Intraphagolysosomal conditions predispose to Staphylococcus epidermidis small colony variants persistence in macrophages.
Identifieur interne : 000570 ( Main/Exploration ); précédent : 000569; suivant : 000571Intraphagolysosomal conditions predispose to Staphylococcus epidermidis small colony variants persistence in macrophages.
Auteurs : Agnieszka Magry [Pologne] ; Kamil Deryło [Pologne] ; Agnieszka Bogut [Pologne] ; Alina Olender [Pologne] ; Marek Tch Rzewski [Pologne]Source :
- PloS one [ 1932-6203 ] ; 2018.
Descripteurs français
- KwdFr :
- MESH :
- microbiologie : Macrophages, Phagosomes.
- métabolisme : Macrophages, Phagosomes, Staphylococcus epidermidis.
- Cellules THP-1, Humains, Viabilité microbienne.
English descriptors
- KwdEn :
- MESH :
- metabolism : Macrophages, Phagosomes, Staphylococcus epidermidis.
- microbiology : Macrophages, Phagosomes.
- Humans, Microbial Viability, THP-1 Cells.
Abstract
Staphylococcus epidermidis small colony variants can survive inside macrophages and their survival has been proposed as a pivotal process in the pathogenesis of biomaterial associated infections. In the present study the intracellular location of clinical isolates of SCV and parental wild type strains inside macrophages was determined. Furthermore, the effect of IFN-γ and rapamycin on the level of SCV/WT as well as lysosomes colocalisation and iNOS induction in THP-activated macrophages in response to WT and SCV strains of Staphylococcus epidermidis were examined. It was demonstrated that SCV strain of S. epidermidis can survive and persist inside macrophages and its intracellular survival is supported by the induction of phagosomal acidification. The ability to reduce the high proportion of LysoTracker positive SCV containing phagosomes was exclusively found when IFN-γ was used. The findings suggest that IFN-γ mediates SCV killing via two distinct mechanisms, phagosome alkalisation and an increased iNOS synthesis, so the cytokine may control S. epidermidis WT and SCV infection in macrophages. Staphylococcus epidermidis SCV is a less potent stimulus of iNOS than the WT strain and the feature may help SCV to persist in hostile environment of macrophages. Rapamycin treatment did not influence the iNOS synthesis but reduced the percentage of both bacterial strains within acidic organelles. However, the percentage of SCV within LysoTracker positive organelles, even though reduced comparing to non-primed cells, was higher than in the WT strain indicating that Staphylococcus epidermidis possesses unique metabolic features allowing SCV to survive within macrophages.
DOI: 10.1371/journal.pone.0207312
PubMed: 30412620
PubMed Central: PMC6226201
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Intraphagolysosomal conditions predispose to Staphylococcus epidermidis small colony variants persistence in macrophages.</title><author><name sortKey="Magry, Agnieszka" sort="Magry, Agnieszka" uniqKey="Magry A" first="Agnieszka" last="Magry">Agnieszka Magry</name><affiliation wicri:level="1"><nlm:affiliation>Chair and Department of Medical Microbiology, Medical University of Lublin, Lublin, Poland.</nlm:affiliation><country xml:lang="fr">Pologne</country><wicri:regionArea>Chair and Department of Medical Microbiology, Medical University of Lublin, Lublin</wicri:regionArea><wicri:noRegion>Lublin</wicri:noRegion></affiliation></author><author><name sortKey="Derylo, Kamil" sort="Derylo, Kamil" uniqKey="Derylo K" first="Kamil" last="Deryło">Kamil Deryło</name><affiliation wicri:level="1"><nlm:affiliation>Department of Molecular Biology, Maria Curie-Skłodowska University, Lublin, Poland.</nlm:affiliation><country xml:lang="fr">Pologne</country><wicri:regionArea>Department of Molecular Biology, Maria Curie-Skłodowska University, Lublin</wicri:regionArea><wicri:noRegion>Lublin</wicri:noRegion></affiliation></author><author><name sortKey="Bogut, Agnieszka" sort="Bogut, Agnieszka" uniqKey="Bogut A" first="Agnieszka" last="Bogut">Agnieszka Bogut</name><affiliation wicri:level="1"><nlm:affiliation>Chair and Department of Medical Microbiology, Medical University of Lublin, Lublin, Poland.</nlm:affiliation><country xml:lang="fr">Pologne</country><wicri:regionArea>Chair and Department of Medical Microbiology, Medical University of Lublin, Lublin</wicri:regionArea><wicri:noRegion>Lublin</wicri:noRegion></affiliation></author><author><name sortKey="Olender, Alina" sort="Olender, Alina" uniqKey="Olender A" first="Alina" last="Olender">Alina Olender</name><affiliation wicri:level="1"><nlm:affiliation>Chair and Department of Medical Microbiology, Medical University of Lublin, Lublin, Poland.