AustralieFrV1, Ncbi, Merge, bibRecord, 004630

High-avidity IgA protects the intestine by enchaining growing bacteria.

Identifieur interne : 004630 ( Ncbi/Merge ); précédent : 004629; suivant : 004631

High-avidity IgA protects the intestine by enchaining growing bacteria.

Auteurs : Kathrin Moor [Suisse] ; Médéric Diard [Suisse] ; Mikael E. Sellin [Suisse] ; Boas Felmy [Suisse] ; Sandra Y. Wotzka [Suisse] ; Albulena Toska [Suisse] ; Erik Bakkeren [Suisse] ; Markus Arnoldini [Suisse] ; Florence Bansept [France] ; Alma Dal Co [Suisse] ; Tom Völler [Suisse] ; Andrea Minola [Suisse] ; Blanca Fernandez-Rodriguez [Suisse] ; Gloria Agatic [Suisse] ; Sonia Barbieri [Suisse] ; Luca Piccoli [Suisse] ; Costanza Casiraghi [Suisse] ; Davide Corti [Suisse] ; Antonio Lanzavecchia [Suisse] ; Roland R. Regoes [Suisse] ; Claude Loverdo [France] ; Roman Stocker [Suisse] ; Douglas R. Brumley [Suisse] ; Wolf-Dietrich Hardt [Suisse] ; Emma Slack [Suisse]

Source :

Nature [ 1476-4687 ] ; 2017.

RBID : pubmed:28405025

Descripteurs français

KwdFr :
- Adhérence bactérienne, Affinité des anticorps, Animaux, Caecum (immunologie), Caecum (microbiologie), Conjugaison génétique, Femelle, Humains, Immunoglobuline A (immunologie), Intestins (immunologie), Intestins (microbiologie), Mâle, Numération de colonies microbiennes, Plasmides (génétique), Salmonella typhimurium (croissance et développement), Salmonella typhimurium (génétique), Salmonella typhimurium (immunologie), Salmonella typhimurium (pathogénicité), Salmonelloses (), Salmonelloses (immunologie), Salmonelloses (microbiologie), Souris, Vaccins antibactériens.
MESH :
- croissance et développement : Salmonella typhimurium.
- génétique : Plasmides, Salmonella typhimurium.
- immunologie : Caecum, Immunoglobuline A, Intestins, Salmonella typhimurium, Salmonelloses.
- microbiologie : Caecum, Intestins, Salmonelloses.
- pathogénicité : Salmonella typhimurium.
- Adhérence bactérienne, Affinité des anticorps, Animaux, Conjugaison génétique, Femelle, Humains, Mâle, Numération de colonies microbiennes, Salmonelloses, Souris, Vaccins antibactériens.

English descriptors

KwdEn :
- Animals, Antibody Affinity, Bacterial Adhesion, Bacterial Vaccines, Cecum (immunology), Cecum (microbiology), Colony Count, Microbial, Conjugation, Genetic, Female, Humans, Immunoglobulin A (immunology), Intestines (immunology), Intestines (microbiology), Male, Mice, Plasmids (genetics), Salmonella Infections (immunology), Salmonella Infections (microbiology), Salmonella Infections (prevention & control), Salmonella typhimurium (genetics), Salmonella typhimurium (growth & development), Salmonella typhimurium (immunology), Salmonella typhimurium (pathogenicity).
MESH :
- chemical , immunology : Immunoglobulin A.
- chemical : Bacterial Vaccines.
- genetics : Plasmids, Salmonella typhimurium.
- growth & development : Salmonella typhimurium.
- immunology : Cecum, Intestines, Salmonella Infections, Salmonella typhimurium.
- microbiology : Cecum, Intestines, Salmonella Infections.
- pathogenicity : Salmonella typhimurium.
- prevention & control : Salmonella Infections.
- Animals, Antibody Affinity, Bacterial Adhesion, Colony Count, Microbial, Conjugation, Genetic, Female, Humans, Male, Mice.

