Legionella pneumophila infection-mediated regulation of RICTOR via miR-218 in U937 macrophage cells.
Identifieur interne : 000304 ( Main/Exploration ); précédent : 000303; suivant : 000305Legionella pneumophila infection-mediated regulation of RICTOR via miR-218 in U937 macrophage cells.
Auteurs : Toyoyasu Koriyama [Japon] ; Munekazu Yamakuchi [Japon] ; Kazunori Takenouchi [Japon] ; Yoko Oyama [Japon] ; Hiroyoshi Takenaka [Japon] ; Takumi Nagakura [Japon] ; Izumi Masamoto [Japon] ; Teruto Hashiguchi [Japon]Source :
- Biochemical and biophysical research communications [ 1090-2104 ] ; 2019.
Descripteurs français
- KwdFr :
- ARN messager (analyse), Cellules U937 (MeSH), Compagnon de mTOR insensible à la rapamycine (métabolisme), Cytokines (MeSH), Humains (MeSH), Inflammation (MeSH), Interactions hôte-pathogène (MeSH), Legionella pneumophila (MeSH), Macrophages (anatomopathologie), Macrophages (microbiologie), Macrophages (métabolisme), Maladie des légionnaires (anatomopathologie), Maladie des légionnaires (métabolisme), Maladie des légionnaires (virologie), microARN (analyse), microARN (métabolisme).
- MESH :
- analyse : ARN messager, microARN.
- anatomopathologie : Macrophages, Maladie des légionnaires.
- microbiologie : Macrophages.
- métabolisme : Compagnon de mTOR insensible à la rapamycine, Macrophages, Maladie des légionnaires, microARN.
- virologie : Maladie des légionnaires.
- Cellules U937, Cytokines, Humains, Inflammation, Interactions hôte-pathogène, Legionella pneumophila.
English descriptors
- KwdEn :
- Cytokines (MeSH), Host-Pathogen Interactions (MeSH), Humans (MeSH), Inflammation (MeSH), Legionella pneumophila (MeSH), Legionnaires' Disease (metabolism), Legionnaires' Disease (pathology), Legionnaires' Disease (virology), Macrophages (metabolism), Macrophages (microbiology), Macrophages (pathology), MicroRNAs (analysis), MicroRNAs (metabolism), RNA, Messenger (analysis), Rapamycin-Insensitive Companion of mTOR Protein (metabolism), U937 Cells (MeSH).
- MESH :
- chemical , analysis : MicroRNAs, RNA, Messenger.
- chemical , metabolism : MicroRNAs, Rapamycin-Insensitive Companion of mTOR Protein.
- chemical : Cytokines.
- metabolism : Legionnaires' Disease, Macrophages.
- microbiology : Macrophages.
- pathology : Legionnaires' Disease, Macrophages.
- virology : Legionnaires' Disease.
- Host-Pathogen Interactions, Humans, Inflammation, Legionella pneumophila, U937 Cells.
Abstract
BACKGROUND
Inhalation of aerosolized Legionella pneumophila, a Gram-negative bacterium, can cause severe pneumonia. During infection, L. pneumophila replicates intracellularly in macrophages. The involvement of host microRNAs (miRNAs) in L. pneumophila infection is not fully understood.
METHODS
The human macrophage-like cell line U937 was infected with L. pneumophila. The levels of miRNA and messenger RNA (mRNA) were measured using reverse transcriptase polymerase chain reaction. Release of lactate dehydrogenase was used to evaluate cytotoxicity. The expression of RICTOR and related proteins was examined by western blotting of cell lysates.
RESULTS
L. pneumophila infection upregulated the expression of miR-218 and the host genes SLIT2 and SLIT3 in U937 cells. The expression of RICTOR, a component of the mechanistic target of rapamycin complex 2 (mTORC2), decreased during L. pneumophila infection. RICTOR protein expression was inhibited by the overexpression of miR-218, whereas knockdown of miR-218 restored the downregulation of RICTOR by L. pneumophila. L. pneumophila infection induced the expression of the proinflammatory cytokines IL-6 and TNF-alpha, which was modulated by knockdown of miR-218 or RICTOR.
CONCLUSIONS
Our study revealed the involvement of miR-218 in regulating the inflammatory response of macrophages against L. pneumophila infection. These findings suggest potential novel roles for miR-218 and RICTOR as therapeutic targets of L. pneumophila infection.
