Staphylococcus aureus subvert autophagy for induction of caspase-independent host cell death.
Identifieur interne : 001683 ( Main/Exploration ); précédent : 001682; suivant : 001684Staphylococcus aureus subvert autophagy for induction of caspase-independent host cell death.
Auteurs : Annabelle Schnaith [Allemagne] ; Hamid Kashkar ; Sonja A. Leggio ; Klaus Addicks ; Martin Krönke ; Oleg KrutSource :
- The Journal of biological chemistry [ 0021-9258 ] ; 2007.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Autophagie (MeSH), Caspases (métabolisme), Cellules HeLa (MeSH), Humains (MeSH), Infections à staphylocoques (anatomopathologie), Infections à staphylocoques (métabolisme), Modèles biologiques (MeSH), Protéine-5 associée à l'autophagie (MeSH), Protéines associées aux microtubules (génétique), Protéines associées aux microtubules (métabolisme), Protéines bactériennes (métabolisme), Souris (MeSH), Staphylococcus aureus (MeSH), Transactivateurs (métabolisme).
- MESH :
- anatomopathologie : Infections à staphylocoques.
- génétique : Protéines associées aux microtubules.
- métabolisme : Caspases, Infections à staphylocoques, Protéines associées aux microtubules, Protéines bactériennes, Transactivateurs.
- Animaux, Autophagie, Cellules HeLa, Humains, Modèles biologiques, Protéine-5 associée à l'autophagie, Souris, Staphylococcus aureus.
English descriptors
- KwdEn :
- Animals (MeSH), Autophagy (MeSH), Autophagy-Related Protein 5 (MeSH), Bacterial Proteins (metabolism), Caspases (metabolism), HeLa Cells (MeSH), Humans (MeSH), Mice (MeSH), Microtubule-Associated Proteins (genetics), Microtubule-Associated Proteins (metabolism), Models, Biological (MeSH), Staphylococcal Infections (metabolism), Staphylococcal Infections (pathology), Staphylococcus aureus (MeSH), Trans-Activators (metabolism).
- MESH :
- chemical , genetics : Microtubule-Associated Proteins.
- chemical , metabolism : Bacterial Proteins, Caspases, Microtubule-Associated Proteins, Trans-Activators.
- chemical : Autophagy-Related Protein 5.
- metabolism : Staphylococcal Infections.
- pathology : Staphylococcal Infections.
- Animals, Autophagy, HeLa Cells, Humans, Mice, Models, Biological, Staphylococcus aureus.
Abstract
Staphylococcus aureus is a common bacterial etiology of serious infectious diseases. S. aureus can invade various types of non-professional phagocytes to produce host cell death. We show here that shortly after invasion of HeLa cells S. aureus transit to autophagosomes was characterized by double membranes and co-localization with LC3. S. aureus were not able to replicate and produce cell death in autophagy-deficient atg5-/- mouse embryonic fibroblasts. S. aureus-containing autophagosomes do not acidify nor do they acquire lysosome-associated membrane protein-2, indicating that S. aureus inhibits autophagosome maturation and fusion with lysosomes. Eventually, S. aureus escape from autophagosomes into the cytoplasm, which results in caspase-independent host cell death. S. aureus strains deficient for agr, a global regulator of S. aureus virulence, were not targeted by autophagy and did not produce host-cell death. Autophagy induction by rapamycin restored both replication and cytotoxicity of agr-deficient S. aureus strains, indicating that an agr-regulated factor(s) is required for autophagy-mediated cytotoxicity. The results of this study suggest that rapid induction of autophagy is essential for S. aureus replication, escape into the cytoplasm, and host cell killing.
