Overlapping and complementary oxidative stress defense mechanisms in nontypeable Haemophilus influenzae.
Identifieur interne : 000524 ( Main/Exploration ); précédent : 000523; suivant : 000525Overlapping and complementary oxidative stress defense mechanisms in nontypeable Haemophilus influenzae.
Auteurs : Alistair Harrison ; Beth D. Baker [États-Unis] ; Robert S. Munson [États-Unis]Source :
- Journal of bacteriology [ 1098-5530 ] ; 2015.
Descripteurs français
- KwdFr :
- Catalase (métabolisme), Fer (métabolisme), Haemophilus influenzae (effets des médicaments et des substances chimiques), Haemophilus influenzae (métabolisme), Oxydants (pharmacologie), Peroxyde d'hydrogène (pharmacologie), Protéines bactériennes (métabolisme), Stress oxydatif (effets des médicaments et des substances chimiques).
- MESH :
- effets des médicaments et des substances chimiques : Haemophilus influenzae, Stress oxydatif.
- métabolisme : Catalase, Fer, Haemophilus influenzae, Protéines bactériennes.
- pharmacologie : Oxydants, Peroxyde d'hydrogène.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Bacterial Proteins, Catalase, Iron.
- drug effects : Haemophilus influenzae, Oxidative Stress.
- metabolism : Haemophilus influenzae.
- chemical , pharmacology : Hydrogen Peroxide, Oxidants.
Abstract
The Gram-negative commensal bacterium nontypeable Haemophilus influenzae (NTHI) can cause respiratory tract diseases that include otitis media, sinusitis, exacerbations of chronic obstructive pulmonary disease, and bronchitis. During colonization and infection, NTHI withstands oxidative stress generated by reactive oxygen species produced endogenously, by the host, and by other copathogens and flora. These reactive oxygen species include superoxide, hydrogen peroxide (H2O2), and hydroxyl radicals, whose killing is amplified by iron via the Fenton reaction. We previously identified genes that encode proteins with putative roles in protection of the NTHI isolate strain 86-028NP against oxidative stress. These include catalase (HktE), peroxiredoxin/glutaredoxin (PgdX), and a ferritin-like protein (Dps). Strains were generated with mutations in hktE, pgdX, and dps. The hktE mutant and a pgdX hktE double mutant were more sensitive than the parent to killing by H2O2. Conversely, the pgdX mutant was more resistant to H2O2 due to increased catalase activity. Supporting the role of killing via the Fenton reaction, binding of iron by Dps significantly mitigated the effect of H2O2-mediated killing. NTHI thus utilizes several effectors to resist oxidative stress, and regulation of free iron is critical to this protection. These mechanisms will be important for successful colonization and infection by this opportunistic human pathogen.
DOI: 10.1128/JB.01973-14
PubMed: 25368297
PubMed Central: PMC4272597
Affiliations:
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Baker</name><affiliation wicri:level="2"><nlm:affiliation>The Center for Microbial Pathogenesis at the Research Institute at Nationwide Children's Hospital and the Center for Microbial Interface Biology and Department of Pediatrics, The Ohio State University, Ohio, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>The Center for Microbial Pathogenesis at the Research Institute at Nationwide Children's Hospital and the Center for Microbial Interface Biology and Department of Pediatrics, The Ohio State University, Ohio</wicri:regionArea><placeName><region type="state">Ohio</region></placeName></affiliation></author><author><name sortKey="Munson, Robert S" sort="Munson, Robert S" uniqKey="Munson R" first="Robert S" last="Munson">Robert S. Munson</name><affiliation wicri:level="2"><nlm:affiliation>The Center for Microbial Pathogenesis at the Research Institute at Nationwide Children's Hospital and the Center for Microbial Interface Biology and Department of Pediatrics, The Ohio State University, Ohio, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>The Center for Microbial Pathogenesis at the Research Institute at Nationwide Children's Hospital and the Center for Microbial Interface Biology and Department of Pediatrics, The Ohio State University, Ohio</wicri:regionArea><placeName><region type="state">Ohio</region></placeName></affiliation></author></analytic><series><title level="j">Journal of bacteriology</title><idno type="eISSN">1098-5530</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Bacterial Proteins (metabolism)</term><term>Catalase (metabolism)</term><term>Haemophilus influenzae (drug effects)</term><term>Haemophilus influenzae (metabolism)</term><term>Hydrogen Peroxide (pharmacology)</term><term>Iron (metabolism)</term><term>Oxidants (pharmacology)</term><term>Oxidative Stress (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Catalase (métabolisme)</term><term>Fer (métabolisme)</term><term>Haemophilus influenzae (effets des médicaments et des substances chimiques)</term><term>Haemophilus influenzae (métabolisme)</term><term>Oxydants (pharmacologie)</term><term>Peroxyde d'hydrogène (pharmacologie)</term><term>Protéines bactériennes (métabolisme)</term><term>Stress oxydatif (effets des médicaments et des substances chimiques)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Bacterial Proteins</term><term>Catalase</term><term>Iron</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Haemophilus influenzae</term><term>Oxidative Stress</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Haemophilus influenzae</term><term>Stress oxydatif</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Haemophilus influenzae</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Catalase</term><term>Fer</term><term>Haemophilus influenzae</term><term>Protéines bactériennes</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Oxydants</term><term>Peroxyde d'hydrogène</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Hydrogen