RapamycinFungusV1, Main, Exploration, bibRecord, 000A27

Rewiring cellular metabolism via the AKT/mTOR pathway contributes to host defence against Mycobacterium tuberculosis in human and murine cells.

Identifieur interne : 000A27 ( Main/Exploration ); précédent : 000A26; suivant : 000A28

Rewiring cellular metabolism via the AKT/mTOR pathway contributes to host defence against Mycobacterium tuberculosis in human and murine cells.

Auteurs : Ekta Lachmandas [Pays-Bas] ; Macarena Beigier-Bompadre [Allemagne] ; Shih-Chin Cheng [Pays-Bas] ; Vinod Kumar [Pays-Bas] ; Arjan Van Laarhoven [Pays-Bas] ; Xinhui Wang [Pays-Bas, République populaire de Chine] ; Anne Ammerdorffer [Pays-Bas] ; Lily Boutens [Pays-Bas] ; Dirk De Jong [Pays-Bas] ; Thirumala-Devi Kanneganti [États-Unis] ; Mark S. Gresnigt [Pays-Bas] ; Tom H M. Ottenhoff [Pays-Bas] ; Leo A B. Joosten [Pays-Bas] ; Rinke Stienstra [Pays-Bas] ; Cisca Wijmenga [Pays-Bas] ; Stefan H E. Kaufmann [Allemagne] ; Reinout Van Crevel [Pays-Bas] ; Mihai G. Netea [Pays-Bas]

Source :

European journal of immunology [ 1521-4141 ] ; 2016.

RBID : pubmed:27624090

Descripteurs français

KwdFr :
- Agranulocytes (immunologie), Agranulocytes (microbiologie), Agranulocytes (métabolisme), Analyse de profil d'expression de gènes (MeSH), Animaux (MeSH), Antibactériens (pharmacologie), Glucose (métabolisme), Glycolyse (génétique), Humains (MeSH), Interactions hôte-pathogène (MeSH), Mycobacterium tuberculosis (immunologie), Phosphorylation oxydative (MeSH), Protéines proto-oncogènes c-akt (métabolisme), Récepteur de type Toll-2 (immunologie), Sirolimus (pharmacologie), Souris (MeSH), Sérine-thréonine kinases TOR (génétique), Sérine-thréonine kinases TOR (immunologie), Sérine-thréonine kinases TOR (métabolisme), Transduction du signal (effets des médicaments et des substances chimiques), Tuberculose (immunologie), Tuberculose (microbiologie), Tuberculose (métabolisme).
MESH :
- effets des médicaments et des substances chimiques : Transduction du signal.
- génétique : Glycolyse, Sérine-thréonine kinases TOR.
- immunologie : Agranulocytes, Mycobacterium tuberculosis, Récepteur de type Toll-2, Sérine-thréonine kinases TOR, Tuberculose.
- microbiologie : Agranulocytes, Tuberculose.
- métabolisme : Agranulocytes, Glucose, Protéines proto-oncogènes c-akt, Sérine-thréonine kinases TOR, Tuberculose.
- pharmacologie : Antibactériens, Sirolimus.
- Analyse de profil d'expression de gènes, Animaux, Humains, Interactions hôte-pathogène, Phosphorylation oxydative, Souris.