DOI: 10.1074/jbc.M609784200
PubMed: 17135247
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Leggio</name></author><author><name sortKey="Addicks, Klaus" sort="Addicks, Klaus" uniqKey="Addicks K" first="Klaus" last="Addicks">Klaus Addicks</name></author><author><name sortKey="Kronke, Martin" sort="Kronke, Martin" uniqKey="Kronke M" first="Martin" last="Krönke">Martin Krönke</name></author><author><name sortKey="Krut, Oleg" sort="Krut, Oleg" uniqKey="Krut O" first="Oleg" last="Krut">Oleg Krut</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2007">2007</date><idno type="RBID">pubmed:17135247</idno><idno type="pmid">17135247</idno><idno type="doi">10.1074/jbc.M609784200</idno><idno type="wicri:Area/Main/Corpus">001742</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">001742</idno><idno type="wicri:Area/Main/Curation">001742</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">001742</idno><idno type="wicri:Area/Main/Exploration">001742</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Staphylococcus aureus subvert autophagy for induction of caspase-independent host cell death.</title><author><name sortKey="Schnaith, Annabelle" sort="Schnaith, Annabelle" uniqKey="Schnaith A" first="Annabelle" last="Schnaith">Annabelle Schnaith</name><affiliation wicri:level="3"><nlm:affiliation>Institute for Medical Microbiology, Immunology and Hygiene, University of Cologne, 50935 Cologne, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Institute for Medical Microbiology, Immunology and Hygiene, University of Cologne, 50935 Cologne</wicri:regionArea><placeName><region type="land" nuts="1">Rhénanie-du-Nord-Westphalie</region><region type="district" nuts="2">District de Cologne</region><settlement type="city">Cologne</settlement></placeName></affiliation></author><author><name sortKey="Kashkar, Hamid" sort="Kashkar, Hamid" uniqKey="Kashkar H" first="Hamid" last="Kashkar">Hamid Kashkar</name></author><author><name sortKey="Leggio, Sonja A" sort="Leggio, Sonja A" uniqKey="Leggio S" first="Sonja A" last="Leggio">Sonja A. Leggio</name></author><author><name sortKey="Addicks, Klaus" sort="Addicks, Klaus" uniqKey="Addicks K" first="Klaus" last="Addicks">Klaus Addicks</name></author><author><name sortKey="Kronke, Martin" sort="Kronke, Martin" uniqKey="Kronke M" first="Martin" last="Krönke">Martin Krönke</name></author><author><name sortKey="Krut, Oleg" sort="Krut, Oleg" uniqKey="Krut O" first="Oleg" last="Krut">Oleg Krut</name></author></analytic><series><title level="j">The Journal of biological chemistry</title><idno type="ISSN">0021-9258</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Autophagy (MeSH)</term><term>Autophagy-Related Protein 5 (MeSH)</term><term>Bacterial Proteins (metabolism)</term><term>Caspases (metabolism)</term><term>HeLa Cells (MeSH)</term><term>Humans (MeSH)</term><term>Mice (MeSH)</term><term>Microtubule-Associated Proteins (genetics)</term><term>Microtubule-Associated Proteins (metabolism)</term><term>Models, Biological (MeSH)</term><term>Staphylococcal Infections (metabolism)</term><term>Staphylococcal Infections (pathology)</term><term>Staphylococcus aureus (MeSH)</term><term>Trans-Activators (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Autophagie (MeSH)</term><term>Caspases (métabolisme)</term><term>Cellules HeLa (MeSH)</term><term>Humains (MeSH)</term><term>Infections à staphylocoques (anatomopathologie)</term><term>Infections à staphylocoques (métabolisme)</term><term>Modèles biologiques (MeSH)</term><term>Protéine-5 associée à l'autophagie (MeSH)</term><term>Protéines associées aux microtubules (génétique)</term><term>Protéines associées aux microtubules (métabolisme)</term><term>Protéines bactériennes (métabolisme)</term><term>Souris (MeSH)</term><term>Staphylococcus aureus (MeSH)</term><term>Transactivateurs (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Microtubule-Associated Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Bacterial Proteins</term><term>Caspases</term><term>Microtubule-Associated Proteins</term><term>Trans-Activators</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Autophagy-Related Protein 5</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Infections à staphylocoques</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Protéines associées aux microtubules</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Staphylococcal Infections</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Caspases</term><term>Infections à staphylocoques</term><term>Protéines associées aux microtubules</term><term>Protéines bactériennes</term><term>Transactivateurs</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Staphylococcal Infections</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Autophagy</term><term>HeLa Cells</term><term>Humans</term><term>Mice</term><term>Models, Biological</term><term>Staphylococcus aureus</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Autophagie</term><term>Cellules HeLa</term><term>Humains</term><term>Modèles biologiques</term><term>Protéine-5 associée à l'autophagie</term><term>Souris</term><term>Staphylococcus aureus</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Staphylococcus aureus is a common bacterial etiology of serious infectious diseases. S. aureus can invade various types of non-professional phagocytes to produce host cell death. We show here that shortly after invasion of HeLa cells S. aureus transit to autophagosomes was characterized by double membranes and co-localization with LC3. S. aureus were not able to replicate and produce cell death in autophagy-deficient atg5-/- mouse embryonic fibroblasts. S. aureus-containing autophagosomes do not acidify nor do they acquire lysosome-associated membrane protein-2, indicating that S. aureus inhibits autophagosome maturation and fusion with lysosomes. Eventually, S. aureus escape from autophagosomes into the cytoplasm, which results in caspase-independent host cell death. S. aureus strains deficient for agr, a global regulator of S. aureus virulence, were not targeted by autophagy and did not produce host-cell death. Autophagy induction by rapamycin restored both replication and cytotoxicity of agr-deficient S. aureus strains, indicating that an agr-regulated factor(s) is required for autophagy-mediated cytotoxicity. The results of this study suggest that rapid induction of autophagy is essential for S. aureus replication, escape into the cytoplasm, and host cell killing.