Mycobacterium tuberculosis EIS gene inhibits macrophage autophagy through up-regulation of IL-10 by increasing the acetylation of histone H3.
Identifieur interne : 000A60 ( Main/Exploration ); précédent : 000A59; suivant : 000A61Mycobacterium tuberculosis EIS gene inhibits macrophage autophagy through up-regulation of IL-10 by increasing the acetylation of histone H3.
Auteurs : Liang Duan [République populaire de Chine] ; Min Yi [République populaire de Chine] ; Juan Chen [République populaire de Chine] ; Shengjin Li [République populaire de Chine] ; Weixian Chen [République populaire de Chine]Source :
- Biochemical and biophysical research communications [ 1090-2104 ] ; 2016.
Descripteurs français
- KwdFr :
- Acetyltransferases (MeSH), Acétylation (MeSH), Antigènes bactériens (métabolisme), Autophagie (physiologie), Histone (métabolisme), Interleukine-10 (métabolisme), Macrophages (microbiologie), Mycobacterium tuberculosis (cytologie), Mycobacterium tuberculosis (physiologie), Protéines bactériennes (métabolisme), Régulation de l'expression des gènes bactériens (physiologie), Régulation positive (physiologie).
- MESH :
- cytologie : Mycobacterium tuberculosis.
- microbiologie : Macrophages.
- métabolisme : Antigènes bactériens, Histone, Interleukine-10, Protéines bactériennes.
- physiologie : Autophagie, Mycobacterium tuberculosis, Régulation de l'expression des gènes bactériens, Régulation positive.
- Acetyltransferases, Acétylation.
English descriptors
- KwdEn :
- Acetylation (MeSH), Acetyltransferases (MeSH), Antigens, Bacterial (metabolism), Autophagy (physiology), Bacterial Proteins (metabolism), Gene Expression Regulation, Bacterial (physiology), Histones (metabolism), Interleukin-10 (metabolism), Macrophages (microbiology), Mycobacterium tuberculosis (cytology), Mycobacterium tuberculosis (physiology), Up-Regulation (physiology).
- MESH :
- chemical , metabolism : Antigens, Bacterial, Bacterial Proteins, Histones, Interleukin-10.
- chemical : Acetyltransferases.
- cytology : Mycobacterium tuberculosis.
- microbiology : Macrophages.
- physiology : Autophagy, Gene Expression Regulation, Bacterial, Mycobacterium tuberculosis, Up-Regulation.
- Acetylation.
Abstract
Autophagy plays a crucial role in the progress of Mycobacterium tuberculosis (MTB) infection. Recently, MTB enhanced intracellular survival (EIS) protein was reported to be secreted from MTB cells and linked to the inhibition of autophagy and the intracellular persistence of the pathogen. Here, we investigated the mechanism of EIS-mediated inhibition of autophagy in a human phorbol myristate acetate (PMA)-treated THP-1 cell line as well as in murine macrophages. We confirmed that the presence of EIS led to the inhibition of rapamycin (Rapa)-induced autophagy, while IL-10 gene expression was increased and Akt/mTOR/p70S6K pathway was activated during the process. IL-10 gene silencing led to a significant recovery of EIS-mediated autophagy suppression and decreased activity of the Akt/mTOR/p70S6K pathway. IL-10 promoter activity was unaffected by EIS. Remarkably, EIS increased the acetylation level of histone H3 (Ac-H3), which binds to the SP1 and STAT3 region of the human IL-10 gene promoter sequence. Thus, EIS protein possibly increased IL-10 expression through the regulation of Ac-H3 of its promoter. Our data demonstrated that one possible mechanism of the MTB evasion of autophagy is that the EIS protein up-regulates IL-10 via Ac-H3 and thus activates Akt/mTOR/p70S6K pathway.
DOI: 10.1016/j.bbrc.2016.04.045
PubMed: 27079235
Affiliations:
Links toward previous steps (curation, corpus...)
