La maladie de Parkinson au Canada (serveur d'exploration)

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Identification of Candidate Adherent-Invasive E. coli Signature Transcripts by Genomic/Transcriptomic Analysis.

Identifieur interne : 000502 ( PubMed/Checkpoint ); précédent : 000501; suivant : 000503

Identification of Candidate Adherent-Invasive E. coli Signature Transcripts by Genomic/Transcriptomic Analysis.

Auteurs : Yuanhao Zhang [États-Unis] ; Leahana Rowehl [États-Unis] ; Julia M. Krumsiek [États-Unis] ; Erika P. Orner [États-Unis] ; Nurmohammad Shaikh [États-Unis] ; Phillip I. Tarr [États-Unis] ; Erica Sodergren [États-Unis] ; George M. Weinstock [États-Unis] ; Edgar C. Boedeker [États-Unis] ; Xuejian Xiong [Canada] ; John Parkinson [Canada] ; Daniel N. Frank [États-Unis] ; Ellen Li [États-Unis] ; Grace Gathungu [États-Unis]

Source :

RBID : pubmed:26125937

English descriptors

Abstract

Adherent-invasive Escherichia coli (AIEC) strains are detected more frequently within mucosal lesions of patients with Crohn's disease (CD). The AIEC phenotype consists of adherence and invasion of intestinal epithelial cells and survival within macrophages of these bacteria in vitro. Our aim was to identify candidate transcripts that distinguish AIEC from non-invasive E. coli (NIEC) strains and might be useful for rapid and accurate identification of AIEC by culture-independent technology. We performed comparative RNA-Sequence (RNASeq) analysis using AIEC strain LF82 and NIEC strain HS during exponential and stationary growth. Differential expression analysis of coding sequences (CDS) homologous to both strains demonstrated 224 and 241 genes with increased and decreased expression, respectively, in LF82 relative to HS. Transition metal transport and siderophore metabolism related pathway genes were up-regulated, while glycogen metabolic and oxidation-reduction related pathway genes were down-regulated, in LF82. Chemotaxis related transcripts were up-regulated in LF82 during the exponential phase, but flagellum-dependent motility pathway genes were down-regulated in LF82 during the stationary phase. CDS that mapped only to the LF82 genome accounted for 747 genes. We applied an in silico subtractive genomics approach to identify CDS specific to AIEC by incorporating the genomes of 10 other previously phenotyped NIEC. From this analysis, 166 CDS mapped to the LF82 genome and lacked homology to any of the 11 human NIEC strains. We compared these CDS across 13 AIEC, but none were homologous in each. Four LF82 gene loci belonging to clustered regularly interspaced short palindromic repeats region (CRISPR)--CRISPR-associated (Cas) genes were identified in 4 to 6 AIEC and absent from all non-pathogenic bacteria. As previously reported, AIEC strains were enriched for pdu operon genes. One CDS, encoding an excisionase, was shared by 9 AIEC strains. Reverse transcription quantitative polymerase chain reaction assays for 6 genes were conducted on fecal and ileal RNA samples from 22 inflammatory bowel disease (IBD), and 32 patients without IBD (non-IBD). The expression of Cas loci was detected in a higher proportion of CD than non-IBD fecal and ileal RNA samples (p <0.05). These results support a comparative genomic/transcriptomic approach towards identifying candidate AIEC signature transcripts.

