ArticleAntimicrobial agents and chemotherapy2015
Oxidative stress enhances cephalosporin resistance of Enterococcus faecalis through activation of a two-component signaling system.
Article in Antimicrobial agents and chemotherapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 55 citations in OpenAlex.
- Phosphorylation of the cell wall hydrolase MltG in response to cell wall stress modulates resistance toward cephalosporins inJournal of bacteriology · 2025Article
- The cell wall hydrolase MltG is essential to maintain cell wall homeostasis ofJournal of bacteriology · 2025Article
- The extracellular segment of CroS is not required for sensing but fine-tunes the magnitude of CroS signaling to regulate cephalosporin resistance inJournal of bacteriology · 2024Article
- The HtrA chaperone monitors sortase-assembled pilus biogenesis in Enterococcus faecalis.PLoS genetics · 2024Article
- Arginine impacts aggregation, biofilm formation, and antibiotic susceptibility inbioRxiv : the preprint server for biology · 2024Article
- CCR2-dependent CX3CR1+ colonic macrophages promoteInfection and immunity · 2024Article
- Arginine impacts aggregation, biofilm formation, and antibiotic susceptibility inFEMS microbes · 2024Article
- CroR Regulates Expression ofmBio · 2022Article
- Article
- Role ofJournal of bacteriology · 2019Article
- Adaptation to Adversity: the Intermingling of Stress Tolerance and Pathogenesis in Enterococci.Microbiology and molecular biology reviews : MMBR · 2019Review
- Article
- Ctt1 catalase activity potentiates antifungal azoles in the emerging opportunistic pathogen Saccharomyces cerevisiae.Scientific reports · 2019Article
- Sortase-Dependent Proteins Promote Gastrointestinal Colonization by Enterococci.Infection and immunity · 2019Article
- Convergence of PASTA Kinase and Two-Component Signaling in Response to Cell Wall Stress in Enterococcus faecalis.Journal of bacteriology · 2018Article
- Modulators of Enterococcus faecalis Cell Envelope Integrity and Antimicrobial Resistance Influence Stable Colonization of the Mammalian Gastrointestinal Tract.Infection and immunity · 2018Article
- Transcriptome Changes ofFrontiers in microbiology · 2018Article
- Extracellular SalB Contributes to Intrinsic Cephalosporin Resistance and Cell Envelope Integrity in Enterococcus faecalis.Journal of bacteriology · 2017Article
- Growth- and Stress-Induced PASTA Kinase Phosphorylation in Enterococcus faecalis.Journal of bacteriology · 2017Article
- PrgU: a suppressor of sex pheromone toxicity in Enterococcus faecalis.Molecular microbiology · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Enterococcus faecalis is a low-GC Gram-positive bacterium, a normal resident of the gastrointestinal (GI) tract, and an important hospital-acquired pathogen. An important risk factor for hospital-acquired enterococcal infections is prior therapy with broad-spectrum cephalosporins, antibiotics that impair cell wall biosynthesis by inhibiting peptidoglycan cross-linking. Enterococci are intrinsically resistant to cephalosporins; however, environmental factors that modulate cephalosporin resistance have not been described. While searching for the genetic determinants of cephalosporin resistance in E. faecalis, we unexpectedly discovered that oxidative stress, whether from external sources or derived from endogenous metabolism, drives enhanced intrinsic resistance to cephalosporins. A particular source of oxidative stress, H2O2, activates signaling through the CroR-CroS two-component signaling system, a known determinant of cephalosporin resistance in E. faecalis. We find that CroR-CroS is required for adaptation to H2O2 stress and that H2O2 potentiates the activities of cephalosporins against E. faecalis when the CroR-CroS signaling system is nonfunctional. Rather than directly detecting H2O2, our data suggest that the CroR-CroS system responds to cell envelope damage caused by H2O2 exposure in order to promote cell envelope repair and enhanced cephalosporin resistance.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.