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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Loss of Antibiotic Tolerance in Sod-Deficient Mutants Is Dependent on the Energy Source and Arginine Catabolism in Enterococci</title><author><name sortKey="Ladjouzi, Rabia" sort="Ladjouzi, Rabia" uniqKey="Ladjouzi R" first="Rabia" last="Ladjouzi">Rabia Ladjouzi</name><affiliation><nlm:aff id="aff1">Université de Caen Basse-Normandie, EA4655 U2RM-Stress et Virulence, Caen, France</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">Université de Bejaia, FSNV, Laboratoire d'Ecologie Microbienne, Bejaia, Algeria</nlm:aff></affiliation></author><author><name sortKey="Bizzini, Alain" sort="Bizzini, Alain" uniqKey="Bizzini A" first="Alain" last="Bizzini">Alain Bizzini</name><affiliation><nlm:aff id="aff1">Université de Caen Basse-Normandie, EA4655 U2RM-Stress et Virulence, Caen, France</nlm:aff></affiliation></author><author><name sortKey="Van Schaik, Willem" sort="Van Schaik, Willem" uniqKey="Van Schaik W" first="Willem" last="Van Schaik">Willem Van Schaik</name><affiliation><nlm:aff id="aff3">Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands</nlm:aff></affiliation></author><author><name sortKey="Zhang, Xinglin" sort="Zhang, Xinglin" uniqKey="Zhang X" first="Xinglin" last="Zhang">Xinglin Zhang</name><affiliation><nlm:aff id="aff3">Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands</nlm:aff></affiliation></author><author><name sortKey="Rince, Alain" sort="Rince, Alain" uniqKey="Rince A" first="Alain" last="Rincé">Alain Rincé</name><affiliation><nlm:aff id="aff1">Université de Caen Basse-Normandie, EA4655 U2RM-Stress et Virulence, Caen, France</nlm:aff></affiliation></author><author><name sortKey="Benachour, Abdellah" sort="Benachour, Abdellah" uniqKey="Benachour A" first="Abdellah" last="Benachour">Abdellah Benachour</name><affiliation><nlm:aff id="aff1">Université de Caen Basse-Normandie, EA4655 U2RM-Stress et Virulence, Caen, France</nlm:aff></affiliation></author><author><name sortKey="Hartke, Axel" sort="Hartke, Axel" uniqKey="Hartke A" first="Axel" last="Hartke">Axel Hartke</name><affiliation><nlm:aff id="aff1">Université de Caen Basse-Normandie, EA4655 U2RM-Stress et Virulence, Caen, France</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">26260456</idno><idno type="pmc">4573725</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4573725</idno><idno type="RBID">PMC:4573725</idno><idno type="doi">10.1128/JB.00389-15</idno><date when="2015">2015</date><idno type="wicri:Area/Pmc/Corpus">000133</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000133</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Loss of Antibiotic Tolerance in Sod-Deficient Mutants Is Dependent on the Energy Source and Arginine Catabolism in Enterococci</title><author><name sortKey="Ladjouzi, Rabia" sort="Ladjouzi, Rabia" uniqKey="Ladjouzi R" first="Rabia" last="Ladjouzi">Rabia Ladjouzi</name><affiliation><nlm:aff id="aff1">Université de Caen Basse-Normandie, EA4655 U2RM-Stress et Virulence, Caen, France</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">Université de Bejaia, FSNV, Laboratoire d'Ecologie Microbienne, Bejaia, Algeria</nlm:aff></affiliation></author><author><name sortKey="Bizzini, Alain" sort="Bizzini, Alain" uniqKey="Bizzini A" first="Alain" last="Bizzini">Alain Bizzini</name><affiliation><nlm:aff id="aff1">Université de Caen Basse-Normandie, EA4655 U2RM-Stress et Virulence, Caen, France</nlm:aff></affiliation></author><author><name sortKey="Van Schaik, Willem" sort="Van Schaik, Willem" uniqKey="Van Schaik W" first="Willem" last="Van Schaik">Willem Van Schaik</name><affiliation><nlm:aff id="aff3">Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands</nlm:aff></affiliation></author><author><name sortKey="Zhang, Xinglin" sort="Zhang, Xinglin" uniqKey="Zhang X" first="Xinglin" last="Zhang">Xinglin Zhang</name><affiliation><nlm:aff id="aff3">Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands</nlm:aff></affiliation></author><author><name sortKey="Rince, Alain" sort="Rince, Alain" uniqKey="Rince A" first="Alain" last="Rincé">Alain Rincé</name><affiliation><nlm:aff id="aff1">Université de Caen Basse-Normandie, EA4655 U2RM-Stress et Virulence, Caen, France</nlm:aff></affiliation></author><author><name sortKey="Benachour, Abdellah" sort="Benachour, Abdellah" uniqKey="Benachour A" first="Abdellah" last="Benachour">Abdellah Benachour</name><affiliation><nlm:aff id="aff1">Université de Caen Basse-Normandie, EA4655 U2RM-Stress et Virulence, Caen, France</nlm:aff></affiliation></author><author><name sortKey="Hartke, Axel" sort="Hartke, Axel" uniqKey="Hartke A" first="Axel" last="Hartke">Axel Hartke</name><affiliation><nlm:aff id="aff1">Université