PlantImRecepV1, Main, Exploration, bibRecord, 000043

TLR2 and endosomal TLR-mediated secretion of IL-10 and immune suppression in response to phagosome-confined Listeria monocytogenes.

Identifieur interne : 000043 ( Main/Exploration ); précédent : 000042; suivant : 000044

TLR2 and endosomal TLR-mediated secretion of IL-10 and immune suppression in response to phagosome-confined Listeria monocytogenes.

Auteurs : Brittney N. Nguyen [États-Unis] ; Alfredo Chávez-Arroyo [États-Unis] ; Mandy I. Cheng [États-Unis] ; Maria Krasilnikov [États-Unis] ; Alexander Louie [États-Unis] ; Daniel A. Portnoy [États-Unis]

Source :

PLoS pathogens [ 1553-7374 ] ; 2020.

RBID : pubmed:32634175

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), Endosomes (immunology), Endosomes (metabolism), Immune Tolerance (immunology), Interleukin-10 (immunology), Interleukin-10 (metabolism), Listeria monocytogenes (immunology), Listeriosis (immunology), Listeriosis (metabolism), Mice (MeSH), Mice, Inbred C57BL (MeSH), Phagosomes (immunology), Phagosomes (metabolism), Toll-Like Receptor 2 (immunology), Toll-Like Receptor 2 (metabolism), Toll-Like Receptors (immunology), Toll-Like Receptors (metabolism).
MESH :
- chemical , immunology : Interleukin-10, Toll-Like Receptor 2, Toll-Like Receptors.
- immunology : Endosomes, Immune Tolerance, Listeria monocytogenes, Listeriosis, Phagosomes.
- metabolism : Endosomes, Interleukin-10, Listeriosis, Phagosomes, Toll-Like Receptor 2, Toll-Like Receptors.
- Animals, Mice, Mice, Inbred C57BL.

Abstract

Listeria monocytogenes is a facultative intracellular bacterial pathogen that escapes from phagosomes and induces a robust adaptive immune response in mice, while mutants unable to escape phagosomes fail to induce a robust adaptive immune response and suppress the immunity to wildtype bacteria when co-administered. The capacity to suppress immunity can be reversed by blocking IL-10. In this study, we sought to understand the host receptors that lead to secretion of IL-10 in response to phagosome-confined L. monocytogenes (Δhly), with the ultimate goal of generating strains that fail to induce IL-10. We conducted a transposon screen to identify Δhly L. monocytogenes mutants that induced significantly more or less IL-10 secretion in bone marrow-derived macrophages (BMMs). A transposon insertion in lgt, which encodes phosphatidylglycerol-prolipoprotein diacylglyceryl transferase and is essential for the formation of lipoproteins, induced significantly reduced IL-10 secretion. Mutants with transposon insertions in pgdA and oatA, which encode peptidoglycan N-acetylglucosamine deacetylase and O-acetyltransferase, are sensitive to lysozyme and induced enhanced IL-10 secretion. A ΔhlyΔpgdAΔoatA strain was killed in BMMs and induced enhanced IL-10 secretion that was dependent on Unc93b1, a trafficking molecule required for signaling of nucleic acid-sensing TLRs. These data revealed that nucleic acids released by bacteriolysis triggered endosomal TLR-mediated IL-10 secretion. Secretion of IL-10 in response to infection with the parental strain was mostly TLR2-dependent, while IL-10 secretion in response to lysozyme-sensitive strains was dependent on TLR2 and Unc93b1. In mice, the IL-10 response to vacuole-confined L. monocytogenes was also dependent on TLR2 and Unc93b1. Co-administration of Δhly and ΔactA resulted in suppressed immunity in WT mice, but not in mice with mutations in Unc93b1. These data revealed that secretion of IL-10 in response to L. monocytogenes infection in vitro is mostly TLR2-dependent and immune suppression by phagosome-confined bacteria in vivo is mostly dependent on endosomal TLRs.

