Hydrogen peroxide scavenging is not a virulence determinant in the pathogenesis of Haemophilus influenzae type b strain Eagan.
Identifieur interne : 000D43 ( Main/Exploration ); précédent : 000D42; suivant : 000D44Hydrogen peroxide scavenging is not a virulence determinant in the pathogenesis of Haemophilus influenzae type b strain Eagan.
Auteurs : Bjorn Vergauwen [Belgique] ; Mark Herbert ; Jozef J. Van BeeumenSource :
- BMC microbiology [ 1471-2180 ] ; 2006.
Descripteurs français
- KwdFr :
- Catalase (génétique), Catalase (métabolisme), Délétion de gène (MeSH), Haemophilus influenzae type B (enzymologie), Haemophilus influenzae type B (génétique), Haemophilus influenzae type B (métabolisme), Haemophilus influenzae type B (pathogénicité), Mutation (MeSH), Peroxidases (génétique), Peroxidases (métabolisme), Peroxyde d'hydrogène (métabolisme), Piégeurs de radicaux libres (métabolisme), Stress oxydatif (MeSH), Virulence (MeSH).
- MESH :
- enzymologie : Haemophilus influenzae type B.
- génétique : Catalase, Haemophilus influenzae type B, Peroxidases.
- métabolisme : Catalase, Haemophilus influenzae type B, Peroxidases, Peroxyde d'hydrogène, Piégeurs de radicaux libres.
- pathogénicité : Haemophilus influenzae type B.
- Délétion de gène, Mutation, Stress oxydatif, Virulence.
English descriptors
- KwdEn :
- Catalase (genetics), Catalase (metabolism), Free Radical Scavengers (metabolism), Gene Deletion (MeSH), Haemophilus influenzae type b (enzymology), Haemophilus influenzae type b (genetics), Haemophilus influenzae type b (metabolism), Haemophilus influenzae type b (pathogenicity), Hydrogen Peroxide (metabolism), Mutation (MeSH), Oxidative Stress (MeSH), Peroxidases (genetics), Peroxidases (metabolism), Virulence (MeSH).
- MESH :
- chemical , genetics : Catalase, Peroxidases.
- chemical , metabolism : Catalase, Free Radical Scavengers, Hydrogen Peroxide, Peroxidases.
- enzymology : Haemophilus influenzae type b.
- genetics : Haemophilus influenzae type b.
- metabolism : Haemophilus influenzae type b.
- pathogenicity : Haemophilus influenzae type b.
- Gene Deletion, Mutation, Oxidative Stress, Virulence.
Abstract
BACKGROUND
A potentially lethal flux of hydrogen peroxide (H2O2) is continuously generated during aerobic metabolism. It follows that aerobic organisms have equipped themselves with specific H2O2 dismutases and H2O2 reductases, of which catalase and the alkyl hydroperoxide reductase (AhpR) are the best-studied prokaryotic members. The sequenced Haemophilus influenzae Rd genome reveals one catalase, designated HktE, and no AhpR. However, Haemophilus influenzae type b strain Eagan (Hib), a causative agent of bacterial sepsis and meningitis in young children, disrupted in its hktE gene is not attenuated in virulence, and retains the ability to rapidly scavenge H2O2. This redundancy in H2O2-scavenging is accounted for by peroxidatic activity which specifically uses glutathione as the reducing substrate.
RESULTS
We show here that inside acatalasaemic H. influenzae all of the residual peroxidatic activity is catalyzed by PGdx, a hybrid peroxiredoxin-glutaredoxin glutathione-dependent peroxidase. In vitro kinetic assays on crude hktE- pgdx- H. influenzae Rd extracts revealed the presence of NAD(P)H:peroxide oxidoreductase activity, which, however, appears to be physiologically insignificant because of its low affinity for H2O2 (Km = 1.1 mM). Hydroperoxidase-deficient hktE- pgdx- H. influenzae Rd showed a slightly affected aerobic growth phenotype in rich broth, while, in chemically defined medium, growth was completely inhibited by aerobic conditions, unless the medium contained an amino acid/vitamin supplement. To study the role of PGdx in virulence and to assess the requirement of H2O2-scavenging during the course of infection, both a pgdx single mutant and a pgdx/hktE double mutant of Hib were assayed for virulence in an infant rat model. The ability of both mutant strains to cause bacteremia was unaffected.