DOI: 10.1016/j.bbrc.2018.11.093
PubMed: 30509489
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Department of Laboratory Medicine, Kagoshima University Hospital, Kagoshima, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan; Department of Laboratory Medicine, Kagoshima University Hospital, Kagoshima</wicri:regionArea><wicri:noRegion>Kagoshima</wicri:noRegion></affiliation></author><author><name sortKey="Yamakuchi, Munekazu" sort="Yamakuchi, Munekazu" uniqKey="Yamakuchi M" first="Munekazu" last="Yamakuchi">Munekazu Yamakuchi</name><affiliation wicri:level="1"><nlm:affiliation>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan. Electronic address: munekazu@m.kufm.kagoshima-u.ac.jp.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima</wicri:regionArea><wicri:noRegion>Kagoshima</wicri:noRegion></affiliation></author><author><name sortKey="Takenouchi, Kazunori" sort="Takenouchi, Kazunori" uniqKey="Takenouchi K" first="Kazunori" last="Takenouchi">Kazunori Takenouchi</name><affiliation wicri:level="1"><nlm:affiliation>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima</wicri:regionArea><wicri:noRegion>Kagoshima</wicri:noRegion></affiliation></author><author><name sortKey="Oyama, Yoko" sort="Oyama, Yoko" uniqKey="Oyama Y" first="Yoko" last="Oyama">Yoko Oyama</name><affiliation wicri:level="1"><nlm:affiliation>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima</wicri:regionArea><wicri:noRegion>Kagoshima</wicri:noRegion></affiliation></author><author><name sortKey="Takenaka, Hiroyoshi" sort="Takenaka, Hiroyoshi" uniqKey="Takenaka H" first="Hiroyoshi" last="Takenaka">Hiroyoshi Takenaka</name><affiliation wicri:level="1"><nlm:affiliation>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima</wicri:regionArea><wicri:noRegion>Kagoshima</wicri:noRegion></affiliation></author><author><name sortKey="Nagakura, Takumi" sort="Nagakura, Takumi" uniqKey="Nagakura T" first="Takumi" last="Nagakura">Takumi Nagakura</name><affiliation wicri:level="1"><nlm:affiliation>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima</wicri:regionArea><wicri:noRegion>Kagoshima</wicri:noRegion></affiliation></author><author><name sortKey="Masamoto, Izumi" sort="Masamoto, Izumi" uniqKey="Masamoto I" first="Izumi" last="Masamoto">Izumi Masamoto</name><affiliation wicri:level="1"><nlm:affiliation>Department of Laboratory Medicine, Kagoshima University Hospital, Kagoshima, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Laboratory Medicine, Kagoshima University Hospital, Kagoshima</wicri:regionArea><wicri:noRegion>Kagoshima</wicri:noRegion></affiliation></author><author><name sortKey="Hashiguchi, Teruto" sort="Hashiguchi, Teruto" uniqKey="Hashiguchi T" first="Teruto" last="Hashiguchi">Teruto Hashiguchi</name><affiliation wicri:level="1"><nlm:affiliation>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima</wicri:regionArea><wicri:noRegion>Kagoshima</wicri:noRegion></affiliation></author></analytic><series><title level="j">Biochemical and biophysical research communications</title><idno type="eISSN">1090-2104</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cytokines (MeSH)</term><term>Host-Pathogen Interactions (MeSH)</term><term>Humans (MeSH)</term><term>Inflammation (MeSH)</term><term>Legionella pneumophila (MeSH)</term><term>Legionnaires' Disease (metabolism)</term><term>Legionnaires' Disease (pathology)</term><term>Legionnaires' Disease (virology)</term><term>Macrophages (metabolism)</term><term>Macrophages (microbiology)</term><term>Macrophages (pathology)</term><term>MicroRNAs (analysis)</term><term>MicroRNAs (metabolism)</term><term>RNA, Messenger (analysis)</term><term>Rapamycin-Insensitive Companion of mTOR Protein (metabolism)</term><term>U937 Cells (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (analyse)</term><term>Cellules U937 (MeSH)</term><term>Compagnon de mTOR insensible à la rapamycine (métabolisme)</term><term>Cytokines (MeSH)</term><term>Humains (MeSH)</term><term>Inflammation (MeSH)</term><term>Interactions hôte-pathogène (MeSH)</term><term>Legionella pneumophila (MeSH)</term><term>Macrophages (anatomopathologie)</term><term>Macrophages (microbiologie)</term><term>Macrophages (métabolisme)</term><term>Maladie des légionnaires (anatomopathologie)</term><term>Maladie des légionnaires (métabolisme)</term><term>Maladie des légionnaires (virologie)</term><term>microARN (analyse)</term><term>microARN (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>MicroRNAs</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>MicroRNAs</term><term>Rapamycin-Insensitive Companion of mTOR Protein</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><term>ARN messager</term><term>microARN</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Macrophages</term><term>Maladie des légionnaires</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Legionnaires' Disease</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" qualifier="métabolisme" xml:lang="fr"><term>Compagnon