Tet38 Efflux Pump Affects Staphylococcus aureus Internalization by Epithelial Cells through Interaction with CD36 and Contributes to Bacterial Escape from Acidic and Nonacidic Phagolysosomes.
Identifieur interne : 000366 ( Ncbi/Merge ); précédent : 000365; suivant : 000367Tet38 Efflux Pump Affects Staphylococcus aureus Internalization by Epithelial Cells through Interaction with CD36 and Contributes to Bacterial Escape from Acidic and Nonacidic Phagolysosomes.
Auteurs : Q C Truong-Bolduc [États-Unis] ; N S Khan [États-Unis] ; J M Vyas [États-Unis] ; D C Hooper [États-Unis]Source :
- Infection and immunity [ 1098-5522 ] ; 2017.
Descripteurs français
- KwdFr :
- Anticorps monoclonaux (pharmacologie), Cellules épithéliales (immunologie), Cellules épithéliales (microbiologie), Cellules épithéliales (métabolisme), Chloroquine (pharmacologie), Humains, Infections à staphylocoques (microbiologie), Infections à staphylocoques (métabolisme), Interactions hôte-pathogène, Liaison aux protéines, Lignée cellulaire, Phagosomes (microbiologie), Protéines bactériennes (métabolisme), Récepteur de type Toll-2 (antagonistes et inhibiteurs), Staphylococcus aureus (physiologie), Viabilité microbienne ().
- MESH :
- antagonistes et inhibiteurs : Récepteur de type Toll-2.
- immunologie : Cellules épithéliales.
- microbiologie : Cellules épithéliales, Infections à staphylocoques, Phagosomes.
- métabolisme : Cellules épithéliales, Infections à staphylocoques, Protéines bactériennes.
- pharmacologie : Anticorps monoclonaux, Chloroquine.
- physiologie : Staphylococcus aureus.
- Humains, Interactions hôte-pathogène, Liaison aux protéines, Lignée cellulaire, Viabilité microbienne.
English descriptors
- KwdEn :
- Antibodies, Monoclonal (pharmacology), Bacterial Proteins (metabolism), CD36 Antigens (antagonists & inhibitors), CD36 Antigens (metabolism), Cell Line, Chloroquine (pharmacology), Epithelial Cells (immunology), Epithelial Cells (metabolism), Epithelial Cells (microbiology), Host-Pathogen Interactions, Humans, Microbial Viability (drug effects), Phagosomes (microbiology), Protein Binding, Staphylococcal Infections (metabolism), Staphylococcal Infections (microbiology), Staphylococcus aureus (physiology), Toll-Like Receptor 2 (antagonists & inhibitors).
- MESH :
- chemical , antagonists & inhibitors : CD36 Antigens, Toll-Like Receptor 2.
- chemical , metabolism : Bacterial Proteins, CD36 Antigens.
- chemical , pharmacology : Antibodies, Monoclonal, Chloroquine.
- drug effects : Microbial Viability.
- immunology : Epithelial Cells.
- metabolism : Epithelial Cells, Staphylococcal Infections.
- microbiology : Epithelial Cells, Phagosomes, Staphylococcal Infections.
- physiology : Staphylococcus aureus.
- Cell Line, Host-Pathogen Interactions, Humans, Protein Binding.
Abstract
We previously reported that the Tet38 efflux pump is involved in internalization of Staphylococcus aureus by A549 lung epithelial cells. A lack of tet38 reduced bacterial uptake by A549 cells to 36% of that of the parental strain RN6390. Using invasion assays coupled with confocal microscopy imaging, we studied the host cell receptor(s) responsible for bacterial uptake via interaction with Tet38. We also assessed the ability of S. aureus to survive following alkalinization of the phagolysosomes by chloroquine. Antibody to the scavenger receptor CD36 reduced the internalization of S. aureus RN6390 by A549 cells, but the dependence on CD36 was reduced in QT7 tet38, suggesting that an interaction between Tet38 and CD36 contributed to S. aureus internalization. Following fusion of the S. aureus-associated endosomes with lysosomes, alkalinization of the acidic environment with chloroquine led to a rapid increase in the number of S. aureus RN6390 bacteria in the cytosol, followed by a decrease shortly thereafter. This effect of chloroquine was not seen in the absence of intact Tet38 in mutant QT7. These data taken together suggest that Tet38 plays a role both in bacterial internalization via interaction with CD36 and in bacterial escape from the phagolysosomes.
