The role of the PI3K/mTOR signaling pathway in Staphylococcus epidermidis small colony variants intracellular survival.
Identifieur interne : 000445 ( Main/Exploration ); précédent : 000444; suivant : 000446The role of the PI3K/mTOR signaling pathway in Staphylococcus epidermidis small colony variants intracellular survival.
Auteurs : Agnieszka Magry [Pologne] ; Agnieszka Bogut [Pologne] ; Michał Kiełbus [Pologne] ; Alina Olender [Pologne]Source :
- Immunological investigations [ 1532-4311 ] ; 2018.
Descripteurs français
- KwdFr :
- Androstadiènes (pharmacologie), Humains (MeSH), Infections dues aux prothèses (MeSH), Infections à staphylocoques (immunologie), Infections à staphylocoques (microbiologie), Infections à staphylocoques (métabolisme), Lignée cellulaire (MeSH), Macrophages (effets des médicaments et des substances chimiques), Macrophages (immunologie), Macrophages (microbiologie), Macrophages (métabolisme), Phosphatidylinositol 3-kinases (métabolisme), Phosphorylation (MeSH), Phénotype (MeSH), Protéines proto-oncogènes c-akt (métabolisme), Sirolimus (pharmacologie), Staphylococcus epidermidis (physiologie), Sérine-thréonine kinases TOR (métabolisme), Transduction du signal (effets des médicaments et des substances chimiques), Viabilité microbienne (immunologie), Wortmannine (MeSH).
- MESH :
- effets des médicaments et des substances chimiques : Macrophages, Transduction du signal.
- immunologie : Infections à staphylocoques, Macrophages, Viabilité microbienne.
- microbiologie : Infections à staphylocoques, Macrophages.
- métabolisme : Infections à staphylocoques, Macrophages, Phosphatidylinositol 3-kinases, Protéines proto-oncogènes c-akt, Sérine-thréonine kinases TOR.
- pharmacologie : Androstadiènes, Sirolimus.
- physiologie : Staphylococcus epidermidis.
- Humains, Infections dues aux prothèses, Lignée cellulaire, Phosphorylation, Phénotype, Wortmannine.
English descriptors
- KwdEn :
- Androstadienes (pharmacology), Cell Line (MeSH), Humans (MeSH), Macrophages (drug effects), Macrophages (immunology), Macrophages (metabolism), Macrophages (microbiology), Microbial Viability (immunology), Phenotype (MeSH), Phosphatidylinositol 3-Kinases (metabolism), Phosphorylation (MeSH), Prosthesis-Related Infections (MeSH), Proto-Oncogene Proteins c-akt (metabolism), Signal Transduction (drug effects), Sirolimus (pharmacology), Staphylococcal Infections (immunology), Staphylococcal Infections (metabolism), Staphylococcal Infections (microbiology), Staphylococcus epidermidis (physiology), TOR Serine-Threonine Kinases (metabolism), Wortmannin (MeSH).
- MESH :
- chemical , metabolism : Phosphatidylinositol 3-Kinases, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases.
- chemical , pharmacology : Androstadienes, Sirolimus.
- drug effects : Macrophages, Signal Transduction.
- immunology : Macrophages, Microbial Viability, Staphylococcal Infections.
- metabolism : Macrophages, Staphylococcal Infections.
- microbiology : Macrophages, Staphylococcal Infections.
- physiology : Staphylococcus epidermidis.
- Cell Line, Humans, Phenotype, Phosphorylation, Prosthesis-Related Infections, Wortmannin.
Abstract
The objective of this study was to analyze how Staphylococcus epidermidis SCV and WT strains manipulate the PI3K/Akt/mTOR signaling pathway. Six S. epidermidis strains with normal phenotype (WT) and six S. epidermidis strains with SCV phenotype were isolated in parallel from six patients with the prosthetic hip joint infections. THP-1 activated cells were incubated with or without PI3K inhibitor-wortmannin or with mTOR inhibitor-rapamycin. Next, macrophages were exposed to S. epidermidis WT and SCV strains. After 4 h incubation, bacterial survival inside macrophages as well as PI3K-mTOR activation was analyzed. SCV strains of S. epidermidis increased the level of Akt phosphorylation, compared to uninfected macrophages and to their parental WT forms. Wild type variants of S. epidermidis phosphorylated Akt at similar or lower levels as control uninfected cells. Next, the induction of mTOR target, phosphorylated ribosomal protein S6, was measured in bacteria-infected macrophages. The level of phosphorylation was significantly reduced when the cells were exposed to WT strains of S. epidermidis. In contrast, the SCV strains activated S6 protein mostly at a level comparable to the control cells. Rapamycin inhibited mTOR activation as the number of p-S6 positive cells decreased in the tested cases. To conclude, the SCV strains activate the PI3K-Akt signaling pathway in opposite to WT strains. This fact however did not influence the increase in the number of live SCV bacteria as compared to the WT strains. Knowing that the PI3K-Akt pathway is involved in proinflammatory cytokines suppression, SCVs seem to use this pathway to reduce the inflammatory response during the infection.