de mTOR insensible à la rapamycine</term><term>Macrophages</term><term>Maladie des légionnaires</term><term>microARN</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Legionnaires' Disease</term><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Maladie des légionnaires</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Legionnaires' Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Host-Pathogen Interactions</term><term>Humans</term><term>Inflammation</term><term>Legionella pneumophila</term><term>U937 Cells</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cellules U937</term><term>Cytokines</term><term>Humains</term><term>Inflammation</term><term>Interactions hôte-pathogène</term><term>Legionella pneumophila</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b></p><p>Inhalation of aerosolized Legionella pneumophila, a Gram-negative bacterium, can cause severe pneumonia. During infection, L. pneumophila replicates intracellularly in macrophages. The involvement of host microRNAs (miRNAs) in L. pneumophila infection is not fully understood.</p></div><div type="abstract" xml:lang="en"><p><b>METHODS</b></p><p>The human macrophage-like cell line U937 was infected with L. pneumophila. The levels of miRNA and messenger RNA (mRNA) were measured using reverse transcriptase polymerase chain reaction. Release of lactate dehydrogenase was used to evaluate cytotoxicity. The expression of RICTOR and related proteins was examined by western blotting of cell lysates.</p></div><div type="abstract" xml:lang="en"><p><b>RESULTS</b></p><p>L. pneumophila infection upregulated the expression of miR-218 and the host genes SLIT2 and SLIT3 in U937 cells. The expression of RICTOR, a component of the mechanistic target of rapamycin complex 2 (mTORC2), decreased during L. pneumophila infection. RICTOR protein expression was inhibited by the overexpression of miR-218, whereas knockdown of miR-218 restored the downregulation of RICTOR by L. pneumophila. L. pneumophila infection induced the expression of the proinflammatory cytokines IL-6 and TNF-alpha, which was modulated by knockdown of miR-218 or RICTOR.</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b></p><p>Our study revealed the involvement of miR-218 in regulating the inflammatory response of macrophages against L. pneumophila infection. These findings suggest potential novel roles for miR-218 and RICTOR as therapeutic targets of L. pneumophila infection.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30509489</PMID><DateCompleted><Year>2019</Year><Month>06</Month><Day>03</Day></DateCompleted><DateRevised><Year>2019</Year><Month>06</Month><Day>03</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1090-2104</ISSN><JournalIssue CitedMedium="Internet"><Volume>508</Volume><Issue>2</Issue><PubDate><Year>2019</Year><Month>01</Month><Day>08</Day></PubDate></JournalIssue><Title>Biochemical and biophysical research communications</Title><ISOAbbreviation>Biochem Biophys Res Commun</ISOAbbreviation></Journal><ArticleTitle>Legionella pneumophila infection-mediated regulation of RICTOR via miR-218 in U937 macrophage cells.</ArticleTitle><Pagination><MedlinePgn>608-613</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0006-291X(18)32517-8</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbrc.2018.11.093</ELocationID><Abstract><AbstractText Label="BACKGROUND">Inhalation of aerosolized Legionella pneumophila, a Gram-negative bacterium, can cause severe pneumonia. During infection, L. pneumophila replicates intracellularly in macrophages. The involvement of host microRNAs (miRNAs) in L. pneumophila infection is not fully understood.</AbstractText><AbstractText Label="METHODS">The human macrophage-like cell line U937 was infected with L. pneumophila. The levels of miRNA and messenger RNA (mRNA) were measured using reverse transcriptase polymerase chain reaction. Release of lactate dehydrogenase was used to evaluate cytotoxicity. The expression of RICTOR and related proteins was examined by western blotting of cell lysates.</AbstractText><AbstractText Label="RESULTS">L. pneumophila infection upregulated the expression of miR-218 and the host genes SLIT2 and SLIT3 in U937 cells. The expression of RICTOR, a component of the mechanistic target of rapamycin complex 2 (mTORC2), decreased during L. pneumophila infection. RICTOR protein expression was inhibited by the overexpression of miR-218, whereas knockdown of miR-218 restored the downregulation of RICTOR by L. pneumophila. L. pneumophila infection induced the expression of the proinflammatory cytokines IL-6 and TNF-alpha, which was modulated by knockdown of miR-218 or RICTOR.