English descriptors

KwdEn :
- Animals (MeSH), Anti-Bacterial Agents (pharmacology), Gene Expression Profiling (MeSH), Glucose (metabolism), Glycolysis (genetics), Host-Pathogen Interactions (MeSH), Humans (MeSH), Leukocytes, Mononuclear (immunology), Leukocytes, Mononuclear (metabolism), Leukocytes, Mononuclear (microbiology), Mice (MeSH), Mycobacterium tuberculosis (immunology), Oxidative Phosphorylation (MeSH), Proto-Oncogene Proteins c-akt (metabolism), Signal Transduction (drug effects), Sirolimus (pharmacology), TOR Serine-Threonine Kinases (genetics), TOR Serine-Threonine Kinases (immunology), TOR Serine-Threonine Kinases (metabolism), Toll-Like Receptor 2 (immunology), Tuberculosis (immunology), Tuberculosis (metabolism), Tuberculosis (microbiology).
MESH :
- chemical , genetics : TOR Serine-Threonine Kinases.
- chemical , immunology : TOR Serine-Threonine Kinases, Toll-Like Receptor 2.
- chemical , metabolism : Glucose, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases.
- chemical , pharmacology : Anti-Bacterial Agents, Sirolimus.
- drug effects : Signal Transduction.
- genetics : Glycolysis.
- immunology : Leukocytes, Mononuclear, Mycobacterium tuberculosis, Tuberculosis.
- metabolism : Leukocytes, Mononuclear, Tuberculosis.
- microbiology : Leukocytes, Mononuclear, Tuberculosis.
- Animals, Gene Expression Profiling, Host-Pathogen Interactions, Humans, Mice, Oxidative Phosphorylation.

Abstract

Cells in homeostasis metabolize glucose mainly through the tricarboxylic acid cycle and oxidative phosphorylation, while activated cells switch their basal metabolism to aerobic glycolysis. In this study, we examined whether metabolic reprogramming toward aerobic glycolysis is important for the host response to Mycobacterium tuberculosis (Mtb). Through transcriptional and metabolite analysis we show that Mtb induces a switch in host cellular metabolism toward aerobic glycolysis in human peripheral blood mononuclear cells (PBMCs). The metabolic switch is TLR2 dependent but NOD2 independent, and is mediated in part through activation of the AKT-mTOR (mammalian target of rapamycin) pathway. We show that pharmacological inhibition of the AKT/mTOR pathway inhibits cellular responses to Mtb both in vitro in human PBMCs, and in vivo in a model of murine tuberculosis. Our findings reveal a novel regulatory layer of host responses to Mtb that will aid understanding of host susceptibility to Mtb, and which may be exploited for host-directed therapy.

DOI: 10.1002/eji.201546259
PubMed: 27624090
PubMed Central: PMC5129526

Affiliations:

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

to stream Main, to step Corpus: 000942
to stream Main, to step Curation: 000942

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en">Rewiring cellular metabolism via the AKT/mTOR pathway contributes to host defence against Mycobacterium tuberculosis in human and murine cells.</title>
<author><name sortKey="Lachmandas, Ekta" sort="Lachmandas, Ekta" uniqKey="Lachmandas E" first="Ekta" last="Lachmandas">Ekta Lachmandas</name>
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<country xml:lang="fr">Pays-Bas</country>
<wicri:regionArea>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen</wicri:regionArea>
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<author><name sortKey="Beigier Bompadre, Macarena" sort="Beigier Bompadre, Macarena" uniqKey="Beigier Bompadre M" first="Macarena" last="Beigier-Bompadre">Macarena Beigier-Bompadre</name>
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<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Immunology, Max Planck Institute for Infection Biology, Berlin</wicri:regionArea>
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<author><name sortKey="Cheng, Shih Chin" sort="Cheng, Shih Chin" uniqKey="Cheng S" first="Shih-Chin" last="Cheng">Shih-Chin Cheng</name>
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<wicri:regionArea>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen</wicri:regionArea>
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<author><name sortKey="Kumar, Vinod" sort="Kumar, Vinod" uniqKey="Kumar V" first="Vinod" last="Kumar">Vinod Kumar</name>
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<author><name sortKey="Wang, Xinhui" sort="Wang, Xinhui" uniqKey="Wang X" first="Xinhui" last="Wang">Xinhui Wang</name>
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<affiliation wicri:level="1"><nlm:affiliation>College of Computer, Qinghai Normal University, Xining, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
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<wicri:noRegion>Xining</wicri:noRegion>
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<author><name sortKey="Ammerdorffer, Anne" sort="Ammerdorffer, Anne" uniqKey="Ammerdorffer A" first="Anne" last="Ammerdorffer">Anne Ammerdorffer</name>
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<wicri:regionArea>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen</wicri:regionArea>
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<author><name sortKey="Boutens, Lily" sort="Boutens, Lily" uniqKey="Boutens L" first="Lily" last="Boutens">Lily Boutens</name>
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<wicri:regionArea>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen</wicri:regionArea>
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<author><name sortKey="De Jong, Dirk" sort="De Jong, Dirk" uniqKey="De Jong D" first="Dirk" last="De Jong">Dirk De Jong</name>
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<country xml:lang="fr">Pays-Bas</country>
<wicri:regionArea>Department of Gastroenterology, Radboud University Medical Center, Nijmegen</wicri:regionArea>
<placeName><settlement type="city">Nimègue</settlement>
<region type="province" nuts="2">Gueldre</region>
</placeName>
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</author>
<author><name sortKey="Kanneganti, Thirumala Devi" sort="Kanneganti, Thirumala Devi" uniqKey="Kanneganti T" first="Thirumala-Devi" last="Kanneganti">Thirumala-Devi Kanneganti</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN</wicri:regionArea>
<placeName><region type="state">Tennessee</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Gresnigt, Mark S" sort="Gresnigt, Mark S" uniqKey="Gresnigt M" first="Mark S" last="Gresnigt">Mark S. Gresnigt</name>
<affiliation wicri:level="3"><nlm:affiliation>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands.</nlm:affiliation>
<country xml:lang="fr">Pays-Bas</country>
<wicri:regionArea>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen</wicri:regionArea>
<placeName><settlement type="city">Nimègue</settlement>
<region type="province" nuts="2">Gueldre</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Ottenhoff, Tom H M" sort="Ottenhoff, Tom H M" uniqKey="Ottenhoff T" first="Tom H M" last="Ottenhoff">Tom H M. Ottenhoff</name>
<affiliation wicri:level="3"><nlm:affiliation>Department of Infectious Diseases, Leiden University Medical Centre, Leiden, The Netherlands.</nlm:affiliation>
<country xml:lang="fr">Pays-Bas</country>
<wicri:regionArea>Department of Infectious Diseases, Leiden University Medical Centre, Leiden</wicri:regionArea>
<placeName><settlement type="city">Leyde</settlement>
<region nuts="2" type="province">Hollande-Méridionale</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Joosten, Leo A B" sort="Joosten, Leo A B" uniqKey="Joosten L" first="Leo A B" last="Joosten">Leo A B. Joosten</name>
<affiliation wicri:level="3"><nlm:affiliation>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands.</nlm:affiliation>
<country xml:lang="fr">Pays-Bas</country>
<wicri:regionArea>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen</wicri:regionArea>
<placeName><settlement type="city">Nimègue</settlement>
