GlutaredoxinV1, Main, Exploration, bibRecord, 000856

Haemophilus influenzae OxyR: characterization of its regulation, regulon and role in fitness.

Identifieur interne : 000856 ( Main/Exploration ); précédent : 000855; suivant : 000857

Haemophilus influenzae OxyR: characterization of its regulation, regulon and role in fitness.

Auteurs : Paul W. Whitby [États-Unis] ; Daniel J. Morton ; Timothy M. Vanwagoner ; Thomas W. Seale ; Brett K. Cole ; Huda J. Mussa ; Phillip A. Mcghee ; Chee Yoon S. Bauer ; Jennifer M. Springer ; Terrence L. Stull

Source :

PloS one [ 1932-6203 ] ; 2012.

RBID : pubmed:23226321

Descripteurs français

KwdFr :
- Animaux (MeSH), Bactériémie (microbiologie), Catalase (métabolisme), Cinétique (MeSH), Espace intracellulaire (métabolisme), Femelle (MeSH), Fer (métabolisme), Grossesse (MeSH), Haemophilus influenzae (cytologie), Haemophilus influenzae (génétique), Haemophilus influenzae (métabolisme), Haemophilus influenzae (physiologie), Hème (métabolisme), Mutation (MeSH), Otite moyenne (microbiologie), Peroxirédoxines (métabolisme), Protéines bactériennes (génétique), Protéines bactériennes (métabolisme), Rats (MeSH), Régulation de l'expression des gènes bactériens (MeSH), Régulon (MeSH), Spécificité d'espèce (MeSH), Stress oxydatif (génétique), Transcription génétique (MeSH).
MESH :
- cytologie : Haemophilus influenzae.
- génétique : Haemophilus influenzae, Protéines bactériennes, Stress oxydatif.
- microbiologie : Bactériémie, Otite moyenne.
- métabolisme : Catalase, Espace intracellulaire, Fer, Haemophilus influenzae, Hème, Peroxirédoxines, Protéines bactériennes.
- physiologie : Haemophilus influenzae.
- Animaux, Cinétique, Femelle, Grossesse, Mutation, Rats, Régulation de l'expression des gènes bactériens, Régulon, Spécificité d'espèce, Transcription génétique.

English descriptors

KwdEn :
- Animals (MeSH), Bacteremia (microbiology), Bacterial Proteins (genetics), Bacterial Proteins (metabolism), Catalase (metabolism), Female (MeSH), Gene Expression Regulation, Bacterial (MeSH), Haemophilus influenzae (cytology), Haemophilus influenzae (genetics), Haemophilus influenzae (metabolism), Haemophilus influenzae (physiology), Heme (metabolism), Intracellular Space (metabolism), Iron (metabolism), Kinetics (MeSH), Mutation (MeSH), Otitis Media (microbiology), Oxidative Stress (genetics), Peroxiredoxins (metabolism), Pregnancy (MeSH), Rats (MeSH), Regulon (MeSH), Species Specificity (MeSH), Transcription, Genetic (MeSH).
MESH :
- chemical , genetics : Bacterial Proteins.
- chemical , metabolism : Bacterial Proteins, Catalase, Heme, Iron, Peroxiredoxins.
- cytology : Haemophilus influenzae.
- genetics : Haemophilus influenzae, Oxidative Stress.
- metabolism : Haemophilus influenzae, Intracellular Space.
- microbiology : Bacteremia, Otitis Media.
- physiology : Haemophilus influenzae.
- Animals, Female, Gene Expression Regulation, Bacterial, Kinetics, Mutation, Pregnancy, Rats, Regulon, Species Specificity, Transcription, Genetic.

Abstract

To prevent damage by reactive oxygen species, many bacteria have evolved rapid detection and response systems, including the OxyR regulon. The OxyR system detects reactive oxygen and coordinates the expression of numerous defensive antioxidants. In many bacterial species the coordinated OxyR-regulated response is crucial for in vivo survival. Regulation of the OxyR regulon of Haemophilus influenzae was examined in vitro, and significant variation in the regulated genes of the OxyR regulon among strains of H. influenzae was observed. Quantitative PCR studies demonstrated a role for the OxyR-regulated peroxiredoxin/glutaredoxin as a mediator of the OxyR response, and also indicated OxyR self-regulation through a negative feedback loop. Analysis of transcript levels in H. influenzae samples derived from an animal model of otitis media demonstrated that the members of the OxyR regulon were actively upregulated within the chinchilla middle ear. H. influenzae mutants lacking the oxyR gene exhibited increased sensitivity to challenge with various peroxides. The impact of mutations in oxyR was assessed in various animal models of H. influenzae disease. In paired comparisons with the corresponding wild-type strains, the oxyR mutants were unaffected in both the chinchilla model of otitis media and an infant model of bacteremia. However, in weanling rats the oxyR mutant was significantly impaired compared to the wild-type strain. In contrast, in all three animal models when infected with a mixture of equal numbers of both wild-type and mutant strains the mutant strain was significantly out competed by the wild-type strain. These findings clearly establish a crucial role for OxyR in bacterial fitness.

