; Polysaccharides; Proteins; Quorum Sensing; Resistance factors; Root canals; Saccharides; Virulence; Virulence factors; polysaccharides; extracellular polymeric substance; bacteria; gelatinases; virulence factors
• ISSN: 2041-1006; 2041-1014
• DOI: 10.1111/omi.12357

Quorum sensing (QS) is a cell‐to‐cell communication process that regulates major pathogenic attributes in bacteria including biofilm formation, secretion of virulence factors, and antimicrobial resistance. The two‐component Fsr–QS system of the nosocomial pathogen Enterococcus faecalis controls the production of extracellular gelatinase that contributes to biofilm development by enhancing the release of nucleic acids into the biofilm matrix. However, the contribution of this system to the deposition of other biofilm matrix components such as polysaccharides and proteins remains unknown. Using wild type and mutant strains, we discovered that biofilm formation was attenuated by inactivation of the Fsr system or its downstream gelatinase production. Inactivation of the Fsr system caused a modest, yet significant reduction in biofilm metabolic activity without affecting cell counts. Inactivation of the QS‐signal sensor FsrC and response regulator FsrA resulted in decreased extracellular polysaccharides and proteins in biofilms in a temporal manner. Irrespective of biofilm age, eDNA levels were reduced in the gelatinase mutant strain. Our results collectively suggest that the Fsr system contributes to the temporal deposition of polysaccharides and proteins into the extracellular polymeric matrix (EPS) of E. faecalis biofilm, without affecting bacterial viability. This understanding of the role of the Fsr–QS system in biofilm development may reveal a novel target to develop effective antibiofilm agents to tackle E. faecalis‐mediated infections such as in dental root canals, heart valves, and surgical sites.