<region type="province" nuts="2">Gueldre</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Stienstra, Rinke" sort="Stienstra, Rinke" uniqKey="Stienstra R" first="Rinke" last="Stienstra">Rinke Stienstra</name>
<affiliation wicri:level="3"><nlm:affiliation>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands.</nlm:affiliation>
<country xml:lang="fr">Pays-Bas</country>
<wicri:regionArea>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen</wicri:regionArea>
<placeName><settlement type="city">Nimègue</settlement>
<region type="province" nuts="2">Gueldre</region>
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<author><name sortKey="Wijmenga, Cisca" sort="Wijmenga, Cisca" uniqKey="Wijmenga C" first="Cisca" last="Wijmenga">Cisca Wijmenga</name>
<affiliation wicri:level="4"><nlm:affiliation>UMC Groningen University of Groningen, Groningen, The Netherlands.</nlm:affiliation>
<country xml:lang="fr">Pays-Bas</country>
<wicri:regionArea>UMC Groningen University of Groningen, Groningen</wicri:regionArea>
<placeName><settlement type="city">Groningue</settlement>
<region nuts="2" type="province">Groningue (province)</region>
</placeName>
<orgName type="university">Université de Groningue</orgName>
</affiliation>
</author>
<author><name sortKey="Kaufmann, Stefan H E" sort="Kaufmann, Stefan H E" uniqKey="Kaufmann S" first="Stefan H E" last="Kaufmann">Stefan H E. Kaufmann</name>
<affiliation wicri:level="3"><nlm:affiliation>Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.</nlm:affiliation>
<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Immunology, Max Planck Institute for Infection Biology, Berlin</wicri:regionArea>
<placeName><region type="land" nuts="3">Berlin</region>
<settlement type="city">Berlin</settlement>
</placeName>
</affiliation>
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<author><name sortKey="Van Crevel, Reinout" sort="Van Crevel, Reinout" uniqKey="Van Crevel R" first="Reinout" last="Van Crevel">Reinout Van Crevel</name>
<affiliation wicri:level="3"><nlm:affiliation>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands.</nlm:affiliation>
<country xml:lang="fr">Pays-Bas</country>
<wicri:regionArea>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen</wicri:regionArea>
<placeName><settlement type="city">Nimègue</settlement>
<region type="province" nuts="2">Gueldre</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Netea, Mihai G" sort="Netea, Mihai G" uniqKey="Netea M" first="Mihai G" last="Netea">Mihai G. Netea</name>
<affiliation wicri:level="3"><nlm:affiliation>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands. mihai.netea@radboudumc.nl.</nlm:affiliation>
<country xml:lang="fr">Pays-Bas</country>
<wicri:regionArea>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen</wicri:regionArea>
<placeName><settlement type="city">Nimègue</settlement>
<region type="province" nuts="2">Gueldre</region>
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<series><title level="j">European journal of immunology</title>
<idno type="eISSN">1521-4141</idno>
<imprint><date when="2016" type="published">2016</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Anti-Bacterial Agents (pharmacology)</term>
<term>Gene Expression Profiling (MeSH)</term>
<term>Glucose (metabolism)</term>
<term>Glycolysis (genetics)</term>
<term>Host-Pathogen Interactions (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Leukocytes, Mononuclear (immunology)</term>
<term>Leukocytes, Mononuclear (metabolism)</term>
<term>Leukocytes, Mononuclear (microbiology)</term>
<term>Mice (MeSH)</term>
<term>Mycobacterium tuberculosis (immunology)</term>
<term>Oxidative Phosphorylation (MeSH)</term>
<term>Proto-Oncogene Proteins c-akt (metabolism)</term>
<term>Signal Transduction (drug effects)</term>
<term>Sirolimus (pharmacology)</term>
<term>TOR Serine-Threonine Kinases (genetics)</term>
<term>TOR Serine-Threonine Kinases (immunology)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
<term>Toll-Like Receptor 2 (immunology)</term>
<term>Tuberculosis (immunology)</term>
<term>Tuberculosis (metabolism)</term>
<term>Tuberculosis (microbiology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Agranulocytes (immunologie)</term>
<term>Agranulocytes (microbiologie)</term>
<term>Agranulocytes (métabolisme)</term>
<term>Analyse de profil d'expression de gènes (MeSH)</term>
<term>Animaux (MeSH)</term>
<term>Antibactériens (pharmacologie)</term>
<term>Glucose (métabolisme)</term>
<term>Glycolyse (génétique)</term>
<term>Humains (MeSH)</term>
<term>Interactions hôte-pathogène (MeSH)</term>
<term>Mycobacterium tuberculosis (immunologie)</term>
<term>Phosphorylation oxydative (MeSH)</term>
<term>Protéines proto-oncogènes c-akt (métabolisme)</term>
<term>Récepteur de type Toll-2 (immunologie)</term>
<term>Sirolimus (pharmacologie)</term>
<term>Souris (MeSH)</term>
<term>Sérine-thréonine kinases TOR (génétique)</term>
<term>Sérine-thréonine kinases TOR (immunologie)</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
<term>Transduction du signal (effets des médicaments et des substances chimiques)</term>
<term>Tuberculose (immunologie)</term>
<term>Tuberculose (microbiologie)</term>
<term>Tuberculose (métabolisme)</term>
</keywords>
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</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>TOR Serine-Threonine Kinases</term>
