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

Author(s):  
Islam A. A. Ali ◽  
Celine M. Lévesque ◽  
Prasanna Neelakantan
2021 ◽  
Author(s):  
Jinglin Yue ◽  
Pengcheng Du ◽  
Mingxi Hua ◽  
Xinzhe Liu ◽  
Ang Duan ◽  
...  

Abstract Enterococcus faecalis, a major nosocomial pathogen, has become a top leading cause of hospital-acquired infections including urinary tract infections, endocarditis and bacteremia. It is important to study the epidemiology and virulence characteristics of E. faecalis isolates in order to tailor infection prevention and antibiotic prescribing. In this study, comparative genomic analysis was conducted on 537 isolates from different human origins. The isolates from bloodstream and intra-abdominal lining had the largest and smallest average genome size respectively, while the isolates from open natural orifices (gastrointestinal tract, urinary tract, respiratory tract, wound and eye) had medium average genome size. The phylogenetic relationships were expounded that the strain isolation niche is uncorrelated with strain phylogeny. Six clonal complexes generally appeared in different isolation sources. Furthermore, genomic analysis revealed differences at the accessory genome, the functions of different genes mainly pointed to the virulence, drug resistance and metabolism of E. faecalis. Interestingly, fsr quorum sensing system genes affecting biofilm formation had a highest proportion in the blood-derived strains. This study showed the genomic characteristics of different human origins and suggested that fsr quorum-sensing system maybe a contributing factor of bacteremia due to E. faecalis infection.


2002 ◽  
Vol 70 (8) ◽  
pp. 4678-4681 ◽  
Author(s):  
Eleftherios Mylonakis ◽  
Michael Engelbert ◽  
Xiang Qin ◽  
Costi D. Sifri ◽  
Barbara E. Murray ◽  
...  

ABSTRACT We used a rabbit endophthalmitis model to explore the role of fsrB, a gene required for the function of the fsr quorum-sensing system of Enterococcus faecalis, in pathogenicity. A nonpolar deletion mutant of fsrB had significantly reduced virulence compared to wild type. Complementation of mutation restored virulence. These data corroborate the role of fsrB in E. faecalis pathogenesis and suggest that the rabbit endophthalmitis model can be used to study the in vivo role of quorum sensing.


2002 ◽  
Vol 68 (6) ◽  
pp. 3152-3155 ◽  
Author(s):  
Jiro Nakayama ◽  
Reiko Kariyama ◽  
Hiromi Kumon

ABSTRACT Expression of virulence-related extracellular proteases, gelatinase, and serine protease of Enterococcus faecalis is regulated by a quorum-sensing system encoded by the fsr gene cluster. In this study, a 23.9-kb chromosomal deletion containing the fsr gene cluster region was found to be present in the majority (79%) of gelatinase-negative clinical isolates of E. faecalis from urine.


2006 ◽  
Vol 188 (23) ◽  
pp. 8321-8326 ◽  
Author(s):  
Jiro Nakayama ◽  
Shengmin Chen ◽  
Nozomi Oyama ◽  
Kenzo Nishiguchi ◽  
Essam A. Azab ◽  
...  

ABSTRACT Gelatinase biosynthesis-activating pheromone (GBAP) is an autoinducing peptide involved in Enterococcus faecalis fsr quorum sensing, and its 11-amino-acid sequence has been identified in the C-terminal region of the 242-residue deduced fsrB product (J. Nakayama et al., Mol. Microbiol. 41:145-154, 2001). In this study, however, we demonstrated the existence of fsrD, encoding the GBAP propeptide, which is in frame with fsrB but is translated independently of fsrB. It was also demonstrated that FsrB′, an FsrD segment-truncated FsrB, functions as a cysteine protease-like processing enzyme to generate GBAP from FsrD. This revised model is consistent with the staphylococcal agr system.


2021 ◽  
Vol 10 (Supplement_1) ◽  
pp. S10-S10
Author(s):  
Artemis Gogos ◽  
Michael J Federle

Abstract Background Streptococcus pyogenes is a human-restricted pathogen most often found in the human nasopharynx. Multiple bacterial factors have been found to contribute to persistent colonization of this niche, and many of these factors are important in mucosal immunity and vaccine development. In this work, we infected mice intranasally with transcriptional regulator mutants of the Rgg2/3 quorum sensing (QS) system—a peptide-based signaling system conserved in all sequenced isolates of S. pyogenes. Methods Three-week-old CD1 mice were intranasally infected with ~107 CFU of S. pyogenes strain MGAS315. Calcium alginate throat swabs were used to monitor nasopharyngeal colonization by the bacteria over time. Luciferase reporters used alongside an IVIS camera were able to show quorum sensing activity levels after inoculation into the mouse nose. Bacterial RNA was isolated from the throat of the mice and quantitative RT–PCR was performed on the samples to corroborate the luciferase reporter data. The nasal-associated lymphoid tissue (NALT) was excised and its supernatants were subjected to 32-plex murine cytokine and chemokine analysis (Millipore). Results Deletion of the QS system’s transcriptional activator (Δrgg2) dramatically diminished the percentage of colonized mice. Deletion of the transcriptional repressor (Δrgg3) increased the percentage of colonized mice compared with wild type. Stimulation of the QS system using synthetic pheromones prior to inoculation did not significantly increase the percentage of animals colonized, indicating that activity of the QS system is responsive to conditions of the host nasopharynx. Mice inoculated with QS-dependent luciferase reporters were subjected to in vivo imaging and showed activation within 1 hour. Bacterial RNA extracted directly from oropharyngeal swabs and evaluated by quantitative RT–PCR subsequently confirmed QS upregulation within 1 hour of inoculation. In the nasal-associated lymphoid tissue (NALT), a muted inflammatory response to the Δrgg2 bacteria suggests that their rapid elimination fails to elicit the previously characterized response to intranasal inoculation of GAS. Conclusions Deletion of the Rgg2 transcriptional activator of the Rgg 2/3 quorum sensing system eliminates colonization of the murine nasopharynx and changes the transcriptional profile of the bacteria in this niche. An existing small-molecule inhibitor of the Rgg2/3 system was unable to inhibit QS activation in vivo, likely due to the suboptimal achievable doses; however, results of our study indicate inhibition of QS may diminish the oropharyngeal colonization of S. pyogenes and argue for further development.


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