</nlm:affiliation><country xml:lang="fr">Pologne</country><wicri:regionArea>Chair and Department of Medical Microbiology, Medical University of Lublin, Lublin</wicri:regionArea><wicri:noRegion>Lublin</wicri:noRegion></affiliation></author><author><name sortKey="Tch Rzewski, Marek" sort="Tch Rzewski, Marek" uniqKey="Tch Rzewski M" first="Marek" last="Tch Rzewski">Marek Tch Rzewski</name><affiliation wicri:level="1"><nlm:affiliation>Department of Molecular Biology, Maria Curie-Skłodowska University, Lublin, Poland.</nlm:affiliation><country xml:lang="fr">Pologne</country><wicri:regionArea>Department of Molecular Biology, Maria Curie-Skłodowska University, Lublin</wicri:regionArea><wicri:noRegion>Lublin</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2018">2018</date><idno type="RBID">pubmed:30412620</idno><idno type="pmid">30412620</idno><idno type="doi">10.1371/journal.pone.0207312</idno><idno type="pmc">PMC6226201</idno><idno type="wicri:Area/Main/Corpus">000408</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000408</idno><idno type="wicri:Area/Main/Curation">000408</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000408</idno><idno type="wicri:Area/Main/Exploration">000408</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Intraphagolysosomal conditions predispose to Staphylococcus epidermidis small colony variants persistence in macrophages.</title><author><name sortKey="Magry, Agnieszka" sort="Magry, Agnieszka" uniqKey="Magry A" first="Agnieszka" last="Magry">Agnieszka Magry</name><affiliation wicri:level="1"><nlm:affiliation>Chair and Department of Medical Microbiology, Medical University of Lublin, Lublin, Poland.</nlm:affiliation><country xml:lang="fr">Pologne</country><wicri:regionArea>Chair and Department of Medical Microbiology, Medical University of Lublin, Lublin</wicri:regionArea><wicri:noRegion>Lublin</wicri:noRegion></affiliation></author><author><name sortKey="Derylo, Kamil" sort="Derylo, Kamil" uniqKey="Derylo K" first="Kamil" last="Deryło">Kamil Deryło</name><affiliation wicri:level="1"><nlm:affiliation>Department of Molecular Biology, Maria Curie-Skłodowska University, Lublin, Poland.</nlm:affiliation><country xml:lang="fr">Pologne</country><wicri:regionArea>Department of Molecular Biology, Maria Curie-Skłodowska University, Lublin</wicri:regionArea><wicri:noRegion>Lublin</wicri:noRegion></affiliation></author><author><name sortKey="Bogut, Agnieszka" sort="Bogut, Agnieszka" uniqKey="Bogut A" first="Agnieszka" last="Bogut">Agnieszka Bogut</name><affiliation wicri:level="1"><nlm:affiliation>Chair and Department of Medical Microbiology, Medical University of Lublin, Lublin, Poland.</nlm:affiliation><country xml:lang="fr">Pologne</country><wicri:regionArea>Chair and Department of Medical Microbiology, Medical University of Lublin, Lublin</wicri:regionArea><wicri:noRegion>Lublin</wicri:noRegion></affiliation></author><author><name sortKey="Olender, Alina" sort="Olender, Alina" uniqKey="Olender A" first="Alina" last="Olender">Alina Olender</name><affiliation wicri:level="1"><nlm:affiliation>Chair and Department of Medical Microbiology, Medical University of Lublin, Lublin, Poland.</nlm:affiliation><country xml:lang="fr">Pologne</country><wicri:regionArea>Chair and Department of Medical Microbiology, Medical University of Lublin, Lublin</wicri:regionArea><wicri:noRegion>Lublin</wicri:noRegion></affiliation></author><author><name sortKey="Tch Rzewski, Marek" sort="Tch Rzewski, Marek" uniqKey="Tch Rzewski M" first="Marek" last="Tch Rzewski">Marek Tch Rzewski</name><affiliation wicri:level="1"><nlm:affiliation>Department of Molecular Biology, Maria Curie-Skłodowska University, Lublin, Poland.</nlm:affiliation><country xml:lang="fr">Pologne</country><wicri:regionArea>Department of Molecular Biology, Maria Curie-Skłodowska University, Lublin</wicri:regionArea><wicri:noRegion>Lublin</wicri:noRegion></affiliation></author></analytic><series><title level="j">PloS one</title><idno type="eISSN">1932-6203</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Humans (MeSH)</term><term>Macrophages (metabolism)</term><term>Macrophages (microbiology)</term><term>Microbial Viability (MeSH)</term><term>Phagosomes (metabolism)</term><term>Phagosomes (microbiology)</term><term>Staphylococcus epidermidis (metabolism)</term><term>THP-1 Cells (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Cellules THP-1 (MeSH)</term><term>Humains (MeSH)</term><term>Macrophages (microbiologie)</term><term>Macrophages (métabolisme)</term><term>Phagosomes (microbiologie)</term><term>Phagosomes (métabolisme)</term><term>Staphylococcus epidermidis (métabolisme)</term><term>Viabilité microbienne (MeSH)</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Macrophages</term><term>Phagosomes</term><term>Staphylococcus epidermidis</term></keywords><keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Macrophages</term><term>Phagosomes</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Macrophages</term><term>Phagosomes</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Macrophages</term><term>Phagosomes</term><term>Staphylococcus epidermidis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term><term>Microbial Viability</term><term>THP-1 Cells</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cellules THP-1</term><term>Humains</term><term>Viabilité microbienne</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Staphylococcus epidermidis small colony variants can survive inside macrophages and their survival has been proposed as a pivotal process in the pathogenesis of biomaterial associated infections. In the present study the intracellular location of clinical isolates of SCV and parental wild type strains inside macrophages was determined. Furthermore, the effect of IFN-γ and rapamycin on the level of SCV/WT as well as lysosomes colocalisation and iNOS induction in THP-activated macrophages in response to WT and SCV strains of Staphylococcus epidermidis were examined. It was demonstrated that SCV strain of S. epidermidis can survive and persist inside macrophages and its intracellular survival is supported by the induction of phagosomal acidification. The ability to reduce the high proportion of LysoTracker positive SCV containing phagosomes was exclusively found when IFN-γ was used. The findings suggest that IFN-γ mediates SCV killing via two distinct mechanisms, phagosome alkalisation and an increased iNOS synthesis, so the cytokine may control S. epidermidis WT and SCV infection in macrophages. Staphylococcus epidermidis SCV is a less potent stimulus of iNOS than the WT strain and the feature may help SCV to persist in hostile environment of macrophages. Rapamycin treatment did not influence the iNOS synthesis but reduced the percentage of both bacterial strains within acidic organelles. However, the percentage of SCV within LysoTracker positive organelles, even though reduced comparing to non-primed cells, was higher than in the WT strain indicating that Staphylococcus epidermidis possesses unique metabolic features allowing SCV to survive within macrophages.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30412620</PMID><DateCompleted><Year>2019</Year><Month>04</Month><Day>16</Day></DateCompleted><DateRevised><Year>2019</Year><Month>04</Month><Day>16</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>13</Volume><Issue>11</Issue><PubDate><Year>2018</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS One</ISOAbbreviation></Journal><ArticleTitle>Intraphagolysosomal conditions predispose to Staphylococcus epidermidis small colony variants persistence in macrophages.</ArticleTitle><Pagination><MedlinePgn>e0207312</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0207312</ELocationID><Abstract><AbstractText>Staphylococcus epidermidis small colony variants can survive inside macrophages and their survival has been proposed as a pivotal process in the pathogenesis of biomaterial associated infections. In the present study the intracellular location of clinical isolates of SCV and parental wild type strains inside macrophages was determined. Furthermore, the effect of IFN-γ and rapamycin on the level of SCV/WT as well as lysosomes colocalisation and iNOS induction in THP-activated macrophages in response to WT and SCV strains of Staphylococcus epidermidis were examined. It was demonstrated that SCV strain of S. epidermidis can survive and persist inside macrophages and its intracellular survival is supported by the induction of phagosomal acidification. The ability to reduce the high proportion of LysoTracker positive SCV containing phagosomes was exclusively found when IFN-γ was used. The findings suggest that IFN-γ mediates SCV killing via two distinct mechanisms, phagosome alkalisation and an increased iNOS synthesis, so the cytokine may control S. epidermidis WT and SCV infection in macrophages. Staphylococcus epidermidis SCV is a less potent stimulus of iNOS than the WT strain and the feature may help SCV to persist in hostile environment of macrophages. Rapamycin treatment did not influence the iNOS synthesis but reduced the percentage of both bacterial strains within acidic organelles. However, the percentage of SCV within LysoTracker positive organelles, even though reduced comparing to non-primed cells, was higher than in the WT strain indicating that Staphylococcus epidermidis possesses unique metabolic features allowing SCV to survive within macrophages.