<term>Toll-Like Receptor 2</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glucose</term>
<term>Proto-Oncogene Proteins c-akt</term>
<term>TOR Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Bacterial Agents</term>
<term>Sirolimus</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Transduction du signal</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Glycolysis</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Glycolyse</term>
<term>Sérine-thréonine kinases TOR</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Agranulocytes</term>
<term>Mycobacterium tuberculosis</term>
<term>Récepteur de type Toll-2</term>
<term>Sérine-thréonine kinases TOR</term>
<term>Tuberculose</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Leukocytes, Mononuclear</term>
<term>Mycobacterium tuberculosis</term>
<term>Tuberculosis</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Leukocytes, Mononuclear</term>
<term>Tuberculosis</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Agranulocytes</term>
<term>Tuberculose</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Leukocytes, Mononuclear</term>
<term>Tuberculosis</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Agranulocytes</term>
<term>Glucose</term>
<term>Protéines proto-oncogènes c-akt</term>
<term>Sérine-thréonine kinases TOR</term>
<term>Tuberculose</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antibactériens</term>
<term>Sirolimus</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Gene Expression Profiling</term>
<term>Host-Pathogen Interactions</term>
<term>Humans</term>
<term>Mice</term>
<term>Oxidative Phosphorylation</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term>
<term>Animaux</term>
<term>Humains</term>
<term>Interactions hôte-pathogène</term>
<term>Phosphorylation oxydative</term>
<term>Souris</term>
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<front><div type="abstract" xml:lang="en">Cells in homeostasis metabolize glucose mainly through the tricarboxylic acid cycle and oxidative phosphorylation, while activated cells switch their basal metabolism to aerobic glycolysis. In this study, we examined whether metabolic reprogramming toward aerobic glycolysis is important for the host response to Mycobacterium tuberculosis (Mtb). Through transcriptional and metabolite analysis we show that Mtb induces a switch in host cellular metabolism toward aerobic glycolysis in human peripheral blood mononuclear cells (PBMCs). The metabolic switch is TLR2 dependent but NOD2 independent, and is mediated in part through activation of the AKT-mTOR (mammalian target of rapamycin) pathway. We show that pharmacological inhibition of the AKT/mTOR pathway inhibits cellular responses to Mtb both in vitro in human PBMCs, and in vivo in a model of murine tuberculosis. Our findings reveal a novel regulatory layer of host responses to Mtb that will aid understanding of host susceptibility to Mtb, and which may be exploited for host-directed therapy.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27624090</PMID>
<DateCompleted><Year>2017</Year>
<Month>07</Month>
<Day>18</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1521-4141</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>46</Volume>
<Issue>11</Issue>
<PubDate><Year>2016</Year>
<Month>11</Month>
</PubDate>
</JournalIssue>
<Title>European journal of immunology</Title>
<ISOAbbreviation>Eur J Immunol</ISOAbbreviation>
</Journal>
<ArticleTitle>Rewiring cellular metabolism via the AKT/mTOR pathway contributes to host defence against Mycobacterium tuberculosis in human and murine cells.</ArticleTitle>
<Pagination><MedlinePgn>2574-2586</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1002/eji.201546259</ELocationID>
<Abstract><AbstractText>Cells in homeostasis metabolize glucose mainly through the tricarboxylic acid cycle and oxidative phosphorylation, while activated cells switch their basal metabolism to aerobic glycolysis. In this study, we examined whether metabolic reprogramming toward aerobic glycolysis is important for the host response to Mycobacterium tuberculosis (Mtb). Through transcriptional and metabolite analysis we show that Mtb induces a switch in host cellular metabolism toward aerobic glycolysis in human peripheral blood mononuclear cells (PBMCs). The metabolic switch is TLR2 dependent but NOD2 independent, and is mediated in part through activation of the AKT-mTOR (mammalian target of rapamycin) pathway. We show that pharmacological inhibition of the AKT/mTOR pathway inhibits cellular responses to Mtb both in vitro in human PBMCs, and in vivo in a model of murine tuberculosis. Our findings reveal a novel regulatory layer of host responses to Mtb that will aid understanding of host susceptibility to Mtb, and which may be exploited for host-directed therapy.</AbstractText>
<CopyrightInformation>© 2016 The Authors. European Journal of Immunology published by WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lachmandas</LastName>
<ForeName>Ekta</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Beigier-Bompadre</LastName>
<ForeName>Macarena</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cheng</LastName>
<ForeName>Shih-Chin</ForeName>
<Initials>SC</Initials>
