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      Real-Time Imaging of the Bacillithiol Redox Potential in the Human Pathogen Staphylococcus aureus Using a Genetically Encoded Bacilliredoxin-Fused Redox Biosensor

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          Abstract

          Aims: Bacillithiol (BSH) is utilized as a major thiol-redox buffer in the human pathogen Staphylococcus aureus. Under oxidative stress, BSH forms mixed disulfides with proteins, termed as S-bacillithiolation, which can be reversed by bacilliredoxins (Brx). In eukaryotes, glutaredoxin-fused roGFP2 biosensors have been applied for dynamic live imaging of the glutathione redox potential. Here, we have constructed a genetically encoded bacilliredoxin-fused redox biosensor (Brx-roGFP2) to monitor dynamic changes in the BSH redox potential in S. aureus.

          Results: The Brx-roGFP2 biosensor showed a specific and rapid response to low levels of bacillithiol disulfide (BSSB) in vitro that required the active-site Cys of Brx. Dynamic live imaging in two methicillin-resistant S. aureus (MRSA) USA300 and COL strains revealed fast and dynamic responses of the Brx-roGFP2 biosensor under hypochlorite and hydrogen peroxide (H 2O 2) stress and constitutive oxidation of the probe in different BSH-deficient mutants. Furthermore, we found that the Brx-roGFP2 expression level and the dynamic range are higher in S. aureus COL compared with the USA300 strain. In phagocytosis assays with THP-1 macrophages, the biosensor was 87% oxidized in S. aureus COL. However, no changes in the BSH redox potential were measured after treatment with different antibiotics classes, indicating that antibiotics do not cause oxidative stress in S. aureus.

          Conclusion and Innovation: This Brx-roGFP2 biosensor catalyzes specific equilibration between the BSH and roGFP2 redox couples and can be applied for dynamic live imaging of redox changes in S. aureus and other BSH-producing Firmicutes. Antioxid. Redox Signal. 26, 835–848.

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          A common mechanism of cellular death induced by bactericidal antibiotics.

          Michael A Kohanski, Daniel Dwyer, Boris Hayete … (2007)
          Antibiotic mode-of-action classification is based upon drug-target interaction and whether the resultant inhibition of cellular function is lethal to bacteria. Here we show that the three major classes of bactericidal antibiotics, regardless of drug-target interaction, stimulate the production of highly deleterious hydroxyl radicals in Gram-negative and Gram-positive bacteria, which ultimately contribute to cell death. We also show, in contrast, that bacteriostatic drugs do not produce hydroxyl radicals. We demonstrate that the mechanism of hydroxyl radical formation induced by bactericidal antibiotics is the end product of an oxidative damage cellular death pathway involving the tricarboxylic acid cycle, a transient depletion of NADH, destabilization of iron-sulfur clusters, and stimulation of the Fenton reaction. Our results suggest that all three major classes of bactericidal drugs can be potentiated by targeting bacterial systems that remediate hydroxyl radical damage, including proteins involved in triggering the DNA damage response, e.g., RecA.
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            Cell death from antibiotics without the involvement of reactive oxygen species.

            Yuanyuan Liu, James Imlay (2013)
            Recent observations have suggested that classic antibiotics kill bacteria by stimulating the formation of reactive oxygen species (ROS). If true, this notion might guide new strategies to improve antibiotic efficacy. In this study, the model was directly tested. Contrary to the hypothesis, antibiotic treatment did not accelerate the formation of hydrogen peroxide in Escherichia coli and did not elevate intracellular free iron, an essential reactant for the production of lethal damage. Lethality persisted in the absence of oxygen, and DNA repair mutants were not hypersensitive, undermining the idea that toxicity arose from oxidative DNA lesions. We conclude that these antibiotic exposures did not produce ROS and that lethality more likely resulted from the direct inhibition of cell-wall assembly, protein synthesis, and DNA replication.
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              Staphylococcus aureus: a well-armed pathogen.

              G L Archer (1998)
              Staphylococcus aureus is a virulent pathogen that is currently the most common cause of infections in hospitalized patients. S. aureus infection can involve any organ system. The success of S. aureus as a pathogen and its ability to cause such a wide range of infections are the result of its extensive virulence factors. The increase in the resistance of this virulent pathogen to antibacterial agents, coupled with its increasing prevalence as a nosocomial pathogen, is of major concern. The core resistance phenotype that seems to be most associated with the persistence of S. aureus in the hospital is methicillin resistance. Methicillin resistance in nosocomial S. aureus isolates has been increasing dramatically in United States hospitals and is also associated with resistance to other useful antistaphylococcal compounds. Possible ways to decrease the incidence of nosocomial S. aureus infections include instituting more effective infection control, decreasing nasal colonization, developing vaccines, and developing new or improved antimicrobials.
              Article 0 comments Cited 140 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Antioxid Redox Signal
                Journal ID (iso-abbrev): Antioxid. Redox Signal
                Journal ID (publisher-id): ars
                Title: Antioxidants & Redox Signaling
                Publisher: Mary Ann Liebert, Inc. (140 Huguenot Street, 3rd FloorNew Rochelle, NY 10801USA )
                ISSN (Print): 1523-0864
                ISSN (Electronic): 1557-7716
                Publication date (Print): 20 May 2017
                Publication date (Electronic): 20 May 2017
                Publication date PMC-release: 20 May 2017
                Volume: 26
                Issue: 15
                Pages: 835-848
                Affiliations
                [ 1 ]Institute for Biology-Microbiology, Freie Universität Berlin , Berlin, Germany.
                [ 2 ]Junior Research Group Pathoproteomics, Ernst-Moritz-Arndt-University of Greifswald , Greifswald, Germany.
                [ 3 ]Institute for Microbiology, Ernst-Moritz-Arndt-University of Greifswald , Greifswald, Germany.
                [ 4 ]School of Pharmacy, University of East Anglia , Norwich Research Park, Norwich, United Kingdom.
                Author notes
                Address correspondence to: Prof. Haike Antelmann, Institute for Biology-Microbiology, Freie Universität Berlin Königin-Luise-Strasse 12-16, Berlin D-14195, Germany

                E-mail: haike.antelmann@ 123456fu-berlin.de
                Article
                Publisher ID: 10.1089/ars.2016.6733
                DOI: 10.1089/ars.2016.6733
                PMC ID: 5444506
                PubMed ID: 27462976
                SO-VID: 73d03f64-95e9-4fcc-af61-fba31cbe302a
                Copyright © © Vu Van Loi, et al., 2017; Published by Mary Ann Liebert, Inc.
                License:

                This article is available under the Creative Commons License CC-BY-NC ( http://creativecommons.org/licenses/by-nc/4.0). This license permits non-commercial use, distribution and reproduction in any medium, provided the original work is properly cited. Permission only needs to be obtained for commercial use and can be done via RightsLink.

                History
                Date received : 26 April 2016
                Date revision received : 01 July 2016
                Date accepted : 05 July 2016
                Page count
                Figures: 6, Equations: 2, References: 41, Pages: 14
                Categories
                Subject: Original Research Communications

                Keywords: staphylococcus aureus,bacillithiol,bacilliredoxin,redox biosensor,rogfp,oxidative stress
                Data availability:
                Keywords: staphylococcus aureus, bacillithiol, bacilliredoxin, redox biosensor, rogfp, oxidative stress

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