Activator of G-Protein Signaling 3-Induced Lysosomal Biogenesis Limits Macrophage Intracellular Bacterial Infection.
Identifieur interne : 000B54 ( Main/Exploration ); précédent : 000B53; suivant : 000B55Activator of G-Protein Signaling 3-Induced Lysosomal Biogenesis Limits Macrophage Intracellular Bacterial Infection.
Auteurs : Ali Vural [États-Unis] ; Souhaila Al-Khodor [États-Unis] ; Gordon Y C. Cheung [États-Unis] ; Chong-Shan Shi [États-Unis] ; Lalitha Srinivasan [États-Unis] ; Travis J. Mcquiston [États-Unis] ; Il-Young Hwang [États-Unis] ; Anthony J. Yeh [États-Unis] ; Joe B. Blumer [États-Unis] ; Volker Briken [États-Unis] ; Peter R. Williamson [États-Unis] ; Michael Otto [États-Unis] ; Iain D C. Fraser [États-Unis] ; John H. Kehrl [États-Unis]Source :
- Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2016.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Cytométrie en flux (MeSH), Immunotransfert (MeSH), Infections bactériennes (immunologie), Inhibiteurs de la dissociation de nucléotides guanyliques (MeSH), Lysosomes (immunologie), Macrophages (immunologie), Macrophages (microbiologie), Microscopie confocale (MeSH), Petit ARN interférent (MeSH), Protéines de transport (immunologie), Réaction de polymérisation en chaîne (MeSH), Souris (MeSH), Souris de lignée C57BL (MeSH), Souris knockout (MeSH).
- MESH :
- immunologie : Infections bactériennes, Lysosomes, Macrophages, Protéines de transport.
- microbiologie : Macrophages.
- Animaux, Cytométrie en flux, Immunotransfert, Inhibiteurs de la dissociation de nucléotides guanyliques, Microscopie confocale, Petit ARN interférent, Réaction de polymérisation en chaîne, Souris, Souris de lignée C57BL, Souris knockout.
English descriptors
- KwdEn :
- Animals (MeSH), Bacterial Infections (immunology), Carrier Proteins (immunology), Flow Cytometry (MeSH), Guanine Nucleotide Dissociation Inhibitors (MeSH), Immunoblotting (MeSH), Lysosomes (immunology), Macrophages (immunology), Macrophages (microbiology), Mice (MeSH), Mice, Inbred C57BL (MeSH), Mice, Knockout (MeSH), Microscopy, Confocal (MeSH), Polymerase Chain Reaction (MeSH), RNA, Small Interfering (MeSH).
- MESH :
- chemical , immunology : Carrier Proteins.
- immunology : Bacterial Infections, Lysosomes, Macrophages.
- microbiology : Macrophages.
- Animals, Flow Cytometry, Guanine Nucleotide Dissociation Inhibitors, Immunoblotting, Mice, Mice, Inbred C57BL, Mice, Knockout, Microscopy, Confocal, Polymerase Chain Reaction, RNA, Small Interfering.
Abstract
Many intracellular pathogens cause disease by subverting macrophage innate immune defense mechanisms. Intracellular pathogens actively avoid delivery to or directly target lysosomes, the major intracellular degradative organelle. In this article, we demonstrate that activator of G-protein signaling 3 (AGS3), an LPS-inducible protein in macrophages, affects both lysosomal biogenesis and activity. AGS3 binds the Gi family of G proteins via its G-protein regulatory (GoLoco) motif, stabilizing the Gα subunit in its GDP-bound conformation. Elevated AGS3 levels in macrophages limited the activity of the mammalian target of rapamycin pathway, a sensor of cellular nutritional status. This triggered the nuclear translocation of transcription factor EB, a known activator of lysosomal gene transcription. In contrast, AGS3-deficient macrophages had increased mammalian target of rapamycin activity, reduced transcription factor EB activity, and a lower lysosomal mass. High levels of AGS3 in macrophages enhanced their resistance to infection by Burkholderia cenocepacia J2315, Mycobacterium tuberculosis, and methicillin-resistant Staphylococcus aureus, whereas AGS3-deficient macrophages were more susceptible. We conclude that LPS priming increases AGS3 levels, which enhances lysosomal function and increases the capacity of macrophages to eliminate intracellular pathogens.