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Electronic address: lsj1025@163.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory, The Second Hospital Affiliated to Chongqing Medical University, Chongqing, 400010</wicri:regionArea><wicri:noRegion>400010</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Weixian" sort="Chen, Weixian" uniqKey="Chen W" first="Weixian" last="Chen">Weixian Chen</name><affiliation wicri:level="1"><nlm:affiliation>Department of Laboratory Medicine, The Second Hospital Affiliated to Chongqing Medical University, Chongqing, 400010, China. Electronic address: chenweixian75@163.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Laboratory Medicine, The Second Hospital Affiliated to Chongqing Medical University, Chongqing, 400010</wicri:regionArea><wicri:noRegion>400010</wicri:noRegion></affiliation></author></analytic><series><title level="j">Biochemical and biophysical research communications</title><idno type="eISSN">1090-2104</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acetylation (MeSH)</term><term>Acetyltransferases (MeSH)</term><term>Antigens, Bacterial (metabolism)</term><term>Autophagy (physiology)</term><term>Bacterial Proteins (metabolism)</term><term>Gene Expression Regulation, Bacterial (physiology)</term><term>Histones (metabolism)</term><term>Interleukin-10 (metabolism)</term><term>Macrophages (microbiology)</term><term>Mycobacterium tuberculosis (cytology)</term><term>Mycobacterium tuberculosis (physiology)</term><term>Up-Regulation (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acetyltransferases (MeSH)</term><term>Acétylation (MeSH)</term><term>Antigènes bactériens (métabolisme)</term><term>Autophagie (physiologie)</term><term>Histone (métabolisme)</term><term>Interleukine-10 (métabolisme)</term><term>Macrophages (microbiologie)</term><term>Mycobacterium tuberculosis (cytologie)</term><term>Mycobacterium tuberculosis (physiologie)</term><term>Protéines bactériennes (métabolisme)</term><term>Régulation de l'expression des gènes bactériens (physiologie)</term><term>Régulation positive (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antigens, Bacterial</term><term>Bacterial Proteins</term><term>Histones</term><term>Interleukin-10</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Acetyltransferases</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Mycobacterium tuberculosis</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Mycobacterium tuberculosis</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>Antigènes bactériens</term><term>Histone</term><term>Interleukine-10</term><term>Protéines bactériennes</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Autophagie</term><term>Mycobacterium tuberculosis</term><term>Régulation de l'expression des gènes bactériens</term><term>Régulation positive</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Autophagy</term><term>Gene Expression Regulation, Bacterial</term><term>Mycobacterium tuberculosis</term><term>Up-Regulation</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Acetylation</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Acetyltransferases</term><term>Acétylation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Autophagy plays a crucial role in the progress of Mycobacterium tuberculosis (MTB) infection. Recently, MTB enhanced intracellular survival (EIS) protein was reported to be secreted from MTB cells and linked to the inhibition of autophagy and the intracellular persistence of the pathogen. Here, we investigated the mechanism of EIS-mediated inhibition of autophagy in a human phorbol myristate acetate (PMA)-treated THP-1 cell line as well as in murine macrophages. We confirmed that the presence of EIS led to the inhibition of rapamycin (Rapa)-induced autophagy, while IL-10 gene expression was increased and Akt/mTOR/p70S6K pathway was activated during the process. IL-10 gene silencing led to a significant recovery of EIS-mediated autophagy suppression and decreased activity of the Akt/mTOR/p70S6K pathway. IL-10 promoter activity was unaffected by EIS. Remarkably, EIS increased the acetylation level of histone H3 (Ac-H3), which binds to the SP1 and STAT3 region of the human IL-10 gene promoter sequence. Thus, EIS protein possibly increased IL-10 expression through the regulation of Ac-H3 of its promoter. Our data demonstrated that one possible mechanism of the MTB evasion of autophagy is that the EIS protein up-regulates IL-10 via Ac-H3 and thus activates Akt/mTOR/p70S6K pathway.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27079235</PMID><DateCompleted><Year>2017</Year><Month>05</Month><Day>05</Day></DateCompleted><DateRevised><Year>2017</Year><Month>11</Month><Day>17</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1090-2104</ISSN><JournalIssue CitedMedium="Internet"><Volume>473</Volume><Issue>4</Issue><PubDate><Year>2016</Year><Month>05</Month><Day>13</Day></PubDate></JournalIssue><Title>Biochemical and biophysical research communications</Title><ISOAbbreviation>Biochem Biophys Res Commun</ISOAbbreviation></Journal><ArticleTitle>Mycobacterium tuberculosis EIS gene inhibits macrophage autophagy through up-regulation of IL-10 by increasing the acetylation of histone H3.