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Magryś</LastName><ForeName>Agnieszka</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0001-8499-8055</Identifier><AffiliationInfo><Affiliation>Chair and Department of Medical Microbiology, Medical University of Lublin, Lublin, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Deryło</LastName><ForeName>Kamil</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Molecular Biology, Maria Curie-Skłodowska University, Lublin, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bogut</LastName><ForeName>Agnieszka</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Chair and Department of Medical Microbiology, Medical University of Lublin, Lublin, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Olender</LastName><ForeName>Alina</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Chair and Department of Medical Microbiology, Medical University of Lublin, Lublin, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tchórzewski</LastName><ForeName>Marek</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Molecular Biology, Maria Curie-Skłodowska University, Lublin, Poland.</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>11</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="Y">Macrophages</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050296" MajorTopicYN="Y">Microbial Viability</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010588" MajorTopicYN="Y">Phagosomes</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013212" MajorTopicYN="N">Staphylococcus epidermidis</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000074084" MajorTopicYN="N">THP-1 Cells</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>The authors have declared that no competing interests exist.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>07</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2018</Year><Month>10</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2018</Year><Month>11</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2018</Year><Month>11</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>4</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30412620</ArticleId><ArticleId IdType="doi">10.1371/journal.pone.0207312</ArticleId><ArticleId IdType="pii">PONE-D-18-22416</ArticleId><ArticleId IdType="pmc">PMC6226201</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>J Cell Sci. 1998 Apr;111 ( Pt 7):897-905</Citation><ArticleIdList><ArticleId IdType="pubmed">9490634</ArticleId></ArticleIdList></Reference><Reference><Citation>Autophagy. 2008 Aug;4(6):744-53</Citation><ArticleIdList><ArticleId IdType="pubmed">18483470</ArticleId></ArticleIdList></Reference><Reference><Citation>Biochim Biophys Acta Mol Cell Res. 2018 Jan;1865(1):34-47</Citation><ArticleIdList><ArticleId IdType="pubmed">28986221</ArticleId></ArticleIdList></Reference><Reference><Citation>Infect Immun. 2001 Oct;69(10):6391-400</Citation><ArticleIdList><ArticleId IdType="pubmed">11553583</ArticleId></ArticleIdList></Reference><Reference><Citation>Infect Immun. 2007 Dec;75(12):5615-26</Citation><ArticleIdList><ArticleId IdType="pubmed">17893127</ArticleId></ArticleIdList></Reference><Reference><Citation>J Microbiol. 2015 Aug;53(8):544-52</Citation><ArticleIdList><ArticleId IdType="pubmed">26224457</ArticleId></ArticleIdList></Reference><Reference><Citation>Front Cell Infect Microbiol. 2014 Jul 28;4:99</Citation><ArticleIdList><ArticleId IdType="pubmed">25120957</ArticleId></ArticleIdList></Reference><Reference><Citation>J Infect Dis. 2016 Jan 15;213(2):305-13</Citation><ArticleIdList><ArticleId IdType="pubmed">26188074</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Microbiol. 2016 Jan;18(1):80-96</Citation><ArticleIdList><ArticleId IdType="pubmed">26248337</ArticleId></ArticleIdList></Reference><Reference><Citation>Virulence. 2017 Nov 17;8(8):1761-1775</Citation><ArticleIdList><ArticleId IdType="pubmed">28762868</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Mol Gastroenterol Hepatol. 