DOI: 10.4049/jimmunol.1501595
PubMed: 26667172
PubMed Central: PMC4811337
Affiliations:
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Le document en format XML
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Yeh</name><affiliation wicri:level="2"><nlm:affiliation>Pathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Pathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda</wicri:cityArea></affiliation></author><author><name sortKey="Blumer, Joe B" sort="Blumer, Joe B" uniqKey="Blumer J" first="Joe B" last="Blumer">Joe B. Blumer</name><affiliation wicri:level="2"><nlm:affiliation>Department of Cell and Molecular Pharmacology and Experimental Therapeutics, Medical University of South Carolina, Charleston, SC 29425.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Caroline du Sud</region></placeName><wicri:cityArea>Department of Cell and Molecular Pharmacology and Experimental Therapeutics, Medical University of South Carolina, Charleston</wicri:cityArea></affiliation></author><author><name sortKey="Briken, Volker" sort="Briken, Volker" uniqKey="Briken V" first="Volker" last="Briken">Volker Briken</name><affiliation wicri:level="2"><nlm:affiliation>Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742;</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Department of Cell Biology and Molecular Genetics, University of Maryland, College Park</wicri:cityArea></affiliation></author><author><name sortKey="Williamson, Peter R" sort="Williamson, Peter R" uniqKey="Williamson P" first="Peter R" last="Williamson">Peter R. 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Fraser</name><affiliation wicri:level="2"><nlm:affiliation>Signaling Systems Unit, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Signaling Systems Unit, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda</wicri:cityArea></affiliation></author><author><name sortKey="Kehrl, John H" sort="Kehrl, John H" uniqKey="Kehrl J" first="John H" last="Kehrl">John H. Kehrl</name><affiliation wicri:level="2"><nlm:affiliation>B-Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; jkehrl@niaid.nih.gov.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>B-Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda</wicri:cityArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:26667172</idno><idno type="pmid">26667172</idno><idno type="doi">10.4049/jimmunol.1501595</idno><idno type="pmc">PMC4811337</idno><idno type="wicri:Area/Main/Corpus">000B38</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000B38</idno><idno type="wicri:Area/Main/Curation">000B38</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000B38</idno><idno type="wicri:Area/Main/Exploration">000B38</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Activator of G-Protein Signaling 3-Induced Lysosomal Biogenesis Limits Macrophage Intracellular Bacterial Infection.</title><author><name sortKey="Vural, Ali" sort="Vural, Ali" uniqKey="Vural A" first="Ali" last="Vural">Ali Vural</name><affiliation wicri:level="2"><nlm:affiliation>B-Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>B-Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda</wicri:cityArea></affiliation></author><author><name sortKey="Al Khodor, Souhaila" sort="Al Khodor, Souhaila" uniqKey="Al Khodor S" first="Souhaila" last="Al-Khodor">Souhaila Al-Khodor</name><affiliation wicri:level="2"><nlm:affiliation>Signaling Systems Unit, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Signaling Systems Unit, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda</wicri:cityArea></affiliation></author><author><name sortKey="Cheung, Gordon Y C" sort="Cheung, Gordon Y C" uniqKey="Cheung G" first="Gordon Y C" last="Cheung">Gordon Y C. Cheung</name><affiliation wicri:level="2"><nlm:affiliation>Pathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Pathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda</wicri:cityArea></affiliation></author><author><name sortKey="Shi, Chong Shan" sort="Shi, Chong Shan" uniqKey="Shi C" first="Chong-Shan" last="Shi">Chong-Shan Shi</name><affiliation wicri:level="2"><nlm:affiliation>B-Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>B-Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda</wicri:cityArea></affiliation></author><author><name sortKey="Srinivasan, Lalitha" sort="Srinivasan, Lalitha" uniqKey="Srinivasan L" first="Lalitha" last="Srinivasan">Lalitha Srinivasan</name><affiliation wicri:level="2"><nlm:affiliation>Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742;</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Department of Cell Biology and Molecular Genetics, University of Maryland, College Park</wicri:cityArea></affiliation></author><author><name sortKey="Mcquiston, Travis J" sort="Mcquiston, Travis J" uniqKey="Mcquiston T" first="Travis J" last="Mcquiston">Travis J. Mcquiston</name><affiliation wicri:level="2"><nlm:affiliation>Translational Mycology Unit, Laboratory of Clinical Infectious Disease, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; and.