de Caen Basse-Normandie, EA4655 U2RM-Stress et Virulence, Caen, France</nlm:aff></affiliation></author></analytic><series><title level="j">Journal of Bacteriology</title><idno type="ISSN">0021-9193</idno><idno type="eISSN">1098-5530</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><title>ABSTRACT</title><p>Enterococci are naturally tolerant to typically bactericidal cell wall-active antibiotics, meaning that their growth is inhibited but they are not killed even when exposed to a high concentration of the drug. The molecular reasons for this extraordinary tolerance are still incompletely understood. Previous work showed that resistance to killing collapsed specifically in mutants affected in superoxide dismutase (Sod) activity, arguing that bactericidal antibiotic treatment led to induction of a superoxide burst. In the present work, we show that loss of antibiotic tolerance in Δ<italic>sodA</italic> mutants of pathogenic enterococci is dependent on the energy source present during antibiotic treatment. Hexoses induce greater killing than the pentose ribose, and no killing was observed with glycerol as the energy source. These results point to glycolytic reactions as crucial for antibiotic-mediated killing of Δ<italic>sodA</italic> mutants. A transposon mutant library was constructed in <named-content content-type="genus-species">Enterococcus faecalis ΔsodA</named-content> mutants and screened for restored tolerance of vancomycin. Partially restored tolerance was observed in mutants with transposon integrations into intergenic regions upstream of regulators implicated in arginine catabolism. In these mutants, the arginine deiminase operon was highly upregulated. A model for the action of cell wall-active antibiotics in tolerant and nontolerant bacteria is proposed.</p><p><bold>IMPORTANCE</bold> Antibiotic tolerance is a serious clinical concern, since tolerant bacteria have considerably increased abilities to resist killing by bactericidal drugs. Using enterococci as models for highly antibiotic-tolerant pathogens, we showed that tolerance of these bacteria is linked to their superoxide dismutase (Sod), arguing that bactericidal antibiotics induce generation of reactive oxygen species inside cells. Wild-type strains are tolerant because they detoxify these deleterious molecules by the activity of Sod, whereas Sod-deficient strains are killed. This study showed that killing depends on the energy source present during treatment and that an increase in arginine catabolism partially restored tolerance of the Sod mutants. These results are used to propose a mode-of-action model of cell wall-active antibiotics in tolerant and nontolerant bacteria.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Bacteriol</journal-id><journal-id journal-id-type="iso-abbrev">J. Bacteriol</journal-id><journal-id journal-id-type="hwp">jb</journal-id><journal-id journal-id-type="pmc">jb</journal-id><journal-id journal-id-type="publisher-id">JB</journal-id><journal-title-group><journal-title>Journal of Bacteriology</journal-title></journal-title-group><issn pub-type="ppub">0021-9193</issn><issn pub-type="epub">1098-5530</issn><publisher><publisher-name>American Society for Microbiology</publisher-name><publisher-loc>1752 N St., N.W., Washington, DC</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">26260456</article-id><article-id pub-id-type="pmc">4573725</article-id><article-id pub-id-type="publisher-id">00389-15</article-id><article-id pub-id-type="doi">10.1128/JB.00389-15</article-id><article-categories><subj-group subj-group-type="heading"><subject>Articles</subject></subj-group></article-categories><title-group><article-title>Loss of Antibiotic Tolerance in Sod-Deficient Mutants Is Dependent on the Energy Source and Arginine Catabolism in Enterococci</article-title><alt-title alt-title-type="running-head">Loss of Antibiotic Tolerance in Enterococci</alt-title><alt-title alt-title-type="short-authors">Ladjouzi et al.</alt-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Ladjouzi</surname><given-names>Rabia</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author"><name><surname>Bizzini</surname><given-names>Alain</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>van Schaik</surname><given-names>Willem</given-names></name><xref ref-type="aff" rid="aff3"><sup>c</sup></xref></contrib><contrib contrib-type="author"><name><surname>Zhang</surname><given-names>Xinglin</given-names></name><xref ref-type="aff" rid="aff3"><sup>c</sup></xref></contrib><contrib contrib-type="author"><name><surname>Rincé</surname><given-names>Alain</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Benachour</surname><given-names>Abdellah</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Hartke</surname><given-names>Axel</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><aff id="aff1"><label>a</label>Université de Caen Basse-Normandie, EA4655 U2RM-Stress et Virulence, Caen, France</aff><aff id="aff2"><label>b</label>Université de Bejaia, FSNV, Laboratoire d'Ecologie Microbienne, Bejaia, Algeria</aff><aff id="aff3"><label>c</label>Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands</aff></contrib-group><contrib-group><contrib contrib-type="editor"><name><surname>Silhavy</surname><given-names>T. J.