DOI: 10.1128/IAI.00862-16
PubMed: 27956597
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Antigens</term><term>Toll-Like Receptor 2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Bacterial Proteins</term><term>CD36 Antigens</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antibodies, Monoclonal</term><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Récepteur de type Toll-2</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Microbial Viability</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cellules épithéliales</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Epithelial Cells</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Epithelial Cells</term><term>Staphylococcal Infections</term></keywords><keywords scheme="MESH" qualifier="microbiologie" 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xml:lang="fr"><term>Humains</term><term>Interactions hôte-pathogène</term><term>Liaison aux protéines</term><term>Lignée cellulaire</term><term>Viabilité microbienne</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We previously reported that the Tet38 efflux pump is involved in internalization of Staphylococcus aureus by A549 lung epithelial cells. A lack of tet38 reduced bacterial uptake by A549 cells to 36% of that of the parental strain RN6390. Using invasion assays coupled with confocal microscopy imaging, we studied the host cell receptor(s) responsible for bacterial uptake via interaction with Tet38. We also assessed the ability of S. aureus to survive following alkalinization of the phagolysosomes by chloroquine. Antibody to the scavenger receptor CD36 reduced the internalization of S. aureus RN6390 by A549 cells, but the dependence on CD36 was reduced in QT7 tet38, suggesting that an interaction between Tet38 and CD36 contributed to S. aureus internalization. Following fusion of the S. aureus-associated endosomes with lysosomes, alkalinization of the acidic environment with chloroquine led to a rapid increase in the number of S. aureus RN6390 bacteria in the cytosol, followed by a decrease shortly thereafter. This effect of chloroquine was not seen in the absence of intact Tet38 in mutant QT7. These data taken together suggest that Tet38 plays a role both in bacterial internalization via interaction with CD36 and in bacterial escape from the phagolysosomes.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27956597</PMID><DateCompleted><Year>2017</Year><Month>05</Month><Day>18</Day></DateCompleted><DateRevised><Year>2019</Year><Month>03</Month><Day>29</Day></DateRevised><Article PubModel="Electronic-Print"><Journal><ISSN IssnType="Electronic">1098-5522</ISSN><JournalIssue CitedMedium="Internet"><Volume>85</Volume><Issue>2</Issue><PubDate><Year>2017</Year><Month>02</Month></PubDate></JournalIssue><Title>Infection and immunity</Title><ISOAbbreviation>Infect. Immun.</ISOAbbreviation></Journal><ArticleTitle>Tet38 Efflux Pump Affects Staphylococcus aureus Internalization by Epithelial Cells through Interaction with CD36 and Contributes to Bacterial Escape from Acidic and Nonacidic Phagolysosomes.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">e00862-16</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1128/IAI.00862-16</ELocationID><Abstract><AbstractText>We previously reported that the Tet38 efflux pump is involved in internalization of Staphylococcus aureus by A549 lung epithelial cells. A lack of tet38 reduced bacterial uptake by A549 cells to 36% of that of the parental strain RN6390. Using invasion assays coupled with confocal microscopy imaging, we studied the host cell receptor(s) responsible for bacterial uptake via interaction with Tet38. We also assessed the ability of S. aureus to survive following alkalinization of the phagolysosomes by chloroquine. Antibody to the scavenger receptor CD36 reduced the internalization of S. aureus RN6390 by A549 cells, but the dependence on CD36 was reduced in QT7 tet38, suggesting that an interaction between Tet38 and CD36 contributed to S. aureus internalization. Following fusion of the S. aureus-associated endosomes with lysosomes, alkalinization of the acidic environment with chloroquine led to a rapid increase in the number of S. aureus RN6390 bacteria in the cytosol, followed by a decrease shortly thereafter. This effect of chloroquine was not seen in the absence of intact Tet38 in mutant QT7. These data taken together suggest that Tet38 plays a role both in bacterial internalization via interaction with CD36 and in bacterial escape from the phagolysosomes.</AbstractText><CopyrightInformation>Copyright © 2017 American Society for Microbiology.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Truong-Bolduc</LastName><ForeName>Q C</ForeName><Initials>QC</Initials><AffiliationInfo><Affiliation>Division of Infectious Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Khan</LastName><ForeName>N S</ForeName><Initials>NS</Initials><AffiliationInfo><Affiliation>Division of Infectious Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vyas</LastName><ForeName>J M</ForeName><Initials>JM</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-9985-9565</Identifier><AffiliationInfo><Affiliation>Division of Infectious Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hooper</LastName><ForeName>D C</ForeName><Initials>DC</Initials><AffiliationInfo><Affiliation>Division of Infectious Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA dhooper@mgh.harvard.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P01 AI083214</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R37 AI023988</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>01</Month><Day>26</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Infect Immun</MedlineTA><NlmUniqueID>0246127</NlmUniqueID><ISSNLinking>0019-9567</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000911">Antibodies, Monoclonal</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001426">Bacterial Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018955">CD36 Antigens</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051195">Toll-Like Receptor 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000911" MajorTopicYN="N">Antibodies, Monoclonal</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001426" MajorTopicYN="N">Bacterial Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018955" MajorTopicYN="N">CD36 Antigens</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002738" MajorTopicYN="N">Chloroquine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</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="D054884" MajorTopicYN="Y">Host-Pathogen Interactions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050296" MajorTopicYN="N">Microbial Viability</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010588" MajorTopicYN="N">Phagosomes</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011485" MajorTopicYN="N">Protein Binding</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013203" MajorTopicYN="N">Staphylococcal Infections</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013211" MajorTopicYN="N">Staphylococcus aureus</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051195" MajorTopicYN="N">Toll-Like Receptor 2</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">CD36</Keyword><Keyword MajorTopicYN="Y">S. aureus</Keyword><Keyword MajorTopicYN="Y">endosomes</Keyword><Keyword MajorTopicYN="Y">internalization</Keyword><Keyword 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