Abstract

Vaccine-induced high-avidity IgA can protect against bacterial enteropathogens by directly neutralizing virulence factors or by poorly defined mechanisms that physically impede bacterial interactions with the gut tissues ('immune exclusion'). IgA-mediated cross-linking clumps bacteria in the gut lumen and is critical for protection against infection by non-typhoidal Salmonella enterica subspecies enterica serovar Typhimurium (S. Typhimurium). However, classical agglutination, which was thought to drive this process, is efficient only at high pathogen densities (≥10(8) non-motile bacteria per gram). In typical infections, much lower densities (10(0)-10(7) colony-forming units per gram) of rapidly dividing bacteria are present in the gut lumen. Here we show that a different physical process drives formation of clumps in vivo: IgA-mediated cross-linking enchains daughter cells, preventing their separation after division, and clumping is therefore dependent on growth. Enchained growth is effective at all realistic pathogen densities, and accelerates pathogen clearance from the gut lumen. Furthermore, IgA enchains plasmid-donor and -recipient clones into separate clumps, impeding conjugative plasmid transfer in vivo. Enchained growth is therefore a mechanism by which IgA can disarm and clear potentially invasive species from the intestinal lumen without requiring high pathogen densities, inflammation or bacterial killing. Furthermore, our results reveal an untapped potential for oral vaccines in combating the spread of antimicrobial resistance.

DOI: 10.1038/nature22058
PubMed: 28405025

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

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to stream PubMed, to step Curation: 000E36
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pubmed:28405025

