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 : 000C92 ( Main/Exploration ); précédent : 000C91; suivant : 000C93Tet38 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
Affiliations:
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Le document en format XML
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Interactions</term><term>Humans</term><term>Microbial Viability (drug effects)</term><term>Phagosomes (microbiology)</term><term>Protein Binding</term><term>Staphylococcal Infections (metabolism)</term><term>Staphylococcal Infections (microbiology)</term><term>Staphylococcus aureus (physiology)</term><term>Toll-Like Receptor 2 (antagonists & inhibitors)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Anticorps monoclonaux (pharmacologie)</term><term>Cellules épithéliales (immunologie)</term><term>Cellules épithéliales (microbiologie)</term><term>Cellules épithéliales (métabolisme)</term><term>Chloroquine (pharmacologie)</term><term>Humains</term><term>Infections à staphylocoques (microbiologie)</term><term>Infections à staphylocoques (métabolisme)</term><term>Interactions hôte-pathogène</term><term>Liaison aux protéines</term><term>Lignée cellulaire</term><term>Phagosomes (microbiologie)</term><term>Protéines bactériennes (métabolisme)</term><term>Récepteur de type Toll-2 (antagonistes et inhibiteurs)</term><term>Staphylococcus aureus (physiologie)</term><term>Viabilité microbienne ()</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>CD36 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" xml:lang="fr"><term>Cellules épithéliales</term><term>Infections à staphylocoques</term><term>Phagosomes</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Epithelial Cells</term><term>Phagosomes</term><term>Staphylococcal Infections</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules épithéliales</term><term>Infections à staphylocoques</term><term>Protéines bactériennes</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Anticorps monoclonaux</term><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Staphylococcus aureus</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Staphylococcus aureus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>Host-Pathogen Interactions</term><term>Humans</term><term>Protein Binding</term></keywords><keywords scheme="MESH" 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><affiliations><list><country><li>États-Unis</li></country><region><li>Massachusetts</li></region></list><tree><country name="États-Unis"><region name="Massachusetts"><name sortKey="Truong Bolduc, Q C" sort="Truong Bolduc, Q C" uniqKey="Truong Bolduc Q" first="Q C" last="Truong-Bolduc">Q C Truong-Bolduc</name></region><name sortKey="Hooper, D C" sort="Hooper, D C" uniqKey="Hooper D" first="D C" last="Hooper">D C Hooper</name><name sortKey="Khan, N S" sort="Khan, N S" uniqKey="Khan N" first="N S" last="Khan">N S Khan</name><name sortKey="Vyas, J M" sort="Vyas, J M" uniqKey="Vyas J" first="J M" last="Vyas">J M Vyas</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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