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Comparative genomics of Crohn's disease-associated adherent-invasive Escherichia coli.

Identifieur interne : 003564 ( Ncbi/Merge ); précédent : 003563; suivant : 003565

Comparative genomics of Crohn's disease-associated adherent-invasive Escherichia coli.

Auteurs : Claire L. O'Brien [Australie] ; Marie-Agnès Bringer [France] ; Kathryn E. Holt [Australie] ; David M. Gordon [Australie] ; Anaëlle L. Dubois [France] ; Nicolas Barnich [France] ; Arlette Darfeuille-Michaud [France] ; Paul Pavli [Australie]

Source :

RBID : pubmed:27196580

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English descriptors

Abstract

Adherent-invasive Escherichia coli (AIEC) are a leading candidate bacterial trigger for Crohn's disease (CD). The AIEC pathovar is defined by in vitro cell-line assays examining specific bacteria/cell interactions. No molecular marker exists for their identification. Our aim was to identify a molecular property common to the AIEC phenotype.

DOI: 10.1136/gutjnl-2015-311059
PubMed: 27196580

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pubmed:27196580

Le document en format XML

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<term>Cell Line</term>
<term>Clustered Regularly Interspaced Short Palindromic Repeats</term>
<term>Crohn Disease (microbiology)</term>
<term>Cytokines (secretion)</term>
<term>DNA, Bacterial (analysis)</term>
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<term>Escherichia coli (genetics)</term>
<term>Escherichia coli (growth & development)</term>
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<term>Genome</term>
<term>Host-Pathogen Interactions</term>
<term>Humans</term>
<term>Interleukin-10 (secretion)</term>
<term>Interleukin-6 (secretion)</term>
<term>Interleukin-8 (secretion)</term>
<term>Macrophages (microbiology)</term>
<term>Macrophages (secretion)</term>
<term>Phenotype</term>
<term>Phylogeny</term>
<term>Sequence Analysis, DNA</term>
<term>Tumor Necrosis Factor-alpha (secretion)</term>
</keywords>
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<term>ADN bactérien (analyse)</term>
<term>Adhérence bactérienne</term>
<term>Analyse de séquence d'ADN</term>
<term>Cellules épithéliales (microbiologie)</term>
<term>Clustered regularly interspaced short palindromic repeats</term>
<term>Cytokines (sécrétion)</term>
<term>Escherichia coli (croissance et développement)</term>
<term>Escherichia coli (génétique)</term>
<term>Facteur de nécrose tumorale alpha (sécrétion)</term>
<term>Génome</term>
<term>Humains</term>
<term>Infections à Escherichia coli ()</term>
<term>Interactions hôte-pathogène</term>
<term>Interleukine-10 (sécrétion)</term>
<term>Interleukine-6 (sécrétion)</term>
<term>Interleukine-8 (sécrétion)</term>
<term>Lignée cellulaire</term>
<term>Macrophages (microbiologie)</term>
<term>Macrophages (sécrétion)</term>
<term>Maladie de Crohn (microbiologie)</term>
<term>Phylogénie</term>
<term>Phénotype</term>
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<term>DNA, Bacterial</term>
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<term>Interleukin-10</term>
<term>Interleukin-6</term>
<term>Interleukin-8</term>
<term>Tumor Necrosis Factor-alpha</term>
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<term>ADN bactérien</term>
</keywords>
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<term>Escherichia coli Infections</term>
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<term>Escherichia coli</term>
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<term>Escherichia coli</term>
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<term>Escherichia coli</term>
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<term>Escherichia coli</term>
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<term>Cellules épithéliales</term>
<term>Macrophages</term>
<term>Maladie de Crohn</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en">
<term>Crohn Disease</term>
<term>Epithelial Cells</term>
<term>Macrophages</term>
</keywords>
<keywords scheme="MESH" qualifier="secretion" xml:lang="en">
<term>Macrophages</term>
</keywords>
<keywords scheme="MESH" qualifier="sécrétion" xml:lang="fr">
<term>Cytokines</term>
<term>Facteur de nécrose tumorale alpha</term>
<term>Interleukine-10</term>
<term>Interleukine-6</term>
<term>Interleukine-8</term>
<term>Macrophages</term>
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<term>Bacterial Adhesion</term>
<term>Cell Line</term>
<term>Clustered Regularly Interspaced Short Palindromic Repeats</term>
<term>Genome</term>
<term>Host-Pathogen Interactions</term>
<term>Humans</term>
<term>Phenotype</term>
<term>Phylogeny</term>
<term>Sequence Analysis, DNA</term>
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<term>Adhérence bactérienne</term>
<term>Analyse de séquence d'ADN</term>
<term>Clustered regularly interspaced short palindromic repeats</term>
<term>Génome</term>
<term>Humains</term>
<term>Infections à Escherichia coli</term>
<term>Interactions hôte-pathogène</term>
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<front>
<div type="abstract" xml:lang="en">Adherent-invasive Escherichia coli (AIEC) are a leading candidate bacterial trigger for Crohn's disease (CD). The AIEC pathovar is defined by in vitro cell-line assays examining specific bacteria/cell interactions. No molecular marker exists for their identification. Our aim was to identify a molecular property common to the AIEC phenotype.</div>
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<Year>2016</Year>
<Month>05</Month>
<Day>19</Day>
</DateCreated>
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<Year>2017</Year>
<Month>09</Month>
<Day>05</Day>
</DateCompleted>