Le document en format XML

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<author><name sortKey="Regoes, Roland R" sort="Regoes, Roland R" uniqKey="Regoes R" first="Roland R" last="Regoes">Roland R. Regoes</name>
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<author><name sortKey="Stocker, Roman" sort="Stocker, Roman" uniqKey="Stocker R" first="Roman" last="Stocker">Roman Stocker</name>
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<author><name sortKey="Sellin, Mikael E" sort="Sellin, Mikael E" uniqKey="Sellin M" first="Mikael E" last="Sellin">Mikael E. Sellin</name>
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<author><name sortKey="Felmy, Boas" sort="Felmy, Boas" uniqKey="Felmy B" first="Boas" last="Felmy">Boas Felmy</name>
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<author><name sortKey="Wotzka, Sandra Y" sort="Wotzka, Sandra Y" uniqKey="Wotzka S" first="Sandra Y" last="Wotzka">Sandra Y. Wotzka</name>
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<front><div type="abstract" xml:lang="en">Vaccine-induced high-avidity IgA can protect against bacterial enteropathogens by directly neutralizing virulence factors or by poorly defined mechanisms that physically impede bacterial interactions with the gut tissues ('immune exclusion'). IgA-mediated cross-linking clumps bacteria in the gut lumen and is critical for protection against infection by non-typhoidal Salmonella enterica subspecies enterica serovar Typhimurium (S. Typhimurium). However, classical agglutination, which was thought to drive this process, is efficient only at high pathogen densities (≥10(8) non-motile bacteria per gram). In typical infections, much lower densities (10(0)-10(7) colony-forming units per gram) of rapidly dividing bacteria are present in the gut lumen. Here we show that a different physical process drives formation of clumps in vivo: IgA-mediated cross-linking enchains daughter cells, preventing their separation after division, and clumping is therefore dependent on growth. Enchained growth is effective at all realistic pathogen densities, and accelerates pathogen clearance from the gut lumen. Furthermore, IgA enchains plasmid-donor and -recipient clones into separate clumps, impeding conjugative plasmid transfer in vivo. Enchained growth is therefore a mechanism by which IgA can disarm and clear potentially invasive species from the intestinal lumen without requiring high pathogen densities, inflammation or bacterial killing. Furthermore, our results reveal an untapped potential for oral vaccines in combating the spread of antimicrobial resistance.</div>
</front>
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<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28405025</PMID>
<DateCreated><Year>2017</Year>
<Month>04</Month>
<Day>13</Day>
</DateCreated>
<DateCompleted><Year>2017</Year>
<Month>08</Month>
<Day>18</Day>
</DateCompleted>
<DateRevised><Year>2017</Year>
<Month>08</Month>
<Day>18</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1476-4687</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>544</Volume>
<Issue>7651</Issue>
<PubDate><Year>2017</Year>
<Month>04</Month>
<Day>27</Day>
</PubDate>
</JournalIssue>
<Title>Nature</Title>
<ISOAbbreviation>Nature</ISOAbbreviation>
</Journal>
<ArticleTitle>High-avidity IgA protects the intestine by enchaining growing bacteria.</ArticleTitle>
<Pagination><MedlinePgn>498-502</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1038/nature22058</ELocationID>
<Abstract><AbstractText>Vaccine-induced high-avidity IgA can protect against bacterial enteropathogens by directly neutralizing virulence factors or by poorly defined mechanisms that physically impede bacterial interactions with the gut tissues ('immune exclusion'). IgA-mediated cross-linking clumps bacteria in the gut lumen and is critical for protection against infection by non-typhoidal Salmonella enterica subspecies enterica serovar Typhimurium (S. Typhimurium). However, classical agglutination, which was thought to drive this process, is efficient only at high pathogen densities (≥10(8) non-motile bacteria per gram). In typical infections, much lower densities (10(0)-10(7) colony-forming units per gram) of rapidly dividing bacteria are present in the gut lumen. Here we show that a different physical process drives formation of clumps in vivo: IgA-mediated cross-linking enchains daughter cells, preventing their separation after division, and clumping is therefore dependent on growth. Enchained growth is effective at all realistic pathogen densities, and accelerates pathogen clearance from the gut lumen. Furthermore, IgA enchains plasmid-donor and -recipient clones into separate clumps, impeding conjugative plasmid transfer in vivo. Enchained growth is therefore a mechanism by which IgA can disarm and clear potentially invasive species from the intestinal lumen without requiring high pathogen densities, inflammation or bacterial killing. Furthermore, our results reveal an untapped potential for oral vaccines in combating the spread of antimicrobial resistance.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Moor</LastName>
<ForeName>Kathrin</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Institute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Diard</LastName>
<ForeName>Médéric</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Institute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sellin</LastName>
<ForeName>Mikael E</ForeName>
<Initials>ME</Initials>
<AffiliationInfo><Affiliation>Institute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Science for Life Laboratory, Department of Medical Biochemistry and Microbiology, Uppsala University, 75124 Uppsala, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
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<ForeName>Boas</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Institute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
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<ForeName>Sandra Y</ForeName>
<Initials>SY</Initials>
<AffiliationInfo><Affiliation>Institute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
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<ForeName>Albulena</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Institute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
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<ForeName>Erik</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>Institute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
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<ForeName>Markus</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Institute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
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<ForeName>Florence</ForeName>
<Initials>F</Initials>
<AffiliationInfo><Affiliation>Laboratoire Jean Perrin (UMR 8237), CNRS - UPMC, 75005 Paris, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Co</LastName>
<ForeName>Alma Dal</ForeName>
<Initials>AD</Initials>
<AffiliationInfo><Affiliation>Department of Environmental Systems Science, ETH Zurich, Zürich, Switzerland.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Environmental Microbiology, Eawag, Swiss Federal Institute of Aquatic Science and Technology, Dübendorf, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Völler</LastName>