CONCLUSION
Catalase (HktE) and a sole peroxidase (PGdx) account for the majority of scavenging of metabolically generated H2O2 in the H. influenzae cytoplasm. Growth experiments with hydroperoxidase-deficient hktE- pgdx- H. influenzae Rd suggest that the cytotoxicity inflicted by the continuous accumulation of H2O2 during aerobic growth brings about bacteriostasis rather than bacterial killing. Finally, H2O2-scavenging is not a determinant of Hib virulence in the infant rat model of infection.
DOI: 10.1186/1471-2180-6-3
PubMed: 16430767
PubMed Central: PMC1361801
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Ledeganckstraat 35, 9000 Gent, Belgium. Bjorn.Vergauwen@Ugent.be</nlm:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Laboratory of Protein Biochemistry and Protein Engineering, Ghent University, K.L. Ledeganckstraat 35, 9000 Gent</wicri:regionArea><placeName><region type="province" nuts="2">Province de Flandre-Orientale</region><settlement type="city">Gand</settlement></placeName><orgName type="university">Université de Gand</orgName></affiliation></author><author><name sortKey="Herbert, Mark" sort="Herbert, Mark" uniqKey="Herbert M" first="Mark" last="Herbert">Mark Herbert</name></author><author><name sortKey="Van Beeumen, Jozef J" sort="Van Beeumen, Jozef J" uniqKey="Van Beeumen J" first="Jozef J" last="Van Beeumen">Jozef J. 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It follows that aerobic organisms have equipped themselves with specific H2O2 dismutases and H2O2 reductases, of which catalase and the alkyl hydroperoxide reductase (AhpR) are the best-studied prokaryotic members. The sequenced Haemophilus influenzae Rd genome reveals one catalase, designated HktE, and no AhpR. However, Haemophilus influenzae type b strain Eagan (Hib), a causative agent of bacterial sepsis and meningitis in young children, disrupted in its hktE gene is not attenuated in virulence, and retains the ability to rapidly scavenge H2O2. This redundancy in H2O2-scavenging is accounted for by peroxidatic activity which specifically uses glutathione as the reducing substrate.</p></div><div type="abstract" xml:lang="en"><p><b>RESULTS</b></p><p>We show here that inside acatalasaemic H. influenzae all of the residual peroxidatic activity is catalyzed by PGdx, a hybrid peroxiredoxin-glutaredoxin glutathione-dependent peroxidase. In vitro kinetic assays on crude hktE- pgdx- H. influenzae Rd extracts revealed the presence of NAD(P)H:peroxide oxidoreductase activity, which, however, appears to be physiologically insignificant because of its low affinity for H2O2 (Km = 1.1 mM). Hydroperoxidase-deficient hktE- pgdx- H. influenzae Rd showed a slightly affected aerobic growth phenotype in rich broth, while, in chemically defined medium, growth was completely inhibited by aerobic conditions, unless the medium contained an amino acid/vitamin supplement. To study the role of PGdx in virulence and to assess the requirement of H2O2-scavenging during the course of infection, both a pgdx single mutant and a pgdx/hktE double mutant of Hib were assayed for virulence in an infant rat model. The ability of both mutant strains to cause bacteremia was unaffected.</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSION</b></p><p>Catalase (HktE) and a sole peroxidase (PGdx) account for the majority of scavenging of metabolically generated H2O2 in the H. influenzae cytoplasm. Growth experiments with hydroperoxidase-deficient hktE- pgdx- H. influenzae Rd suggest that the cytotoxicity inflicted by the continuous accumulation of H2O2 during aerobic growth brings about bacteriostasis rather than bacterial killing. Finally, H2O2-scavenging is not a determinant of Hib virulence in the infant rat model of infection.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16430767</PMID><DateCompleted><Year>2006</Year><Month>12</Month><Day>14</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1471-2180</ISSN><JournalIssue CitedMedium="Internet"><Volume>6</Volume><PubDate><Year>2006</Year><Month>Jan</Month><Day>23</Day></PubDate></JournalIssue><Title>BMC microbiology</Title><ISOAbbreviation>BMC Microbiol</ISOAbbreviation></Journal><ArticleTitle>Hydrogen peroxide scavenging is not a virulence determinant in the pathogenesis of Haemophilus influenzae type b strain Eagan.</ArticleTitle><Pagination><MedlinePgn>3</MedlinePgn></Pagination><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">A potentially lethal flux of hydrogen peroxide (H2O2) is continuously generated during aerobic metabolism. It follows that aerobic organisms have equipped themselves with specific H2O2 dismutases and H2O2 reductases, of which catalase and the alkyl hydroperoxide reductase (AhpR) are the best-studied prokaryotic members. The sequenced Haemophilus influenzae Rd genome reveals one catalase, designated HktE, and no AhpR. However, Haemophilus influenzae type b strain Eagan (Hib), a causative agent of bacterial sepsis and meningitis in young children, disrupted in its hktE gene is not attenuated in virulence, and retains the ability to rapidly scavenge H2O2. This redundancy in H2O2-scavenging is accounted for by peroxidatic activity which specifically uses glutathione as the reducing substrate.