DOI: 10.1371/journal.pone.0050588
PubMed: 23226321
PubMed Central: PMC3511568

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Bacteremia (microbiology)</term>
<term>Bacterial Proteins (genetics)</term>
<term>Bacterial Proteins (metabolism)</term>
<term>Catalase (metabolism)</term>
<term>Female (MeSH)</term>
<term>Gene Expression Regulation, Bacterial (MeSH)</term>
<term>Haemophilus influenzae (cytology)</term>
<term>Haemophilus influenzae (genetics)</term>
<term>Haemophilus influenzae (metabolism)</term>
<term>Haemophilus influenzae (physiology)</term>
<term>Heme (metabolism)</term>
<term>Intracellular Space (metabolism)</term>
<term>Iron (metabolism)</term>
<term>Kinetics (MeSH)</term>
<term>Mutation (MeSH)</term>
<term>Otitis Media (microbiology)</term>
<term>Oxidative Stress (genetics)</term>
<term>Peroxiredoxins (metabolism)</term>
<term>Pregnancy (MeSH)</term>
<term>Rats (MeSH)</term>
<term>Regulon (MeSH)</term>
<term>Species Specificity (MeSH)</term>
<term>Transcription, Genetic (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Bactériémie (microbiologie)</term>
<term>Catalase (métabolisme)</term>
<term>Cinétique (MeSH)</term>
<term>Espace intracellulaire (métabolisme)</term>
<term>Femelle (MeSH)</term>
<term>Fer (métabolisme)</term>
<term>Grossesse (MeSH)</term>
<term>Haemophilus influenzae (cytologie)</term>
<term>Haemophilus influenzae (génétique)</term>
<term>Haemophilus influenzae (métabolisme)</term>
<term>Haemophilus influenzae (physiologie)</term>
<term>Hème (métabolisme)</term>
<term>Mutation (MeSH)</term>
<term>Otite moyenne (microbiologie)</term>
<term>Peroxirédoxines (métabolisme)</term>
<term>Protéines bactériennes (génétique)</term>
<term>Protéines bactériennes (métabolisme)</term>
<term>Rats (MeSH)</term>
<term>Régulation de l'expression des gènes bactériens (MeSH)</term>
<term>Régulon (MeSH)</term>
<term>Spécificité d'espèce (MeSH)</term>
<term>Stress oxydatif (génétique)</term>
<term>Transcription génétique (MeSH)</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Bacterial Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Bacterial Proteins</term>
<term>Catalase</term>
<term>Heme</term>
<term>Iron</term>
<term>Peroxiredoxins</term>
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<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Haemophilus influenzae</term>
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<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Haemophilus influenzae</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Haemophilus influenzae</term>
<term>Oxidative Stress</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Haemophilus influenzae</term>
<term>Protéines bactériennes</term>
<term>Stress oxydatif</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Haemophilus influenzae</term>
<term>Intracellular Space</term>
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<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Bactériémie</term>
<term>Otite moyenne</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Bacteremia</term>
<term>Otitis Media</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Catalase</term>
<term>Espace intracellulaire</term>
<term>Fer</term>
<term>Haemophilus influenzae</term>
<term>Hème</term>
<term>Peroxirédoxines</term>
<term>Protéines bactériennes</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Haemophilus influenzae</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Haemophilus influenzae</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Female</term>
<term>Gene Expression Regulation, Bacterial</term>
<term>Kinetics</term>
<term>Mutation</term>
<term>Pregnancy</term>
<term>Rats</term>
<term>Regulon</term>
<term>Species Specificity</term>
<term>Transcription, Genetic</term>
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<term>Cinétique</term>
<term>Femelle</term>
<term>Grossesse</term>
<term>Mutation</term>
<term>Rats</term>
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<front><div type="abstract" xml:lang="en">To prevent damage by reactive oxygen species, many bacteria have evolved rapid detection and response systems, including the OxyR regulon. The OxyR system detects reactive oxygen and coordinates the expression of numerous defensive antioxidants. In many bacterial species the coordinated OxyR-regulated response is crucial for in vivo survival. Regulation of the OxyR regulon of Haemophilus influenzae was examined in vitro, and significant variation in the regulated genes of the OxyR regulon among strains of H. influenzae was observed. Quantitative PCR studies demonstrated a role for the OxyR-regulated peroxiredoxin/glutaredoxin as a mediator of the OxyR response, and also indicated OxyR self-regulation through a negative feedback loop. Analysis of transcript levels in H. influenzae samples derived from an animal model of otitis media demonstrated that the members of the OxyR regulon were actively upregulated within the chinchilla middle ear. H. influenzae mutants lacking the oxyR gene exhibited increased sensitivity to challenge with various peroxides. The impact of mutations in oxyR was assessed in various animal models of H. influenzae disease. In paired comparisons with the corresponding wild-type strains, the oxyR mutants were unaffected in both the chinchilla model of otitis media and an infant model of bacteremia. However, in weanling rats the oxyR mutant was significantly impaired compared to the wild-type strain. In contrast, in all three animal models when infected with a mixture of equal numbers of both wild-type and mutant strains the mutant strain was significantly out competed by the wild-type strain. These findings clearly establish a crucial role for OxyR in bacterial fitness.</div>
