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      Toxin-Antitoxin Systems in Clinical Pathogens

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          Abstract

          Toxin-antitoxin (TA) systems are prevalent in bacteria and archaea. Although not essential for normal cell growth, TA systems are implicated in multiple cellular functions associated with survival under stress conditions. Clinical strains of bacteria are currently causing major human health problems as a result of their multidrug resistance, persistence and strong pathogenicity. Here, we present a review of the TA systems described to date and their biological role in human pathogens belonging to the ESKAPE group ( Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa and Enterobacter spp.) and others of clinical relevance ( Escherichia coli, Burkholderia spp., Streptococcus spp. and Mycobacterium tuberculosis). Better understanding of the mechanisms of action of TA systems will enable the development of new lines of treatment for infections caused by the above-mentioned pathogens.

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          Persister cells, dormancy and infectious disease.

          Kim Lewis (2007)
          Several well-recognized puzzles in microbiology have remained unsolved for decades. These include latent bacterial infections, unculturable microorganisms, persister cells and biofilm multidrug tolerance. Accumulating evidence suggests that these seemingly disparate phenomena result from the ability of bacteria to enter into a dormant (non-dividing) state. The molecular mechanisms that underlie the formation of dormant persister cells are now being unravelled and are the focus of this Review.
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            Persister cells and tolerance to antimicrobials.

            Iris Keren, Niilo Kaldalu, Amy L Spoering … (2004)
            Bacterial populations produce persister cells that neither grow nor die in the presence of microbicidal antibiotics. Persisters are largely responsible for high levels of biofilm tolerance to antimicrobials, but virtually nothing was known about their biology. Tolerance of Escherichia coli to ampicillin and ofloxacin was tested at different growth stages to gain insight into the nature of persisters. The number of persisters did not change in lag or early exponential phase, and increased dramatically in mid-exponential phase. Similar dynamics were observed with Pseudomonas aeruginosa (ofloxacin) and Staphylococcus aureus (ciprofloxacin and penicillin). This shows that production of persisters depends on growth stage. Maintaining a culture of E. coli at early exponential phase by reinoculation eliminated persisters. This suggests that persisters are not at a particular stage in the cell cycle, neither are they defective cells nor cells created in response to antibiotics. Our data indicate that persisters are specialized survivor cells.
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              The phage abortive infection system, ToxIN, functions as a protein-RNA toxin-antitoxin pair.

              Peter Fineran, Tim R. Blower, Ian J Foulds … (2009)
              Various mechanisms exist that enable bacteria to resist bacteriophage infection. Resistance strategies include the abortive infection (Abi) systems, which promote cell death and limit phage replication within a bacterial population. A highly effective 2-gene Abi system from the phytopathogen Erwinia carotovora subspecies atroseptica, designated ToxIN, is described. The ToxIN Abi system also functions as a toxin-antitoxin (TA) pair, with ToxN inhibiting bacterial growth and the tandemly repeated ToxI RNA antitoxin counteracting the toxicity. TA modules are currently divided into 2 classes, protein and RNA antisense. We provide evidence that ToxIN defines an entirely new TA class that functions via a novel protein-RNA mechanism, with analogous systems present in diverse bacteria. Despite the debated role of TA systems, we demonstrate that ToxIN provides viral resistance in a range of bacterial genera against multiple phages. This is the first demonstration of a novel mechanistic class of TA systems and of an Abi system functioning in different bacterial genera, both with implications for the dynamics of phage-bacterial interactions.
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                Author and article information

                Contributors
                Anton Meinhart: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Toxins (Basel)
                Journal ID (iso-abbrev): Toxins (Basel)
                Journal ID (publisher-id): toxins
                Title: Toxins
                Publisher: MDPI
                ISSN (Electronic): 2072-6651
                Publication date (Electronic): 20 July 2016
                Publication date Collection: July 2016
                Volume: 8
                Issue: 7
                Electronic Location Identifier: 227
                Affiliations
                [1 ]Servicio de Microbiología, Complejo Hospitalario Universitario A Coruña-INIBIC, A Coruña 15006, Spain; laugemis@ 123456gmail.com (L.F.-G.); lucia.blasco@ 123456gmail.com (L.B.); maria.lopez.diaz@ 123456sergas.es (M.L.); german.bou.arevalo@ 123456sergas.es (G.B.)
                [2 ]Spanish Network for Research in Infectious Diseases (REIPI), Seville 41071, Spain
                [3 ]Departamento de Microbiología y Parasitología, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México 04510, México; rgarc@ 123456bq.unam.mx
                [4 ]Department of Chemical Engineering Pennsylvania State University, University Park, 16802 PA, USA; tuw14@ 123456psu.edu
                [5 ]Department of Biochemistry and Molecular Biology, Pennsylvania State University, University Park, 16802 PA, USA
                Author notes
                [* ]Correspondence: ma.del.mar.tomas.carmona@ 123456sergas.es ; Tel.: +34-981176399; Fax: +34-981178273
                Article
                Publisher ID: toxins-08-00227
                DOI: 10.3390/toxins8070227
                PMC ID: 4963858
                PubMed ID: 27447671
                SO-VID: 6769e361-c2b0-443f-ae3c-27ed498356dd
                Copyright © © 2016 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 09 May 2016
                Date accepted : 07 July 2016
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular medicine
                Keywords: clinical,pathogens,toxin-antitoxin,plasmids,chromosome,resistance,persistance,virulence
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: clinical, pathogens, toxin-antitoxin, plasmids, chromosome, resistance, persistance, virulence

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