2017 May 06;4(2):237-243</Citation><ArticleIdList><ArticleId IdType="pubmed">28660242</ArticleId></ArticleIdList></Reference><Reference><Citation>J Infect Dis. 2002 Jan 1;185(1):91-7</Citation><ArticleIdList><ArticleId IdType="pubmed">11756986</ArticleId></ArticleIdList></Reference><Reference><Citation>Med Microbiol Immunol. 2006 Dec;195(4):185-94</Citation><ArticleIdList><ArticleId IdType="pubmed">16596413</ArticleId></ArticleIdList></Reference><Reference><Citation>PLoS One. 2016 Jun 08;11(6):e0153289</Citation><ArticleIdList><ArticleId IdType="pubmed">27276061</ArticleId></ArticleIdList></Reference><Reference><Citation>PLoS One. 2011 May 02;6(5):e19105</Citation><ArticleIdList><ArticleId IdType="pubmed">21559306</ArticleId></ArticleIdList></Reference><Reference><Citation>Autophagy. 2016 Nov;12(11):2069-2084</Citation><ArticleIdList><ArticleId IdType="pubmed">27629870</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Rev Microbiol. 2006 Apr;4(4):295-305</Citation><ArticleIdList><ArticleId IdType="pubmed">16541137</ArticleId></ArticleIdList></Reference><Reference><Citation>Scientifica (Cairo). 2014;2014:825463</Citation><ArticleIdList><ArticleId IdType="pubmed">24818040</ArticleId></ArticleIdList></Reference><Reference><Citation>Infect Immun. 2005 Jun;73(6):3445-52</Citation><ArticleIdList><ArticleId IdType="pubmed">15908373</ArticleId></ArticleIdList></Reference><Reference><Citation>J Clin Invest. 2015 Jan;125(1):25-32</Citation><ArticleIdList><ArticleId IdType="pubmed">25654547</ArticleId></ArticleIdList></Reference><Reference><Citation>Infect Immun. 1998 Mar;66(3):1017-22</Citation><ArticleIdList><ArticleId IdType="pubmed">9488390</ArticleId></ArticleIdList></Reference><Reference><Citation>J Med Microbiol. 2014 Feb;63(Pt 2):176-85</Citation><ArticleIdList><ArticleId IdType="pubmed">24257683</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 2002 Oct 15;169(8):4488-95</Citation><ArticleIdList><ArticleId IdType="pubmed">12370385</ArticleId></ArticleIdList></Reference><Reference><Citation>Biol Pharm Bull. 2009 Jun;32(6):988-92</Citation><ArticleIdList><ArticleId IdType="pubmed">19483303</ArticleId></ArticleIdList></Reference><Reference><Citation>Microbes Infect. 2007 Apr;9(4):460-5</Citation><ArticleIdList><ArticleId IdType="pubmed">17331787</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neuroinflammation. 2011 Jan 05;8(1):1</Citation><ArticleIdList><ArticleId IdType="pubmed">21208419</ArticleId></ArticleIdList></Reference><Reference><Citation>Front Microbiol. 2017 Aug 02;8:1401</Citation><ArticleIdList><ArticleId IdType="pubmed">28824556</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Host Microbe. 2009 Jun 18;5(6):593-601</Citation><ArticleIdList><ArticleId IdType="pubmed">19527886</ArticleId></ArticleIdList></Reference><Reference><Citation>J Cell Sci. 2004 Jun 15;117(Pt 14):2865-7</Citation><ArticleIdList><ArticleId IdType="pubmed">15197240</ArticleId></ArticleIdList></Reference><Reference><Citation>Immunol Invest. 2018 Apr;47(3):251-263</Citation><ArticleIdList><ArticleId IdType="pubmed">29336620</ArticleId></ArticleIdList></Reference><Reference><Citation>J Antimicrob Chemother. 2005 Dec;56(6):1126-9</Citation><ArticleIdList><ArticleId IdType="pubmed">16287983</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>Pologne</li></country></list><tree><country name="Pologne"><noRegion><name sortKey="Magry, Agnieszka" sort="Magry, Agnieszka" uniqKey="Magry A" first="Agnieszka" last="Magry">Agnieszka Magry</name></noRegion><name sortKey="Bogut, Agnieszka" sort="Bogut, Agnieszka" uniqKey="Bogut A" first="Agnieszka" last="Bogut">Agnieszka Bogut</name><name sortKey="Derylo, Kamil" sort="Derylo, Kamil" uniqKey="Derylo K" first="Kamil" last="Deryło">Kamil Deryło</name><name sortKey="Olender, Alina" sort="Olender, Alina" uniqKey="Olender A" first="Alina" last="Olender">Alina Olender</name><name sortKey="Tch Rzewski, Marek" sort="Tch Rzewski, Marek" uniqKey="Tch Rzewski M" first="Marek" last="Tch Rzewski">Marek Tch Rzewski</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Bois/explor/RapamycinFungusV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000570 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000570 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Bois
|area= RapamycinFungusV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= pubmed:30412620
|texte= Intraphagolysosomal conditions predispose to Staphylococcus epidermidis small colony variants persistence in macrophages.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:30412620" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a RapamycinFungusV1
| This area was generated with Dilib version V0.6.38. |  |