<ForeName>Tom</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Institute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
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<ForeName>Andrea</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Humabs BioMed SA, 6500 Bellinzona, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Fernandez-Rodriguez</LastName>
<ForeName>Blanca</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Institute for Research in Biomedicine, Università della Svizzera italiana, Bellinzona 6500, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Agatic</LastName>
<ForeName>Gloria</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Humabs BioMed SA, 6500 Bellinzona, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Barbieri</LastName>
<ForeName>Sonia</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Institute for Research in Biomedicine, Università della Svizzera italiana, Bellinzona 6500, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Piccoli</LastName>
<ForeName>Luca</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Institute for Research in Biomedicine, Università della Svizzera italiana, Bellinzona 6500, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Casiraghi</LastName>
<ForeName>Costanza</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Institute for Research in Biomedicine, Università della Svizzera italiana, Bellinzona 6500, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Corti</LastName>
<ForeName>Davide</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Humabs BioMed SA, 6500 Bellinzona, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lanzavecchia</LastName>
<ForeName>Antonio</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Institute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Institute for Research in Biomedicine, Università della Svizzera italiana, Bellinzona 6500, Switzerland.</Affiliation>
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<Author ValidYN="Y"><LastName>Loverdo</LastName>
<ForeName>Claude</ForeName>
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<AffiliationInfo><Affiliation>School of Mathematics and Statistics, The University of Melbourne, Parkville, Victoria 3010, Australia.</Affiliation>
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<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
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<MeshHeading><DescriptorName UI="D007422" MajorTopicYN="N">Intestines</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName>
</MeshHeading>
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<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
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<MeshHeading><DescriptorName UI="D010957" MajorTopicYN="N">Plasmids</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012480" MajorTopicYN="N">Salmonella Infections</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
<QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012486" MajorTopicYN="N">Salmonella typhimurium</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000254" MajorTopicYN="Y">growth & development</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
<QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName>
</MeshHeading>
</MeshHeadingList>
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<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year>
<Month>01</Month>
<Day>20</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2017</Year>
<Month>03</Month>
<Day>10</Day>
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<ArticleIdList><ArticleId IdType="pubmed">28405025</ArticleId>
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<affiliations><list><country><li>France</li>
<li>Suisse</li>
</country>
<region><li>Canton de Zurich</li>
<li>Île-de-France</li>
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<settlement><li>Paris</li>
<li>Zurich</li>
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<tree><country name="Suisse"><region name="Canton de Zurich"><name sortKey="Moor, Kathrin" sort="Moor, Kathrin" uniqKey="Moor K" first="Kathrin" last="Moor">Kathrin Moor</name>
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<name sortKey="Casiraghi, Costanza" sort="Casiraghi, Costanza" uniqKey="Casiraghi C" first="Costanza" last="Casiraghi">Costanza Casiraghi</name>
<name sortKey="Co, Alma Dal" sort="Co, Alma Dal" uniqKey="Co A" first="Alma Dal" last="Co">Alma Dal Co</name>
<name sortKey="Corti, Davide" sort="Corti, Davide" uniqKey="Corti D" first="Davide" last="Corti">Davide Corti</name>
<name sortKey="Diard, Mederic" sort="Diard, Mederic" uniqKey="Diard M" first="Médéric" last="Diard">Médéric Diard</name>
<name sortKey="Felmy, Boas" sort="Felmy, Boas" uniqKey="Felmy B" first="Boas" last="Felmy">Boas Felmy</name>
<name sortKey="Fernandez Rodriguez, Blanca" sort="Fernandez Rodriguez, Blanca" uniqKey="Fernandez Rodriguez B" first="Blanca" last="Fernandez-Rodriguez">Blanca Fernandez-Rodriguez</name>
<name sortKey="Hardt, Wolf Dietrich" sort="Hardt, Wolf Dietrich" uniqKey="Hardt W" first="Wolf-Dietrich" last="Hardt">Wolf-Dietrich Hardt</name>
<name sortKey="Lanzavecchia, Antonio" sort="Lanzavecchia, Antonio" uniqKey="Lanzavecchia A" first="Antonio" last="Lanzavecchia">Antonio Lanzavecchia</name>
<name sortKey="Minola, Andrea" sort="Minola, Andrea" uniqKey="Minola A" first="Andrea" last="Minola">Andrea Minola</name>
<name sortKey="Piccoli, Luca" sort="Piccoli, Luca" uniqKey="Piccoli L" first="Luca" last="Piccoli">Luca Piccoli</name>
<name sortKey="Regoes, Roland R" sort="Regoes, Roland R" uniqKey="Regoes R" first="Roland R" last="Regoes">Roland R. Regoes</name>
<name sortKey="Sellin, Mikael E" sort="Sellin, Mikael E" uniqKey="Sellin M" first="Mikael E" last="Sellin">Mikael E. Sellin</name>
<name sortKey="Slack, Emma" sort="Slack, Emma" uniqKey="Slack E" first="Emma" last="Slack">Emma Slack</name>
<name sortKey="Stocker, Roman" sort="Stocker, Roman" uniqKey="Stocker R" first="Roman" last="Stocker">Roman Stocker</name>
<name sortKey="Toska, Albulena" sort="Toska, Albulena" uniqKey="Toska A" first="Albulena" last="Toska">Albulena Toska</name>
<name sortKey="Voller, Tom" sort="Voller, Tom" uniqKey="Voller T" first="Tom" last="Völler">Tom Völler</name>
<name sortKey="Wotzka, Sandra Y" sort="Wotzka, Sandra Y" uniqKey="Wotzka S" first="Sandra Y" last="Wotzka">Sandra Y. Wotzka</name>
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<country name="France"><region name="Île-de-France"><name sortKey="Bansept, Florence" sort="Bansept, Florence" uniqKey="Bansept F" first="Florence" last="Bansept">Florence Bansept</name>
</region>
<name sortKey="Loverdo, Claude" sort="Loverdo, Claude" uniqKey="Loverdo C" first="Claude" last="Loverdo">Claude Loverdo</name>
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   |area=    AustralieFrV1
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   |clé=     pubmed:28405025
   |texte=   High-avidity IgA protects the intestine by enchaining growing bacteria.
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	Serveur d'exploration sur les relations entre la France et l'Australie
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration sur les relations entre la France et l'Australie

High-avidity IgA protects the intestine by enchaining growing bacteria.

High-avidity IgA protects the intestine by enchaining growing bacteria.

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