</given-names></name><role>Editor</role></contrib></contrib-group><author-notes><corresp id="cor1">Address correspondence to Axel Hartke, <email>axel.hartke@unicaen.fr</email>.</corresp><fn fn-type="other"><p><bold>Citation</bold> Ladjouzi R, Bizzini A, van Schaik W, Zhang X, Rincé A, Benachour A, Hartke A. 2015. Loss of antibiotic tolerance in Sod-deficient mutants is dependent on the energy source and arginine catabolism in enterococci. J Bacteriol 197:3283–3293. doi:<ext-link ext-link-type="uri" xlink:href="http://dx.doi.org/10.1128/JB.00389-15">10.1128/JB.00389-15</ext-link>.</p></fn></author-notes><pub-date pub-type="epreprint"><day>10</day><month>8</month><year>2015</year></pub-date><pub-date pub-type="epub"><day>17</day><month>9</month><year>2015</year></pub-date><pub-date pub-type="ppub"><month>10</month><year>2015</year></pub-date><volume>197</volume><issue>20</issue><fpage>3283</fpage><lpage>3293</lpage><history><date date-type="received"><day>21</day><month>5</month><year>2015</year></date><date date-type="accepted"><day>31</day><month>7</month><year>2015</year></date></history><permissions><copyright-statement>Copyright © 2015, American Society for Microbiology. All Rights Reserved.</copyright-statement><copyright-year>2015</copyright-year><copyright-holder>American Society for Microbiology</copyright-holder></permissions><self-uri content-type="pdf" xlink:href="zjb02015003283.pdf"></self-uri><abstract><title>ABSTRACT</title><p>Enterococci are naturally tolerant to typically bactericidal cell wall-active antibiotics, meaning that their growth is inhibited but they are not killed even when exposed to a high concentration of the drug. The molecular reasons for this extraordinary tolerance are still incompletely understood. Previous work showed that resistance to killing collapsed specifically in mutants affected in superoxide dismutase (Sod) activity, arguing that bactericidal antibiotic treatment led to induction of a superoxide burst. In the present work, we show that loss of antibiotic tolerance in Δ<italic>sodA</italic> mutants of pathogenic enterococci is dependent on the energy source present during antibiotic treatment. Hexoses induce greater killing than the pentose ribose, and no killing was observed with glycerol as the energy source. These results point to glycolytic reactions as crucial for antibiotic-mediated killing of Δ<italic>sodA</italic> mutants. A transposon mutant library was constructed in <named-content content-type="genus-species">Enterococcus faecalis ΔsodA</named-content> mutants and screened for restored tolerance of vancomycin. Partially restored tolerance was observed in mutants with transposon integrations into intergenic regions upstream of regulators implicated in arginine catabolism. In these mutants, the arginine deiminase operon was highly upregulated. A model for the action of cell wall-active antibiotics in tolerant and nontolerant bacteria is proposed.</p><p><bold>IMPORTANCE</bold> Antibiotic tolerance is a serious clinical concern, since tolerant bacteria have considerably increased abilities to resist killing by bactericidal drugs. Using enterococci as models for highly antibiotic-tolerant pathogens, we showed that tolerance of these bacteria is linked to their superoxide dismutase (Sod), arguing that bactericidal antibiotics induce generation of reactive oxygen species inside cells. Wild-type strains are tolerant because they detoxify these deleterious molecules by the activity of Sod, whereas Sod-deficient strains are killed. This study showed that killing depends on the energy source present during treatment and that an increase in arginine catabolism partially restored tolerance of the Sod mutants. These results are used to propose a mode-of-action model of cell wall-active antibiotics in tolerant and nontolerant bacteria.</p></abstract><counts><fig-count count="6"></fig-count><table-count count="2"></table-count><equation-count count="0"></equation-count><ref-count count="38"></ref-count><page-count count="11"></page-count><word-count count="9030"></word-count></counts></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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