<AffiliationInfo><Affiliation>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kumar</LastName>
<ForeName>Vinod</ForeName>
<Initials>V</Initials>
<AffiliationInfo><Affiliation>UMC Groningen University of Groningen, Groningen, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>van Laarhoven</LastName>
<ForeName>Arjan</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Xinhui</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>College of Computer, Qinghai Normal University, Xining, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ammerdorffer</LastName>
<ForeName>Anne</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Boutens</LastName>
<ForeName>Lily</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>de Jong</LastName>
<ForeName>Dirk</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Department of Gastroenterology, Radboud University Medical Center, Nijmegen, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kanneganti</LastName>
<ForeName>Thirumala-Devi</ForeName>
<Initials>TD</Initials>
<AffiliationInfo><Affiliation>Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gresnigt</LastName>
<ForeName>Mark S</ForeName>
<Initials>MS</Initials>
<AffiliationInfo><Affiliation>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ottenhoff</LastName>
<ForeName>Tom H M</ForeName>
<Initials>TH</Initials>
<AffiliationInfo><Affiliation>Department of Infectious Diseases, Leiden University Medical Centre, Leiden, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Joosten</LastName>
<ForeName>Leo A B</ForeName>
<Initials>LA</Initials>
<AffiliationInfo><Affiliation>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Stienstra</LastName>
<ForeName>Rinke</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wijmenga</LastName>
<ForeName>Cisca</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>UMC Groningen University of Groningen, Groningen, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kaufmann</LastName>
<ForeName>Stefan H E</ForeName>
<Initials>SH</Initials>
<AffiliationInfo><Affiliation>Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>van Crevel</LastName>
<ForeName>Reinout</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Netea</LastName>
<ForeName>Mihai G</ForeName>
<Initials>MG</Initials>
<AffiliationInfo><Affiliation>Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands. mihai.netea@radboudumc.nl.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>310372</GrantID>
<Agency>European Research Council</Agency>
<Country>International</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2016</Year>
<Month>09</Month>
<Day>27</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Germany</Country>
<MedlineTA>Eur J Immunol</MedlineTA>
<NlmUniqueID>1273201</NlmUniqueID>
<ISSNLinking>0014-2980</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000900">Anti-Bacterial Agents</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C495342">TLR2 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C493486">Tlr2 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D051195">Toll-Like Receptor 2</NameOfSubstance>
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<Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber>
<NameOfSubstance UI="C546842">MTOR protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber>
<NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance>
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<Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber>
<NameOfSubstance UI="C546843">mTOR protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="C494918">AKT1 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="C514862">Akt1 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D051057">Proto-Oncogene Proteins c-akt</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>IY9XDZ35W2</RegistryNumber>
<NameOfSubstance UI="D005947">Glucose</NameOfSubstance>
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<Chemical><RegistryNumber>W36ZG6FT64</RegistryNumber>
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</MeshHeading>
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<MeshHeading><DescriptorName UI="D020869" MajorTopicYN="N">Gene Expression Profiling</DescriptorName>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D006019" MajorTopicYN="Y">Glycolysis</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054884" MajorTopicYN="N">Host-Pathogen Interactions</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007963" MajorTopicYN="N">Leukocytes, Mononuclear</DescriptorName>
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<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009169" MajorTopicYN="N">Mycobacterium tuberculosis</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010085" MajorTopicYN="N">Oxidative Phosphorylation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051057" MajorTopicYN="N">Proto-Oncogene Proteins c-akt</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
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Rewiring cellular metabolism via the AKT/mTOR pathway contributes to host defence against Mycobacterium tuberculosis in human and murine cells.

Rewiring cellular metabolism via the AKT/mTOR pathway contributes to host defence against Mycobacterium tuberculosis in human and murine cells.

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