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Published on: February 10, 2011
Uncovering Antibiotic Resistance Signatures in Endodontic Enterococcus faecalis
Nezar Boreak1, Wafa Faqehi2, Raghad E Ageeli3
1Department of Restorative Dental Sciences, College of Dentistry, Jazan University, Jazan, Saudi Arabia, Phone: +966599016688, e-mail: nboraak@jazanu.edu.sa, Orcid: https://orcid.org/0000-0001-9017-9224.
Enterococcus faecalis exhibits adaptable transcriptional responses to antibiotics, developing drug-specific survival strategies. Understanding these resistance mechanisms is key to improving endodontic treatment and combating antibiotic resistance.
Area of Science:
- Microbiology
- Genomics
- Endodontics
Background:
- Enterococcus faecalis (E. faecalis) is a resilient pathogen causing persistent endodontic infections.
- E. faecalis exhibits increasing resistance to cell wall-targeting antibiotics, contributing to endodontic treatment failure.
- Limited understanding exists regarding E. faecalis's global transcriptional response to common endodontic antibiotics.
Purpose of the Study:
- To investigate the global transcriptional changes in E. faecalis upon exposure to beta-lactam and glycopeptide antibiotics.
- To identify conserved and drug-specific gene expression patterns associated with antibiotic resistance in E. faecalis.
Main Methods:
- Utilized Affymetrix E. faecalis OG1RF microarray data (GSE45306) with 15 samples.
- Exposed E. faecalis cultures to 10x Minimum Inhibitory Concentration (MIC) of Ampicillin, Bacitracin, Cephalothin, and Vancomycin.
- Employed GEO2R/limma for differential gene expression analysis (adjusted p < 0.05, |log2 fold change| > 1.5) and visualized results using heatmaps, Venn diagrams, and volcano plots.
Main Results:
- Vancomycin induced the most significant transcriptional shift (552 differentially expressed genes, DEGs), followed by Cephalothin (77 DEGs) and Bacitracin (10 DEGs).
- Identified a core set of 55 stress-responsive genes consistently altered across all antibiotic treatments.
- Observed increased expression of efflux transporters, metabolic alterations (ATP synthase, pyruvate dehydrogenase), cell wall remodeling, and antibiotic-specific regulators like membrane-associated sensors and the LytR-CpsA-Psr family.
Conclusions:
- E. faecalis demonstrates a sophisticated and adaptable transcriptional response to antibiotic stress.
- The pathogen employs both drug-specific and conserved survival strategies to resist antibiotic pressure.
- Antibiotic-specific regulators represent promising molecular targets for enhancing root canal disinfection and combating resistance.
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