DOI: 10.1371/journal.ppat.1008622
PubMed: 32634175
PubMed Central: PMC7340287

Affiliations:

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

to stream Main, to step Corpus: 000094
to stream Main, to step Curation: 000094

Le document en format XML

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<series><title level="j">PLoS pathogens</title>
<idno type="eISSN">1553-7374</idno>
<imprint><date when="2020" type="published">2020</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Endosomes (immunology)</term>
<term>Endosomes (metabolism)</term>
<term>Immune Tolerance (immunology)</term>
<term>Interleukin-10 (immunology)</term>
<term>Interleukin-10 (metabolism)</term>
<term>Listeria monocytogenes (immunology)</term>
<term>Listeriosis (immunology)</term>
<term>Listeriosis (metabolism)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Phagosomes (immunology)</term>
<term>Phagosomes (metabolism)</term>
<term>Toll-Like Receptor 2 (immunology)</term>
<term>Toll-Like Receptor 2 (metabolism)</term>
<term>Toll-Like Receptors (immunology)</term>
<term>Toll-Like Receptors (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Endosomes (immunologie)</term>
<term>Endosomes (métabolisme)</term>
<term>Infections à Listeria (immunologie)</term>
<term>Infections à Listeria (métabolisme)</term>
<term>Interleukine-10 (immunologie)</term>
<term>Interleukine-10 (métabolisme)</term>
<term>Listeria monocytogenes (immunologie)</term>
<term>Phagosomes (immunologie)</term>
<term>Phagosomes (métabolisme)</term>
<term>Récepteur de type Toll-2 (immunologie)</term>
<term>Récepteur de type Toll-2 (métabolisme)</term>
<term>Récepteurs de type Toll (immunologie)</term>
<term>Récepteurs de type Toll (métabolisme)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Tolérance immunitaire (immunologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Interleukin-10</term>
<term>Toll-Like Receptor 2</term>
<term>Toll-Like Receptors</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Endosomes</term>
<term>Infections à Listeria</term>
<term>Interleukine-10</term>
<term>Listeria monocytogenes</term>
<term>Phagosomes</term>
<term>Récepteur de type Toll-2</term>
<term>Récepteurs de type Toll</term>
<term>Tolérance immunitaire</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Endosomes</term>
<term>Immune Tolerance</term>
<term>Listeria monocytogenes</term>
<term>Listeriosis</term>
<term>Phagosomes</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endosomes</term>
<term>Interleukin-10</term>
<term>Listeriosis</term>
<term>Phagosomes</term>
<term>Toll-Like Receptor 2</term>
<term>Toll-Like Receptors</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Endosomes</term>
<term>Infections à Listeria</term>
<term>Interleukine-10</term>
<term>Phagosomes</term>
<term>Récepteur de type Toll-2</term>
<term>Récepteurs de type Toll</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
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<front><div type="abstract" xml:lang="en">Listeria monocytogenes is a facultative intracellular bacterial pathogen that escapes from phagosomes and induces a robust adaptive immune response in mice, while mutants unable to escape phagosomes fail to induce a robust adaptive immune response and suppress the immunity to wildtype bacteria when co-administered. The capacity to suppress immunity can be reversed by blocking IL-10. In this study, we sought to understand the host receptors that lead to secretion of IL-10 in response to phagosome-confined L. monocytogenes (Δhly), with the ultimate goal of generating strains that fail to induce IL-10. We conducted a transposon screen to identify Δhly L. monocytogenes mutants that induced significantly more or less IL-10 secretion in bone marrow-derived macrophages (BMMs). A transposon insertion in lgt, which encodes phosphatidylglycerol-prolipoprotein diacylglyceryl transferase and is essential for the formation of lipoproteins, induced significantly reduced IL-10 secretion. Mutants with transposon insertions in pgdA and oatA, which encode peptidoglycan N-acetylglucosamine deacetylase and O-acetyltransferase, are sensitive to lysozyme and induced enhanced IL-10 secretion. A ΔhlyΔpgdAΔoatA strain was killed in BMMs and induced enhanced IL-10 secretion that was dependent on Unc93b1, a trafficking molecule required for signaling of nucleic acid-sensing TLRs. These data revealed that nucleic acids released by bacteriolysis triggered endosomal TLR-mediated IL-10 secretion. Secretion of IL-10 in response to infection with the parental strain was mostly TLR2-dependent, while IL-10 secretion in response to lysozyme-sensitive strains was dependent on TLR2 and Unc93b1. In mice, the IL-10 response to vacuole-confined L. monocytogenes was also dependent on TLR2 and Unc93b1. Co-administration of Δhly and ΔactA resulted in suppressed immunity in WT mice, but not in mice with mutations in Unc93b1. These data revealed that secretion of IL-10 in response to L. monocytogenes infection in vitro is mostly TLR2-dependent and immune suppression by phagosome-confined bacteria in vivo is mostly dependent on endosomal TLRs.</div>
</front>