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Translational Mycology Unit, Laboratory of Clinical Infectious Disease, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda</wicri:cityArea></affiliation></author><author><name sortKey="Hwang, Il Young" sort="Hwang, Il Young" uniqKey="Hwang I" first="Il-Young" last="Hwang">Il-Young Hwang</name><affiliation wicri:level="2"><nlm:affiliation>B-Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>B-Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda</wicri:cityArea></affiliation></author><author><name sortKey="Yeh, Anthony J" sort="Yeh, Anthony J" uniqKey="Yeh A" first="Anthony J" last="Yeh">Anthony J. Yeh</name><affiliation wicri:level="2"><nlm:affiliation>Pathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Pathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda</wicri:cityArea></affiliation></author><author><name sortKey="Blumer, Joe B" sort="Blumer, Joe B" uniqKey="Blumer J" first="Joe B" last="Blumer">Joe B. Blumer</name><affiliation wicri:level="2"><nlm:affiliation>Department of Cell and Molecular Pharmacology and Experimental Therapeutics, Medical University of South Carolina, Charleston, SC 29425.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Caroline du Sud</region></placeName><wicri:cityArea>Department of Cell and Molecular Pharmacology and Experimental Therapeutics, Medical University of South Carolina, Charleston</wicri:cityArea></affiliation></author><author><name sortKey="Briken, Volker" sort="Briken, Volker" uniqKey="Briken V" first="Volker" last="Briken">Volker Briken</name><affiliation wicri:level="2"><nlm:affiliation>Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742;</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Department of Cell Biology and Molecular Genetics, University of Maryland, College Park</wicri:cityArea></affiliation></author><author><name sortKey="Williamson, Peter R" sort="Williamson, Peter R" uniqKey="Williamson P" first="Peter R" last="Williamson">Peter R. Williamson</name><affiliation wicri:level="2"><nlm:affiliation>Translational Mycology Unit, Laboratory of Clinical Infectious Disease, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; and.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Translational Mycology Unit, Laboratory of Clinical Infectious Disease, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda</wicri:cityArea></affiliation></author><author><name sortKey="Otto, Michael" sort="Otto, Michael" uniqKey="Otto M" first="Michael" last="Otto">Michael Otto</name><affiliation wicri:level="2"><nlm:affiliation>Pathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Pathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda</wicri:cityArea></affiliation></author><author><name sortKey="Fraser, Iain D C" sort="Fraser, Iain D C" uniqKey="Fraser I" first="Iain D C" last="Fraser">Iain D C. Fraser</name><affiliation wicri:level="2"><nlm:affiliation>Signaling Systems Unit, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Signaling Systems Unit, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda</wicri:cityArea></affiliation></author><author><name sortKey="Kehrl, John H" sort="Kehrl, John H" uniqKey="Kehrl J" first="John H" last="Kehrl">John H. Kehrl</name><affiliation wicri:level="2"><nlm:affiliation>B-Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; jkehrl@niaid.nih.gov.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>B-Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda</wicri:cityArea></affiliation></author></analytic><series><title level="j">Journal of immunology (Baltimore, Md. : 1950)</title><idno type="eISSN">1550-6606</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Bacterial Infections (immunology)</term><term>Carrier Proteins (immunology)</term><term>Flow Cytometry (MeSH)</term><term>Guanine Nucleotide Dissociation Inhibitors (MeSH)</term><term>Immunoblotting (MeSH)</term><term>Lysosomes (immunology)</term><term>Macrophages (immunology)</term><term>Macrophages (microbiology)</term><term>Mice (MeSH)</term><term>Mice, Inbred C57BL (MeSH)</term><term>Mice, Knockout (MeSH)</term><term>Microscopy, Confocal (MeSH)</term><term>Polymerase Chain Reaction (MeSH)</term><term>RNA, Small Interfering (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Cytométrie en flux (MeSH)</term><term>Immunotransfert (MeSH)</term><term>Infections bactériennes (immunologie)</term><term>Inhibiteurs de la dissociation de nucléotides guanyliques (MeSH)</term><term>Lysosomes (immunologie)</term><term>Macrophages (immunologie)</term><term>Macrophages (microbiologie)</term><term>Microscopie confocale (MeSH)</term><term>Petit ARN interférent (MeSH)</term><term>Protéines de transport (immunologie)</term><term>Réaction de polymérisation en chaîne (MeSH)</term><term>Souris (MeSH)</term><term>Souris de lignée C57BL (MeSH)</term><term>Souris knockout (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Carrier Proteins</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Infections bactériennes</term><term>Lysosomes</term><term>Macrophages</term><term>Protéines de transport</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Bacterial Infections</term><term>Lysosomes</term><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Macrophages</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Flow