DOI: 10.1371/journal.pone.0130902
PubMed: 26125937


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Le document en format XML

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<term>Crohn Disease (microbiology)</term>
<term>Down-Regulation (genetics)</term>
<term>Escherichia coli (genetics)</term>
<term>Escherichia coli Infections (microbiology)</term>
<term>Genome, Bacterial (genetics)</term>
<term>Genomics</term>
<term>Humans</term>
<term>Ileum (microbiology)</term>
<term>Intestinal Mucosa (microbiology)</term>
<term>Macrophages (microbiology)</term>
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<div type="abstract" xml:lang="en">Adherent-invasive Escherichia coli (AIEC) strains are detected more frequently within mucosal lesions of patients with Crohn's disease (CD). The AIEC phenotype consists of adherence and invasion of intestinal epithelial cells and survival within macrophages of these bacteria in vitro. Our aim was to identify candidate transcripts that distinguish AIEC from non-invasive E. coli (NIEC) strains and might be useful for rapid and accurate identification of AIEC by culture-independent technology. We performed comparative RNA-Sequence (RNASeq) analysis using AIEC strain LF82 and NIEC strain HS during exponential and stationary growth. Differential expression analysis of coding sequences (CDS) homologous to both strains demonstrated 224 and 241 genes with increased and decreased expression, respectively, in LF82 relative to HS. Transition metal transport and siderophore metabolism related pathway genes were up-regulated, while glycogen metabolic and oxidation-reduction related pathway genes were down-regulated, in LF82. Chemotaxis related transcripts were up-regulated in LF82 during the exponential phase, but flagellum-dependent motility pathway genes were down-regulated in LF82 during the stationary phase. CDS that mapped only to the LF82 genome accounted for 747 genes. We applied an in silico subtractive genomics approach to identify CDS specific to AIEC by incorporating the genomes of 10 other previously phenotyped NIEC. From this analysis, 166 CDS mapped to the LF82 genome and lacked homology to any of the 11 human NIEC strains. We compared these CDS across 13 AIEC, but none were homologous in each. Four LF82 gene loci belonging to clustered regularly interspaced short palindromic repeats region (CRISPR)--CRISPR-associated (Cas) genes were identified in 4 to 6 AIEC and absent from all non-pathogenic bacteria. As previously reported, AIEC strains were enriched for pdu operon genes. One CDS, encoding an excisionase, was shared by 9 AIEC strains. Reverse transcription quantitative polymerase chain reaction assays for 6 genes were conducted on fecal and ileal RNA samples from 22 inflammatory bowel disease (IBD), and 32 patients without IBD (non-IBD). The expression of Cas loci was detected in a higher proportion of CD than non-IBD fecal and ileal RNA samples (p <0.05). These results support a comparative genomic/transcriptomic approach towards identifying candidate AIEC signature transcripts.</div>
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</DateCompleted>
<DateRevised>
<Year>2016</Year>
<Month>10</Month>
<Day>19</Day>
</DateRevised>
<Article PubModel="Electronic-eCollection">
<Journal>
<ISSN IssnType="Electronic">1932-6203</ISSN>
<JournalIssue CitedMedium="Internet">
<Volume>10</Volume>
<Issue>6</Issue>
<PubDate>
<Year>2015</Year>
</PubDate>
</JournalIssue>
<Title>PloS one</Title>
<ISOAbbreviation>PLoS ONE</ISOAbbreviation>
</Journal>
<ArticleTitle>Identification of Candidate Adherent-Invasive E. coli Signature Transcripts by Genomic/Transcriptomic Analysis.</ArticleTitle>
<Pagination>
<MedlinePgn>e0130902</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0130902</ELocationID>
<Abstract>
<AbstractText>Adherent-invasive Escherichia coli (AIEC) strains are detected more frequently within mucosal lesions of patients with Crohn's disease (CD). The AIEC phenotype consists of adherence and invasion of intestinal epithelial cells and survival within macrophages of these bacteria in vitro. Our aim was to identify candidate transcripts that distinguish AIEC from non-invasive E. coli (NIEC) strains and might be useful for rapid and accurate identification of AIEC by culture-independent technology. We performed comparative RNA-Sequence (RNASeq) analysis using AIEC strain LF82 and NIEC strain HS during exponential and stationary growth. Differential expression analysis of coding sequences (CDS) homologous to both strains demonstrated 224 and 241 genes with increased and decreased expression, respectively, in LF82 relative to HS. Transition metal transport and siderophore metabolism related pathway genes were up-regulated, while glycogen metabolic and oxidation-reduction related pathway genes were down-regulated, in LF82. Chemotaxis related transcripts were up-regulated in LF82 during the exponential phase, but flagellum-dependent motility pathway genes were down-regulated in LF82 during the stationary phase. CDS that mapped only to the LF82 genome accounted for 747 genes. We applied an in silico subtractive genomics approach to identify CDS specific to AIEC by incorporating the genomes of 10 other previously phenotyped NIEC. From this analysis, 166 CDS mapped to the LF82 genome and lacked homology to any of the 11 human NIEC strains. We compared these CDS across 13 AIEC, but none were homologous in each. Four LF82 gene loci belonging to clustered regularly interspaced short palindromic repeats region (CRISPR)--CRISPR-associated (Cas) genes were identified in 4 to 6 AIEC and absent from all non-pathogenic bacteria. As previously reported, AIEC strains were enriched for pdu operon genes. One CDS, encoding an excisionase, was shared by 9 AIEC strains. Reverse transcription quantitative polymerase chain reaction assays for 6 genes were conducted on fecal and ileal RNA samples from 22 inflammatory bowel disease (IBD), and 32 patients without IBD (non-IBD). The expression of Cas loci was detected in a higher proportion of CD than non-IBD fecal and ileal RNA samples (p <0.05). These results support a comparative genomic/transcriptomic approach towards identifying candidate AIEC signature transcripts.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y">
<Author ValidYN="Y">
<LastName>Zhang</LastName>
<ForeName>Yuanhao</ForeName>
<Initials>Y</Initials>
<AffiliationInfo>
<Affiliation>Department of Applied Mathematics and Statistics, Stony Brook University, Stony Brook, New York, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Rowehl</LastName>