Peroxide</term><term>Oxidants</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The Gram-negative commensal bacterium nontypeable Haemophilus influenzae (NTHI) can cause respiratory tract diseases that include otitis media, sinusitis, exacerbations of chronic obstructive pulmonary disease, and bronchitis. During colonization and infection, NTHI withstands oxidative stress generated by reactive oxygen species produced endogenously, by the host, and by other copathogens and flora. These reactive oxygen species include superoxide, hydrogen peroxide (H2O2), and hydroxyl radicals, whose killing is amplified by iron via the Fenton reaction. We previously identified genes that encode proteins with putative roles in protection of the NTHI isolate strain 86-028NP against oxidative stress. These include catalase (HktE), peroxiredoxin/glutaredoxin (PgdX), and a ferritin-like protein (Dps). Strains were generated with mutations in hktE, pgdX, and dps. The hktE mutant and a pgdX hktE double mutant were more sensitive than the parent to killing by H2O2. Conversely, the pgdX mutant was more resistant to H2O2 due to increased catalase activity. Supporting the role of killing via the Fenton reaction, binding of iron by Dps significantly mitigated the effect of H2O2-mediated killing. NTHI thus utilizes several effectors to resist oxidative stress, and regulation of free iron is critical to this protection. These mechanisms will be important for successful colonization and infection by this opportunistic human pathogen. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25368297</PMID><DateCompleted><Year>2015</Year><Month>02</Month><Day>25</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5530</ISSN><JournalIssue CitedMedium="Internet"><Volume>197</Volume><Issue>2</Issue><PubDate><Year>2015</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Journal of bacteriology</Title><ISOAbbreviation>J Bacteriol</ISOAbbreviation></Journal><ArticleTitle>Overlapping and complementary oxidative stress defense mechanisms in nontypeable Haemophilus influenzae.</ArticleTitle><Pagination><MedlinePgn>277-85</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/JB.01973-14</ELocationID><Abstract><AbstractText>The Gram-negative commensal bacterium nontypeable Haemophilus influenzae (NTHI) can cause respiratory tract diseases that include otitis media, sinusitis, exacerbations of chronic obstructive pulmonary disease, and bronchitis. During colonization and infection, NTHI withstands oxidative stress generated by reactive oxygen species produced endogenously, by the host, and by other copathogens and flora. These reactive oxygen species include superoxide, hydrogen peroxide (H2O2), and hydroxyl radicals, whose killing is amplified by iron via the Fenton reaction. We previously identified genes that encode proteins with putative roles in protection of the NTHI isolate strain 86-028NP against oxidative stress. These include catalase (HktE), peroxiredoxin/glutaredoxin (PgdX), and a ferritin-like protein (Dps). Strains were generated with mutations in hktE, pgdX, and dps. The hktE mutant and a pgdX hktE double mutant were more sensitive than the parent to killing by H2O2. Conversely, the pgdX mutant was more resistant to H2O2 due to increased catalase activity. Supporting the role of killing via the Fenton reaction, binding of iron by Dps significantly mitigated the effect of H2O2-mediated killing. NTHI thus utilizes several effectors to resist oxidative stress, and regulation of free iron is critical to this protection. These mechanisms will be important for successful colonization and infection by this opportunistic human pathogen. </AbstractText><CopyrightInformation>Copyright © 2015, American Society for Microbiology. All Rights Reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Harrison</LastName><ForeName>Alistair</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>The Center for Microbial Pathogenesis at the Research Institute at Nationwide Children's Hospital and the Center for Microbial Interface Biology and Department of Pediatrics, The Ohio State University, Ohio, USA alistair.harrison@nationwidechildrens.org.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Baker</LastName><ForeName>Beth D</ForeName><Initials>BD</Initials><AffiliationInfo><Affiliation>The Center for Microbial Pathogenesis at the Research Institute at Nationwide Children's Hospital and the Center for Microbial Interface Biology and Department of Pediatrics, The Ohio State University, Ohio, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Munson</LastName><ForeName>Robert S</ForeName><Initials>RS</Initials><Suffix>Jr</Suffix><AffiliationInfo><Affiliation>The Center for Microbial Pathogenesis at the Research Institute at Nationwide Children's Hospital and the Center for Microbial Interface Biology and Department of Pediatrics, The Ohio State University, Ohio, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 AI077897</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01-AI077897</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>11</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Bacteriol</MedlineTA><NlmUniqueID>2985120R</NlmUniqueID><ISSNLinking>0021-9193</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001426">Bacterial Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016877">Oxidants</NameOfSubstance></Chemical><Chemical><RegistryNumber>BBX060AN9V</RegistryNumber><NameOfSubstance UI="D006861">Hydrogen Peroxide</NameOfSubstance></Chemical><Chemical><RegistryNumber>E1UOL152H7</RegistryNumber><NameOfSubstance UI="D007501">Iron</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.11.1.6</RegistryNumber><NameOfSubstance UI="D002374">Catalase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001426" 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