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17135247</PMID><DateCompleted><Year>2007</Year><Month>04</Month><Day>09</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>24</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0021-9258</ISSN><JournalIssue CitedMedium="Print"><Volume>282</Volume><Issue>4</Issue><PubDate><Year>2007</Year><Month>Jan</Month><Day>26</Day></PubDate></JournalIssue><Title>The Journal of biological chemistry</Title><ISOAbbreviation>J Biol Chem</ISOAbbreviation></Journal><ArticleTitle>Staphylococcus aureus subvert autophagy for induction of caspase-independent host cell death.</ArticleTitle><Pagination><MedlinePgn>2695-706</MedlinePgn></Pagination><Abstract><AbstractText>Staphylococcus aureus is a common bacterial etiology of serious infectious diseases. S. aureus can invade various types of non-professional phagocytes to produce host cell death. We show here that shortly after invasion of HeLa cells S. aureus transit to autophagosomes was characterized by double membranes and co-localization with LC3. S. aureus were not able to replicate and produce cell death in autophagy-deficient atg5-/- mouse embryonic fibroblasts. S. aureus-containing autophagosomes do not acidify nor do they acquire lysosome-associated membrane protein-2, indicating that S. aureus inhibits autophagosome maturation and fusion with lysosomes. Eventually, S. aureus escape from autophagosomes into the cytoplasm, which results in caspase-independent host cell death. S. aureus strains deficient for agr, a global regulator of S. aureus virulence, were not targeted by autophagy and did not produce host-cell death. Autophagy induction by rapamycin restored both replication and cytotoxicity of agr-deficient S. aureus strains, indicating that an agr-regulated factor(s) is required for autophagy-mediated cytotoxicity. The results of this study suggest that rapid induction of autophagy is essential for S. aureus replication, escape into the cytoplasm, and host cell killing.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Schnaith</LastName><ForeName>Annabelle</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Institute for Medical Microbiology, Immunology and Hygiene, University of Cologne, 50935 Cologne, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kashkar</LastName><ForeName>Hamid</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Leggio</LastName><ForeName>Sonja A</ForeName><Initials>SA</Initials></Author><Author ValidYN="Y"><LastName>Addicks</LastName><ForeName>Klaus</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Krönke</LastName><ForeName>Martin</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Krut</LastName><ForeName>Oleg</ForeName><Initials>O</Initials></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>2006</Year><Month>11</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Biol Chem</MedlineTA><NlmUniqueID>2985121R</NlmUniqueID><ISSNLinking>0021-9258</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C502778">ATG5 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C095698">Agr protein, Staphylococcus aureus</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C495773">Atg5 protein, 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MajorTopicYN="N">Autophagy-Related Protein 5</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001426" MajorTopicYN="N">Bacterial Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020169" MajorTopicYN="N">Caspases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006367" MajorTopicYN="N">HeLa Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008869" MajorTopicYN="N">Microtubule-Associated Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008954" MajorTopicYN="N">Models, Biological</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013203" MajorTopicYN="Y">Staphylococcal Infections</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013211" MajorTopicYN="Y">Staphylococcus aureus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015534" MajorTopicYN="N">Trans-Activators</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>12</Month><Day>1</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>4</Month><Day>10</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>12</Month><Day>1</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17135247</ArticleId><ArticleId IdType="pii">M609784200</ArticleId><ArticleId IdType="doi">10.1074/jbc.M609784200</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li></country><region><li>District de Cologne</li><li>Rhénanie-du-Nord-Westphalie</li></region><settlement><li>Cologne</li></settlement></list><tree><noCountry><name sortKey="Addicks, Klaus" sort="Addicks, Klaus" uniqKey="Addicks K" first="Klaus" last="Addicks">Klaus Addicks</name><name sortKey="Kashkar, Hamid" sort="Kashkar, Hamid" uniqKey="Kashkar H" first="Hamid" last="Kashkar">Hamid Kashkar</name><name sortKey="Kronke, Martin" sort="Kronke, Martin" uniqKey="Kronke M" first="Martin" last="Krönke">Martin Krönke</name><name sortKey="Krut, Oleg" sort="Krut, Oleg" uniqKey="Krut O" first="Oleg" last="Krut">Oleg Krut</name><name sortKey="Leggio, Sonja A" sort="Leggio, Sonja A" uniqKey="Leggio S" first="Sonja A" last="Leggio">Sonja A. Leggio</name></noCountry><country name="Allemagne"><region name="Rhénanie-du-Nord-Westphalie"><name sortKey="Schnaith, Annabelle" sort="Schnaith, Annabelle" uniqKey="Schnaith A" first="Annabelle" last="Schnaith">Annabelle Schnaith</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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