<ForeName>Leahana</ForeName>
<Initials>L</Initials>
<AffiliationInfo>
<Affiliation>Department of Medicine, Stony Brook University, Stony Brook, New York, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Krumsiek</LastName>
<ForeName>Julia M</ForeName>
<Initials>JM</Initials>
<AffiliationInfo>
<Affiliation>Department of Pediatrics, Stony Brook University, Stony Brook, New York, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Orner</LastName>
<ForeName>Erika P</ForeName>
<Initials>EP</Initials>
<AffiliationInfo>
<Affiliation>Department of Medicine, Stony Brook University, Stony Brook, New York, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Shaikh</LastName>
<ForeName>Nurmohammad</ForeName>
<Initials>N</Initials>
<AffiliationInfo>
<Affiliation>Department of Pediatrics, Washington University St. Louis, St. Louis, Missouri, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Tarr</LastName>
<ForeName>Phillip I</ForeName>
<Initials>PI</Initials>
<AffiliationInfo>
<Affiliation>Department of Pediatrics, Washington University St. Louis, St. Louis, Missouri, United States of America; Department of Molecular Microbiology, Washington University St. Louis, St. Louis, Missouri, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Sodergren</LastName>
<ForeName>Erica</ForeName>
<Initials>E</Initials>
<AffiliationInfo>
<Affiliation>The Genome Institute, Washington University St. Louis, St. Louis, Missouri, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Weinstock</LastName>
<ForeName>George M</ForeName>
<Initials>GM</Initials>
<AffiliationInfo>
<Affiliation>The Genome Institute, Washington University St. Louis, St. Louis, Missouri, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Boedeker</LastName>
<ForeName>Edgar C</ForeName>
<Initials>EC</Initials>
<AffiliationInfo>
<Affiliation>Department of Medicine, University of New Mexico, Albuquerque, New Mexico, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Xiong</LastName>
<ForeName>Xuejian</ForeName>
<Initials>X</Initials>
<AffiliationInfo>
<Affiliation>Program in Molecular Structure and Function, The Hospital for Sick Children, Toronto, Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Parkinson</LastName>
<ForeName>John</ForeName>
<Initials>J</Initials>
<AffiliationInfo>
<Affiliation>Department of Biochemistry & Molecular and Medical Genetics, University of Toronto, Toronto, Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Frank</LastName>
<ForeName>Daniel N</ForeName>
<Initials>DN</Initials>
<AffiliationInfo>
<Affiliation>Department of Medicine, University of Colorado, Denver, Colorado, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Li</LastName>
<ForeName>Ellen</ForeName>
<Initials>E</Initials>
<AffiliationInfo>
<Affiliation>Department of Medicine, Stony Brook University, Stony Brook, New York, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Gathungu</LastName>
<ForeName>Grace</ForeName>
<Initials>G</Initials>
<AffiliationInfo>
<Affiliation>Department of Pediatrics, Stony Brook University, Stony Brook, New York, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y">
<Grant>
<GrantID>5P30 DK052574</GrantID>
<Acronym>DK</Acronym>
<Agency>NIDDK 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>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic">
<Year>2015</Year>
<Month>06</Month>
<Day>30</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo>
<Country>United States</Country>
<MedlineTA>PLoS One</MedlineTA>
<NlmUniqueID>101285081</NlmUniqueID>
<ISSNLinking>1932-6203</ISSNLinking>
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<ChemicalList>
<Chemical>
<RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D012329">RNA, Bacterial</NameOfSubstance>
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<MeshHeadingList>
<MeshHeading>
<DescriptorName UI="D001422" MajorTopicYN="N">Bacterial Adhesion</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D003424" MajorTopicYN="N">Crohn Disease</DescriptorName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D015536" MajorTopicYN="N">Down-Regulation</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D004926" MajorTopicYN="N">Escherichia coli</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D004927" MajorTopicYN="N">Escherichia coli Infections</DescriptorName>
<QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D016680" MajorTopicYN="N">Genome, Bacterial</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D023281" MajorTopicYN="N">Genomics</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D007082" MajorTopicYN="N">Ileum</DescriptorName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D007413" MajorTopicYN="N">Intestinal Mucosa</DescriptorName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D012329" MajorTopicYN="N">RNA, Bacterial</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D017423" MajorTopicYN="N">Sequence Analysis, RNA</DescriptorName>
<QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D059467" MajorTopicYN="N">Transcriptome</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D015854" MajorTopicYN="N">Up-Regulation</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
</MeshHeadingList>
<OtherID Source="NLM">PMC4509574</OtherID>
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<PubmedData>
<History>
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<Year>2015</Year>
<Month>02</Month>
<Day>27</Day>
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<ArticleId IdType="pmc">PMC4509574</ArticleId>
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<li>Colorado</li>
<li>Missouri (État)</li>
<li>Nouveau-Mexique</li>
<li>Ontario</li>
<li>État de New York</li>
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<li>Toronto</li>
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<li>Université de Toronto</li>
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<name sortKey="Boedeker, Edgar C" sort="Boedeker, Edgar C" uniqKey="Boedeker E" first="Edgar C" last="Boedeker">Edgar C. Boedeker</name>
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<name sortKey="Shaikh, Nurmohammad" sort="Shaikh, Nurmohammad" uniqKey="Shaikh N" first="Nurmohammad" last="Shaikh">Nurmohammad Shaikh</name>
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<name sortKey="Tarr, Phillip I" sort="Tarr, Phillip I" uniqKey="Tarr P" first="Phillip I" last="Tarr">Phillip I. Tarr</name>
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<name sortKey="Parkinson, John" sort="Parkinson, John" uniqKey="Parkinson J" first="John" last="Parkinson">John Parkinson</name>
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