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">We show here that inside acatalasaemic H. influenzae all of the residual peroxidatic activity is catalyzed by PGdx, a hybrid peroxiredoxin-glutaredoxin glutathione-dependent peroxidase. In vitro kinetic assays on crude hktE- pgdx- H. influenzae Rd extracts revealed the presence of NAD(P)H:peroxide oxidoreductase activity, which, however, appears to be physiologically insignificant because of its low affinity for H2O2 (Km = 1.1 mM). Hydroperoxidase-deficient hktE- pgdx- H. influenzae Rd showed a slightly affected aerobic growth phenotype in rich broth, while, in chemically defined medium, growth was completely inhibited by aerobic conditions, unless the medium contained an amino acid/vitamin supplement. To study the role of PGdx in virulence and to assess the requirement of H2O2-scavenging during the course of infection, both a pgdx single mutant and a pgdx/hktE double mutant of Hib were assayed for virulence in an infant rat model. The ability of both mutant strains to cause bacteremia was unaffected.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Catalase (HktE) and a sole peroxidase (PGdx) account for the majority of scavenging of metabolically generated H2O2 in the H. influenzae cytoplasm. Growth experiments with hydroperoxidase-deficient hktE- pgdx- H. influenzae Rd suggest that the cytotoxicity inflicted by the continuous accumulation of H2O2 during aerobic growth brings about bacteriostasis rather than bacterial killing. Finally, H2O2-scavenging is not a determinant of Hib virulence in the infant rat model of infection.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Vergauwen</LastName><ForeName>Bjorn</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Laboratory of Protein Biochemistry and Protein Engineering, Ghent University, K.L. Ledeganckstraat 35, 9000 Gent, Belgium. Bjorn.Vergauwen@Ugent.be</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Herbert</LastName><ForeName>Mark</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Van Beeumen</LastName><ForeName>Jozef J</ForeName><Initials>JJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2006</Year><Month>01</Month><Day>23</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMC Microbiol</MedlineTA><NlmUniqueID>100966981</NlmUniqueID><ISSNLinking>1471-2180</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016166">Free Radical Scavengers</NameOfSubstance></Chemical><Chemical><RegistryNumber>BBX060AN9V</RegistryNumber><NameOfSubstance 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Scavengers</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017353" MajorTopicYN="N">Gene Deletion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019741" MajorTopicYN="N">Haemophilus influenzae type b</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000472" MajorTopicYN="Y">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006861" MajorTopicYN="N">Hydrogen Peroxide</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010544" MajorTopicYN="N">Peroxidases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014774" MajorTopicYN="N">Virulence</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2005</Year><Month>08</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2006</Year><Month>01</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>1</Month><Day>25</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>12</Month><Day>15</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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IdType="pubmed">1987145</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>Belgique</li></country><region><li>Province de Flandre-Orientale</li></region><settlement><li>Gand</li></settlement><orgName><li>Université de Gand</li></orgName></list><tree><noCountry><name sortKey="Herbert, Mark" sort="Herbert, Mark" uniqKey="Herbert M" first="Mark" last="Herbert">Mark Herbert</name><name sortKey="Van Beeumen, Jozef J" sort="Van Beeumen, Jozef J" uniqKey="Van Beeumen J" first="Jozef J" last="Van Beeumen">Jozef J. Van Beeumen</name></noCountry><country name="Belgique"><region name="Province de Flandre-Orientale"><name sortKey="Vergauwen, Bjorn" sort="Vergauwen, Bjorn" uniqKey="Vergauwen B" first="Bjorn" last="Vergauwen">Bjorn Vergauwen</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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