Cytometry</term><term>Guanine Nucleotide Dissociation Inhibitors</term><term>Immunoblotting</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Microscopy, Confocal</term><term>Polymerase Chain Reaction</term><term>RNA, Small Interfering</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cytométrie en flux</term><term>Immunotransfert</term><term>Inhibiteurs de la dissociation de nucléotides guanyliques</term><term>Microscopie confocale</term><term>Petit ARN interférent</term><term>Réaction de polymérisation en chaîne</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Souris knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Many intracellular pathogens cause disease by subverting macrophage innate immune defense mechanisms. Intracellular pathogens actively avoid delivery to or directly target lysosomes, the major intracellular degradative organelle. In this article, we demonstrate that activator of G-protein signaling 3 (AGS3), an LPS-inducible protein in macrophages, affects both lysosomal biogenesis and activity. AGS3 binds the Gi family of G proteins via its G-protein regulatory (GoLoco) motif, stabilizing the Gα subunit in its GDP-bound conformation. Elevated AGS3 levels in macrophages limited the activity of the mammalian target of rapamycin pathway, a sensor of cellular nutritional status. This triggered the nuclear translocation of transcription factor EB, a known activator of lysosomal gene transcription. In contrast, AGS3-deficient macrophages had increased mammalian target of rapamycin activity, reduced transcription factor EB activity, and a lower lysosomal mass. High levels of AGS3 in macrophages enhanced their resistance to infection by Burkholderia cenocepacia J2315, Mycobacterium tuberculosis, and methicillin-resistant Staphylococcus aureus, whereas AGS3-deficient macrophages were more susceptible. We conclude that LPS priming increases AGS3 levels, which enhances lysosomal function and increases the capacity of macrophages to eliminate intracellular pathogens. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26667172</PMID><DateCompleted><Year>2016</Year><Month>05</Month><Day>23</Day></DateCompleted><DateRevised><Year>2019</Year><Month>12</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1550-6606</ISSN><JournalIssue CitedMedium="Internet"><Volume>196</Volume><Issue>2</Issue><PubDate><Year>2016</Year><Month>Jan</Month><Day>15</Day></PubDate></JournalIssue><Title>Journal of immunology (Baltimore, Md. : 1950)</Title><ISOAbbreviation>J Immunol</ISOAbbreviation></Journal><ArticleTitle>Activator of G-Protein Signaling 3-Induced Lysosomal Biogenesis Limits Macrophage Intracellular Bacterial Infection.</ArticleTitle><Pagination><MedlinePgn>846-56</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.4049/jimmunol.1501595</ELocationID><Abstract><AbstractText>Many intracellular pathogens cause disease by subverting macrophage innate immune defense mechanisms. Intracellular pathogens actively avoid delivery to or directly target lysosomes, the major intracellular degradative organelle. In this article, we demonstrate that activator of G-protein signaling 3 (AGS3), an LPS-inducible protein in macrophages, affects both lysosomal biogenesis and activity. AGS3 binds the Gi family of G proteins via its G-protein regulatory (GoLoco) motif, stabilizing the Gα subunit in its GDP-bound conformation. Elevated AGS3 levels in macrophages limited the activity of the mammalian target of rapamycin pathway, a sensor of cellular nutritional status. This triggered the nuclear translocation of transcription factor EB, a known activator of lysosomal gene transcription. In contrast, AGS3-deficient macrophages had increased mammalian target of rapamycin activity, reduced transcription factor EB activity, and a lower lysosomal mass. High levels of AGS3 in macrophages enhanced their resistance to infection by Burkholderia cenocepacia J2315, Mycobacterium tuberculosis, and methicillin-resistant Staphylococcus aureus, whereas AGS3-deficient macrophages were more susceptible. We conclude that LPS priming increases AGS3 levels, which enhances lysosomal function and increases the capacity of macrophages to eliminate intracellular pathogens. </AbstractText><CopyrightInformation>Copyright © 2016 by The American Association of Immunologists, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Vural</LastName><ForeName>Ali</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>B-Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Al-Khodor</LastName><ForeName>Souhaila</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Signaling Systems Unit, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cheung</LastName><ForeName>Gordon Y C</ForeName><Initials>GY</Initials><Identifier Source="ORCID">http://orcid.org/0000-0003-1796-6058</Identifier><AffiliationInfo><Affiliation>Pathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shi</LastName><ForeName>Chong-Shan</ForeName><Initials>CS</Initials><AffiliationInfo><Affiliation>B-Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Srinivasan</LastName><ForeName>Lalitha</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McQuiston</LastName><ForeName>Travis