</AbstractText><AbstractText Label="CONCLUSIONS">Our study revealed the involvement of miR-218 in regulating the inflammatory response of macrophages against L. pneumophila infection. These findings suggest potential novel roles for miR-218 and RICTOR as therapeutic targets of L. pneumophila infection.</AbstractText><CopyrightInformation>Copyright © 2018 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Koriyama</LastName><ForeName>Toyoyasu</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan; Department of Laboratory Medicine, Kagoshima University Hospital, Kagoshima, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yamakuchi</LastName><ForeName>Munekazu</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan. Electronic address: munekazu@m.kufm.kagoshima-u.ac.jp.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Takenouchi</LastName><ForeName>Kazunori</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Oyama</LastName><ForeName>Yoko</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Takenaka</LastName><ForeName>Hiroyoshi</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nagakura</LastName><ForeName>Takumi</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Masamoto</LastName><ForeName>Izumi</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Department of Laboratory Medicine, Kagoshima University Hospital, Kagoshima, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hashiguchi</LastName><ForeName>Teruto</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>12</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Biochem Biophys Res Commun</MedlineTA><NlmUniqueID>0372516</NlmUniqueID><ISSNLinking>0006-291X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C547471">MIRN218 microRNA, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D035683">MicroRNAs</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000076226">Rapamycin-Insensitive Companion of mTOR Protein</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054884" MajorTopicYN="N">Host-Pathogen Interactions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016952" MajorTopicYN="Y">Legionella pneumophila</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007877" MajorTopicYN="N">Legionnaires' Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D035683" MajorTopicYN="N">MicroRNAs</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000076226" MajorTopicYN="N">Rapamycin-Insensitive Companion of mTOR Protein</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020298" MajorTopicYN="N">U937 Cells</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Legionella</Keyword><Keyword MajorTopicYN="Y">Macrophage</Keyword><Keyword MajorTopicYN="Y">Rictor</Keyword><Keyword MajorTopicYN="Y">microRNA</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>10</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2018</Year><Month>11</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2018</Year><Month>12</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>6</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2018</Year><Month>12</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30509489</ArticleId><ArticleId IdType="pii">S0006-291X(18)32517-8</ArticleId><ArticleId IdType="doi">10.1016/j.bbrc.2018.11.093</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Japon</li></country></list><tree><country name="Japon"><noRegion><name sortKey="Koriyama, Toyoyasu" sort="Koriyama, Toyoyasu" uniqKey="Koriyama T" first="Toyoyasu" last="Koriyama">Toyoyasu Koriyama</name></noRegion><name sortKey="Hashiguchi, Teruto" sort="Hashiguchi, Teruto" uniqKey="Hashiguchi T" first="Teruto" last="Hashiguchi">Teruto Hashiguchi</name><name sortKey="Masamoto, Izumi" sort="Masamoto, Izumi" uniqKey="Masamoto I" first="Izumi" last="Masamoto">Izumi Masamoto</name><name sortKey="Nagakura, Takumi" sort="Nagakura, Takumi" uniqKey="Nagakura T" first="Takumi" last="Nagakura">Takumi Nagakura</name><name sortKey="Oyama, Yoko" sort="Oyama, Yoko" uniqKey="Oyama Y" first="Yoko" last="Oyama">Yoko Oyama</name><name sortKey="Takenaka, Hiroyoshi" sort="Takenaka, Hiroyoshi" uniqKey="Takenaka H" first="Hiroyoshi" last="Takenaka">Hiroyoshi Takenaka</name><name sortKey="Takenouchi, Kazunori" sort="Takenouchi, Kazunori" uniqKey="Takenouchi K" first="Kazunori" last="Takenouchi">Kazunori Takenouchi</name><name sortKey="Yamakuchi, Munekazu" sort="Yamakuchi, Munekazu" uniqKey="Yamakuchi M" first="Munekazu" last="Yamakuchi">Munekazu Yamakuchi</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Bois/explor/RapamycinFungusV1/Data/Main/Exploration
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{{Explor lien
|wiki= Bois
|area= RapamycinFungusV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= pubmed:30509489
|texte= Legionella pneumophila infection-mediated regulation of RICTOR via miR-218 in U937 macrophage cells.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:30509489" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
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