</ArticleTitle><Pagination><MedlinePgn>1229-1234</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0006-291X(16)30540-X</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbrc.2016.04.045</ELocationID><Abstract><AbstractText>Autophagy plays a crucial role in the progress of Mycobacterium tuberculosis (MTB) infection. Recently, MTB enhanced intracellular survival (EIS) protein was reported to be secreted from MTB cells and linked to the inhibition of autophagy and the intracellular persistence of the pathogen. Here, we investigated the mechanism of EIS-mediated inhibition of autophagy in a human phorbol myristate acetate (PMA)-treated THP-1 cell line as well as in murine macrophages. We confirmed that the presence of EIS led to the inhibition of rapamycin (Rapa)-induced autophagy, while IL-10 gene expression was increased and Akt/mTOR/p70S6K pathway was activated during the process. IL-10 gene silencing led to a significant recovery of EIS-mediated autophagy suppression and decreased activity of the Akt/mTOR/p70S6K pathway. IL-10 promoter activity was unaffected by EIS. Remarkably, EIS increased the acetylation level of histone H3 (Ac-H3), which binds to the SP1 and STAT3 region of the human IL-10 gene promoter sequence. Thus, EIS protein possibly increased IL-10 expression through the regulation of Ac-H3 of its promoter. Our data demonstrated that one possible mechanism of the MTB evasion of autophagy is that the EIS protein up-regulates IL-10 via Ac-H3 and thus activates Akt/mTOR/p70S6K pathway.</AbstractText><CopyrightInformation>Copyright © 2016 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Duan</LastName><ForeName>Liang</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Laboratory Medicine, The Second Hospital Affiliated to Chongqing Medical University, Chongqing, 400010, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yi</LastName><ForeName>Min</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Respiratory, The Second Hospital Affiliated to Chongqing Medical University, Chongqing, 400010, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Juan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Laboratory Medicine, The Second Hospital Affiliated to Chongqing Medical University, Chongqing, 400010, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Shengjin</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Respiratory, The Second Hospital Affiliated to Chongqing Medical University, Chongqing, 400010, China. Electronic address: lsj1025@163.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Weixian</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Laboratory Medicine, The Second Hospital Affiliated to Chongqing Medical University, Chongqing, 400010, China. Electronic address: chenweixian75@163.com.</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>2016</Year><Month>04</Month><Day>11</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="D000942">Antigens, Bacterial</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001426">Bacterial Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006657">Histones</NameOfSubstance></Chemical><Chemical><RegistryNumber>130068-27-8</RegistryNumber><NameOfSubstance UI="D016753">Interleukin-10</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.1.-</RegistryNumber><NameOfSubstance UI="D000123">Acetyltransferases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.1.-</RegistryNumber><NameOfSubstance UI="C430563">Eis protein, Mycobacterium tuberculosis</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000107" MajorTopicYN="N">Acetylation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000123" MajorTopicYN="N">Acetyltransferases</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000942" MajorTopicYN="N">Antigens, Bacterial</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001426" MajorTopicYN="N">Bacterial Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015964" MajorTopicYN="N">Gene Expression Regulation, Bacterial</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006657" MajorTopicYN="N">Histones</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016753" MajorTopicYN="N">Interleukin-10</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009169" MajorTopicYN="N">Mycobacterium tuberculosis</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015854" MajorTopicYN="N">Up-Regulation</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Autophagy</Keyword><Keyword MajorTopicYN="Y">Histone acetylation</Keyword><Keyword MajorTopicYN="Y">Interleukin 10</Keyword><Keyword MajorTopicYN="Y">Mycobacterium tuberculosis</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>03</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>04</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>4</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>4</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>5</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27079235</ArticleId><ArticleId IdType="pii">S0006-291X(16)30540-X</ArticleId><ArticleId IdType="doi">10.1016/j.bbrc.2016.04.045</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Duan, Liang" sort="Duan, Liang" uniqKey="Duan L" first="Liang" last="Duan">Liang Duan</name></noRegion><name sortKey="Chen, Juan" sort="Chen, Juan" uniqKey="Chen J" first="Juan" last="Chen">Juan Chen</name><name sortKey="Chen, Weixian" sort="Chen, Weixian" uniqKey="Chen W" first="Weixian" last="Chen">Weixian Chen</name><name sortKey="Li, Shengjin" sort="Li, Shengjin" uniqKey="Li S" first="Shengjin" last="Li">Shengjin Li</name><name sortKey="Yi, Min" sort="Yi, Min" uniqKey="Yi M" first="Min" last="Yi">Min Yi</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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