</front>
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<ArticleTitle>Haemophilus influenzae OxyR: characterization of its regulation, regulon and role in fitness.</ArticleTitle>
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<Abstract><AbstractText>To prevent damage by reactive oxygen species, many bacteria have evolved rapid detection and response systems, including the OxyR regulon. The OxyR system detects reactive oxygen and coordinates the expression of numerous defensive antioxidants. In many bacterial species the coordinated OxyR-regulated response is crucial for in vivo survival. Regulation of the OxyR regulon of Haemophilus influenzae was examined in vitro, and significant variation in the regulated genes of the OxyR regulon among strains of H. influenzae was observed. Quantitative PCR studies demonstrated a role for the OxyR-regulated peroxiredoxin/glutaredoxin as a mediator of the OxyR response, and also indicated OxyR self-regulation through a negative feedback loop. Analysis of transcript levels in H. influenzae samples derived from an animal model of otitis media demonstrated that the members of the OxyR regulon were actively upregulated within the chinchilla middle ear. H. influenzae mutants lacking the oxyR gene exhibited increased sensitivity to challenge with various peroxides. The impact of mutations in oxyR was assessed in various animal models of H. influenzae disease. In paired comparisons with the corresponding wild-type strains, the oxyR mutants were unaffected in both the chinchilla model of otitis media and an infant model of bacteremia. However, in weanling rats the oxyR mutant was significantly impaired compared to the wild-type strain. In contrast, in all three animal models when infected with a mixture of equal numbers of both wild-type and mutant strains the mutant strain was significantly out competed by the wild-type strain. These findings clearly establish a crucial role for OxyR in bacterial fitness.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Whitby</LastName>
<ForeName>Paul W</ForeName>
<Initials>PW</Initials>
<AffiliationInfo><Affiliation>Department of Pediatrics, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America. pwhitby@ouhsc.edu</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Morton</LastName>
<ForeName>Daniel J</ForeName>
<Initials>DJ</Initials>
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<Author ValidYN="Y"><LastName>Vanwagoner</LastName>
<ForeName>Timothy M</ForeName>
<Initials>TM</Initials>
</Author>
<Author ValidYN="Y"><LastName>Seale</LastName>
<ForeName>Thomas W</ForeName>
<Initials>TW</Initials>
</Author>
<Author ValidYN="Y"><LastName>Cole</LastName>
<ForeName>Brett K</ForeName>
<Initials>BK</Initials>
</Author>
<Author ValidYN="Y"><LastName>Mussa</LastName>
<ForeName>Huda J</ForeName>
<Initials>HJ</Initials>
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<Author ValidYN="Y"><LastName>McGhee</LastName>
<ForeName>Phillip A</ForeName>
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<Author ValidYN="Y"><LastName>Bauer</LastName>
<ForeName>Chee Yoon S</ForeName>
<Initials>CY</Initials>
</Author>
<Author ValidYN="Y"><LastName>Springer</LastName>
<ForeName>Jennifer M</ForeName>
<Initials>JM</Initials>
</Author>
<Author ValidYN="Y"><LastName>Stull</LastName>
<ForeName>Terrence L</ForeName>
<Initials>TL</Initials>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016470" MajorTopicYN="N">Bacteremia</DescriptorName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001426" MajorTopicYN="N">Bacterial Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002374" MajorTopicYN="N">Catalase</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015964" MajorTopicYN="Y">Gene Expression Regulation, Bacterial</DescriptorName>
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<MeshHeading><DescriptorName UI="D006193" MajorTopicYN="N">Haemophilus influenzae</DescriptorName>
<QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006418" MajorTopicYN="N">Heme</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<MeshHeading><DescriptorName UI="D042541" MajorTopicYN="N">Intracellular Space</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007501" MajorTopicYN="N">Iron</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007700" MajorTopicYN="N">Kinetics</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010033" MajorTopicYN="N">Otitis Media</DescriptorName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054464" MajorTopicYN="N">Peroxiredoxins</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
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Haemophilus influenzae OxyR: characterization of its regulation, regulon and role in fitness.

Haemophilus influenzae OxyR: characterization of its regulation, regulon and role in fitness.

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