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<Abstract><AbstractText>Listeria monocytogenes is a facultative intracellular bacterial pathogen that escapes from phagosomes and induces a robust adaptive immune response in mice, while mutants unable to escape phagosomes fail to induce a robust adaptive immune response and suppress the immunity to wildtype bacteria when co-administered. The capacity to suppress immunity can be reversed by blocking IL-10. In this study, we sought to understand the host receptors that lead to secretion of IL-10 in response to phagosome-confined L. monocytogenes (Δhly), with the ultimate goal of generating strains that fail to induce IL-10. We conducted a transposon screen to identify Δhly L. monocytogenes mutants that induced significantly more or less IL-10 secretion in bone marrow-derived macrophages (BMMs). A transposon insertion in lgt, which encodes phosphatidylglycerol-prolipoprotein diacylglyceryl transferase and is essential for the formation of lipoproteins, induced significantly reduced IL-10 secretion. Mutants with transposon insertions in pgdA and oatA, which encode peptidoglycan N-acetylglucosamine deacetylase and O-acetyltransferase, are sensitive to lysozyme and induced enhanced IL-10 secretion. A ΔhlyΔpgdAΔoatA strain was killed in BMMs and induced enhanced IL-10 secretion that was dependent on Unc93b1, a trafficking molecule required for signaling of nucleic acid-sensing TLRs. These data revealed that nucleic acids released by bacteriolysis triggered endosomal TLR-mediated IL-10 secretion. Secretion of IL-10 in response to infection with the parental strain was mostly TLR2-dependent, while IL-10 secretion in response to lysozyme-sensitive strains was dependent on TLR2 and Unc93b1. In mice, the IL-10 response to vacuole-confined L. monocytogenes was also dependent on TLR2 and Unc93b1. Co-administration of Δhly and ΔactA resulted in suppressed immunity in WT mice, but not in mice with mutations in Unc93b1. These data revealed that secretion of IL-10 in response to L. monocytogenes infection in vitro is mostly TLR2-dependent and immune suppression by phagosome-confined bacteria in vivo is mostly dependent on endosomal TLRs.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Nguyen</LastName>
<ForeName>Brittney N</ForeName>
<Initials>BN</Initials>
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<AffiliationInfo><Affiliation>Graduate Group in Microbiology, University of California, Berkeley, Berkeley, California, United States of America.</Affiliation>
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<AffiliationInfo><Affiliation>Graduate Group in Microbiology, University of California, Berkeley, Berkeley, California, United States of America.</Affiliation>
</AffiliationInfo>
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<ForeName>Mandy I</ForeName>
<Initials>MI</Initials>
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<AffiliationInfo><Affiliation>Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, United States of America.</Affiliation>
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<AffiliationInfo><Affiliation>Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, United States of America.</Affiliation>
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<ForeName>Alexander</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, United States of America.</Affiliation>
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<ForeName>Daniel A</ForeName>
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<AffiliationInfo><Affiliation>Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, United States of America.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Plant and Microbial Biology, University of California, Berkeley, Berkeley, California, United States of America.</Affiliation>
</AffiliationInfo>
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<Acronym>AI</Acronym>
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<Country>United States</Country>
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<ArticleDate DateType="Electronic"><Year>2020</Year>
<Month>07</Month>
<Day>07</Day>
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<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C556062">IL10 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C493486">Tlr2 protein, mouse</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D051195">Toll-Like Receptor 2</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
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<Chemical><RegistryNumber>130068-27-8</RegistryNumber>
<NameOfSubstance UI="D016753">Interleukin-10</NameOfSubstance>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011992" MajorTopicYN="N">Endosomes</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007108" MajorTopicYN="N">Immune Tolerance</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
</MeshHeading>
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	Serveur d'exploration sur les récepteurs immunitaires végétaux
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TLR2 and endosomal TLR-mediated secretion of IL-10 and immune suppression in response to phagosome-confined Listeria monocytogenes.

TLR2 and endosomal TLR-mediated secretion of IL-10 and immune suppression in response to phagosome-confined Listeria monocytogenes.

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