DOI: 10.1080/08820139.2018.1423569
PubMed: 29336620
Affiliations:
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type="abstract" xml:lang="en">The objective of this study was to analyze how Staphylococcus epidermidis SCV and WT strains manipulate the PI3K/Akt/mTOR signaling pathway. Six S. epidermidis strains with normal phenotype (WT) and six S. epidermidis strains with SCV phenotype were isolated in parallel from six patients with the prosthetic hip joint infections. THP-1 activated cells were incubated with or without PI3K inhibitor-wortmannin or with mTOR inhibitor-rapamycin. Next, macrophages were exposed to S. epidermidis WT and SCV strains. After 4 h incubation, bacterial survival inside macrophages as well as PI3K-mTOR activation was analyzed. SCV strains of S. epidermidis increased the level of Akt phosphorylation, compared to uninfected macrophages and to their parental WT forms. Wild type variants of S. epidermidis phosphorylated Akt at similar or lower levels as control uninfected cells. Next, the induction of mTOR target, phosphorylated ribosomal protein S6, was measured in bacteria-infected macrophages. The level of phosphorylation was significantly reduced when the cells were exposed to WT strains of S. epidermidis. In contrast, the SCV strains activated S6 protein mostly at a level comparable to the control cells. Rapamycin inhibited mTOR activation as the number of p-S6 positive cells decreased in the tested cases. To conclude, the SCV strains activate the PI3K-Akt signaling pathway in opposite to WT strains. This fact however did not influence the increase in the number of live SCV bacteria as compared to the WT strains. Knowing that the PI3K-Akt pathway is involved in proinflammatory cytokines suppression, SCVs seem to use this pathway to reduce the inflammatory response during the infection.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29336620</PMID><DateCompleted><Year>2018</Year><Month>09</Month><Day>07</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1532-4311</ISSN><JournalIssue CitedMedium="Internet"><Volume>47</Volume><Issue>3</Issue><PubDate><Year>2018</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Immunological investigations</Title><ISOAbbreviation>Immunol Invest</ISOAbbreviation></Journal><ArticleTitle>The role of the PI3K/mTOR signaling pathway in Staphylococcus epidermidis small colony variants intracellular survival.</ArticleTitle><Pagination><MedlinePgn>251-263</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1080/08820139.2018.1423569</ELocationID><Abstract><AbstractText>The objective of this study was to analyze how Staphylococcus epidermidis SCV and WT strains manipulate the PI3K/Akt/mTOR signaling pathway. Six S. epidermidis strains with normal phenotype (WT) and six S. epidermidis strains with SCV phenotype were isolated in parallel from six patients with the prosthetic hip joint infections. THP-1 activated cells were incubated with or without PI3K inhibitor-wortmannin or with mTOR inhibitor-rapamycin. Next, macrophages were exposed to S. epidermidis WT and SCV strains. After 4 h incubation, bacterial survival inside macrophages as well as PI3K-mTOR activation was analyzed. SCV strains of S. epidermidis increased the level of Akt phosphorylation, compared to uninfected macrophages and to their parental WT forms. Wild type variants of S. epidermidis phosphorylated Akt at similar or lower levels as control uninfected cells. Next, the induction of mTOR target, phosphorylated ribosomal protein S6, was measured in bacteria-infected macrophages. The level of phosphorylation was significantly reduced when the cells were exposed to WT strains of S. epidermidis. In contrast, the SCV strains activated S6 protein mostly at a level comparable to the control cells. Rapamycin inhibited mTOR activation as the number of p-S6 positive cells decreased in the tested cases. To conclude, the SCV strains activate the PI3K-Akt signaling pathway in opposite to WT strains. This fact however did not influence the increase in the number of live SCV bacteria as compared to the WT strains. Knowing that the PI3K-Akt pathway is involved in proinflammatory cytokines suppression, SCVs seem to use this pathway to reduce the inflammatory response during the infection.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Magryś</LastName><ForeName>Agnieszka</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>a Chair and Department of Medical Microbiology , Medical University of Lublin , Lublin , Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bogut</LastName><ForeName>Agnieszka</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>a Chair and Department of Medical Microbiology , Medical University of Lublin , Lublin , Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kiełbus</LastName><ForeName>Michał</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>b Chair and Department of Biochemistry and Molecular Biology , Medical University of Lublin , Lublin , Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Olender</LastName><ForeName>Alina</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>a Chair and Department of Medical Microbiology , Medical University of Lublin , Lublin , Poland.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>01</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Immunol Invest</MedlineTA><NlmUniqueID>8504629</NlmUniqueID><ISSNLinking>0882-0139</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000730">Androstadienes</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.-</RegistryNumber><NameOfSubstance UI="D019869">Phosphatidylinositol 3-Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D051057">Proto-Oncogene Proteins c-akt</NameOfSubstance></Chemical><Chemical><RegistryNumber>W36ZG6FT64</RegistryNumber><NameOfSubstance UI="D020123">Sirolimus</NameOfSubstance></Chemical><Chemical><RegistryNumber>XVA4O219QW</RegistryNumber><NameOfSubstance UI="D000077191">Wortmannin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000730" MajorTopicYN="N">Androstadienes</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050296" MajorTopicYN="N">Microbial Viability</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010641" MajorTopicYN="Y">Phenotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019869" MajorTopicYN="N">Phosphatidylinositol 3-Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010766" MajorTopicYN="N">Phosphorylation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016459" MajorTopicYN="N">Prosthesis-Related Infections</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051057" MajorTopicYN="N">Proto-Oncogene Proteins c-akt</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="Y">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013203" MajorTopicYN="N">Staphylococcal Infections</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013212" MajorTopicYN="N">Staphylococcus epidermidis</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000077191" MajorTopicYN="N">Wortmannin</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">PI3K</Keyword><Keyword MajorTopicYN="N">Staphylococcus epidermidis</Keyword><Keyword MajorTopicYN="N">mTOR</Keyword><Keyword MajorTopicYN="N">small colony variants</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2018</Year><Month>1</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2018</Year><Month>9</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2018</Year><Month>1</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29336620</ArticleId><ArticleId IdType="doi">10.1080/08820139.2018.1423569</ArticleId></ArticleIdList></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="Kielbus, Michal" sort="Kielbus, Michal" uniqKey="Kielbus M" first="Michał" last="Kiełbus">Michał Kiełbus</name><name sortKey="Olender, Alina" 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