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<Month>09</Month>
<Day>06</Day>
</DateRevised>
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<ISSN IssnType="Electronic">1468-3288</ISSN>
<JournalIssue CitedMedium="Internet">
<Volume>66</Volume>
<Issue>8</Issue>
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<Year>2017</Year>
<Month>Aug</Month>
</PubDate>
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<Title>Gut</Title>
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<ArticleTitle>Comparative genomics of Crohn's disease-associated adherent-invasive Escherichia coli.</ArticleTitle>
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<Abstract>
<AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">Adherent-invasive Escherichia coli (AIEC) are a leading candidate bacterial trigger for Crohn's disease (CD). The AIEC pathovar is defined by in vitro cell-line assays examining specific bacteria/cell interactions. No molecular marker exists for their identification. Our aim was to identify a molecular property common to the AIEC phenotype.</AbstractText>
<AbstractText Label="DESIGN" NlmCategory="METHODS">41 B2 phylogroup E. coli strains were isolated from 36 Australian subjects: 19 patients with IBD and 17 without. Adherence/invasion assays were conducted using the I-407 epithelial cell line and survival/replication assays using the THP-1 macrophage cell line. Cytokine secretion tumour necrosis factor ((TNF)-α, interleukin (IL) 6, IL-8 and IL-10) was measured using ELISA. The genomes were assembled and annotated, and cluster analysis performed using CD-HIT. The resulting matrices were analysed to identify genes unique/more frequent in AIEC strains compared with non-AIEC strains. Base composition differences and clustered regularly interspaced palindromic repeat (CRISPR) analyses were conducted.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">Of all B2 phylogroup strains assessed, 79% could survive and replicate in macrophages. Among them, 11/41 strains (5 CD, 2 UCs, 5 non-IBD) also adhere to and invade epithelial cells, a phenotype assigning them to the AIEC pathovar. The AIEC strains were phylogenetically heterogeneous. We did not identify a gene (or nucleic acid base composition differences) common to all, or the majority of, AIEC. Cytokine secretion and CRISPRs were not associated with the AIEC phenotype.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Comparative genomic analysis of AIEC and non-AIEC strains did not identify a molecular property exclusive to the AIEC phenotype. We recommend a broader approach to the identification of the bacteria-host interactions that are important in the pathogenesis of Crohn's disease.</AbstractText>
<CopyrightInformation>Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.</CopyrightInformation>
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<LastName>O'Brien</LastName>
<ForeName>Claire L</ForeName>
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<Affiliation>Medical School, Australian National University, Canberra, Australian Capital Territory, Australia.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Gastroenterology and Hepatology Unit, Canberra Hospital, Canberra, Australian Capital Territory, Australia.</Affiliation>
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<ForeName>Marie-Agnès</ForeName>
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<Affiliation>INRA UMR1324, CNRS UMR6265, Université Bourgogne-Franche-Comté, Centre des Sciences du Goût et de l'Alimentation, Dijon, France.</Affiliation>
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<AffiliationInfo>
<Affiliation>UMR1071 Inserm/University of Auvergne, INRA USC2018, M2iSH, Clermont-Ferrand, France.</Affiliation>
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<LastName>Pavli</LastName>
<ForeName>Paul</ForeName>
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<Affiliation>Medical School, Australian National University, Canberra, Australian Capital Territory, Australia.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Gastroenterology and Hepatology Unit, Canberra Hospital, Canberra, Australian Capital Territory, Australia.</Affiliation>
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<Country>England</Country>
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<Keyword MajorTopicYN="N">CROHN'S DISEASE</Keyword>
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<li>Australie</li>
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<li>Auvergne (région administrative)</li>
<li>Auvergne-Rhône-Alpes</li>
<li>Bourgogne</li>
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<name sortKey="Gordon, David M" sort="Gordon, David M" uniqKey="Gordon D" first="David M" last="Gordon">David M. Gordon</name>
<name sortKey="Holt, Kathryn E" sort="Holt, Kathryn E" uniqKey="Holt K" first="Kathryn E" last="Holt">Kathryn E. Holt</name>
<name sortKey="Pavli, Paul" sort="Pavli, Paul" uniqKey="Pavli P" first="Paul" last="Pavli">Paul Pavli</name>
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<name sortKey="Bringer, Marie Agnes" sort="Bringer, Marie Agnes" uniqKey="Bringer M" first="Marie-Agnès" last="Bringer">Marie-Agnès Bringer</name>
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<name sortKey="Barnich, Nicolas" sort="Barnich, Nicolas" uniqKey="Barnich N" first="Nicolas" last="Barnich">Nicolas Barnich</name>
<name sortKey="Darfeuille Michaud, Arlette" sort="Darfeuille Michaud, Arlette" uniqKey="Darfeuille Michaud A" first="Arlette" last="Darfeuille-Michaud">Arlette Darfeuille-Michaud</name>
<name sortKey="Dubois, Anaelle L" sort="Dubois, Anaelle L" uniqKey="Dubois A" first="Anaëlle L" last="Dubois">Anaëlle L. Dubois</name>
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