J</ForeName><Initials>TJ</Initials><Identifier Source="ORCID">http://orcid.org/0000-0001-7826-8101</Identifier><AffiliationInfo><Affiliation>Translational Mycology Unit, Laboratory of Clinical Infectious Disease, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hwang</LastName><ForeName>Il-Young</ForeName><Initials>IY</Initials><AffiliationInfo><Affiliation>B-Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yeh</LastName><ForeName>Anthony J</ForeName><Initials>AJ</Initials><AffiliationInfo><Affiliation>Pathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Blumer</LastName><ForeName>Joe B</ForeName><Initials>JB</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-0020-3815</Identifier><AffiliationInfo><Affiliation>Department of Cell and Molecular Pharmacology and Experimental Therapeutics, Medical University of South Carolina, Charleston, SC 29425.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Briken</LastName><ForeName>Volker</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Williamson</LastName><ForeName>Peter R</ForeName><Initials>PR</Initials><AffiliationInfo><Affiliation>Translational Mycology Unit, Laboratory of Clinical Infectious Disease, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Otto</LastName><ForeName>Michael</ForeName><Initials>M</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-2222-4115</Identifier><AffiliationInfo><Affiliation>Pathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fraser</LastName><ForeName>Iain D C</ForeName><Initials>ID</Initials><AffiliationInfo><Affiliation>Signaling Systems Unit, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kehrl</LastName><ForeName>John H</ForeName><Initials>JH</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-6526-159X</Identifier><AffiliationInfo><Affiliation>B-Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; jkehrl@niaid.nih.gov.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>Z01 AI000738-13</GrantID><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>ZIA AI001106-08</GrantID><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>ZIA AI001107-08</GrantID><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052060">Research Support, N.I.H., Intramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>12</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Immunol</MedlineTA><NlmUniqueID>2985117R</NlmUniqueID><ISSNLinking>0022-1767</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002352">Carrier Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C498915">Gpsm1 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020730">Guanine Nucleotide Dissociation Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D034741">RNA, Small Interfering</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001424" MajorTopicYN="N">Bacterial Infections</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002352" MajorTopicYN="N">Carrier Proteins</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005434" MajorTopicYN="N">Flow Cytometry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020730" MajorTopicYN="N">Guanine Nucleotide Dissociation Inhibitors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015151" MajorTopicYN="N">Immunoblotting</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008247" MajorTopicYN="N">Lysosomes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018613" MajorTopicYN="N">Microscopy, Confocal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016133" MajorTopicYN="N">Polymerase Chain Reaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D034741" MajorTopicYN="N">RNA, Small 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Blumer</name><name sortKey="Briken, Volker" sort="Briken, Volker" uniqKey="Briken V" first="Volker" last="Briken">Volker Briken</name><name sortKey="Cheung, Gordon Y C" sort="Cheung, Gordon Y C" uniqKey="Cheung G" first="Gordon Y C" last="Cheung">Gordon Y C. Cheung</name><name sortKey="Fraser, Iain D C" sort="Fraser, Iain D C" uniqKey="Fraser I" first="Iain D C" last="Fraser">Iain D C. Fraser</name><name sortKey="Hwang, Il Young" sort="Hwang, Il Young" uniqKey="Hwang I" first="Il-Young" last="Hwang">Il-Young Hwang</name><name sortKey="Kehrl, John H" sort="Kehrl, John H" uniqKey="Kehrl J" first="John H" last="Kehrl">John H. Kehrl</name><name sortKey="Mcquiston, Travis J" sort="Mcquiston, Travis J" uniqKey="Mcquiston T" first="Travis J" last="Mcquiston">Travis J. Mcquiston</name><name sortKey="Otto, Michael" sort="Otto, Michael" uniqKey="Otto M" first="Michael" last="Otto">Michael Otto</name><name sortKey="Shi, Chong Shan" sort="Shi, Chong Shan" uniqKey="Shi C" first="Chong-Shan" last="Shi">Chong-Shan Shi</name><name sortKey="Srinivasan, Lalitha" sort="Srinivasan, Lalitha" uniqKey="Srinivasan L" first="Lalitha" last="Srinivasan">Lalitha Srinivasan</name><name sortKey="Williamson, Peter R" sort="Williamson, Peter R" uniqKey="Williamson P" first="Peter R" last="Williamson">Peter R. Williamson</name><name sortKey="Yeh, Anthony J" sort="Yeh, Anthony J" uniqKey="Yeh A" first="Anthony J" last="Yeh">Anthony J. Yeh</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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