Staphylococcus aureus induces type I IFN signaling in dendritic cells via TLR9.
Identifieur interne : 001300 ( Main/Exploration ); précédent : 001299; suivant : 001301Staphylococcus aureus induces type I IFN signaling in dendritic cells via TLR9.
Auteurs : Dane Parker [États-Unis] ; Alice PrinceSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2012.
Descripteurs français
- KwdFr :
- Animaux, Cellules cultivées, Cellules dendritiques (immunologie), Cellules dendritiques (microbiologie), Cellules dendritiques (métabolisme), Granulocytes neutrophiles (anatomopathologie), Infiltration par les neutrophiles (immunologie), Interféron de type I (physiologie), Pneumopathie bactérienne (immunologie), Pneumopathie bactérienne (microbiologie), Pneumopathie bactérienne (métabolisme), Récepteur-9 de type Toll-like (déficit), Récepteur-9 de type Toll-like (génétique), Récepteur-9 de type Toll-like (physiologie), Régulation négative (immunologie), Souris, Souris de lignée C57BL, Souris knockout, Staphylococcus aureus (immunologie), Transduction du signal (génétique), Transduction du signal (immunologie).
- MESH :
- anatomopathologie : Granulocytes neutrophiles.
- déficit : Récepteur-9 de type Toll-like.
- génétique : Récepteur-9 de type Toll-like, Transduction du signal.
- immunologie : Cellules dendritiques, Infiltration par les neutrophiles, Pneumopathie bactérienne, Régulation négative, Staphylococcus aureus, Transduction du signal.
- microbiologie : Cellules dendritiques, Pneumopathie bactérienne.
- métabolisme : Cellules dendritiques, Pneumopathie bactérienne.
- physiologie : Interféron de type I, Récepteur-9 de type Toll-like.
- Animaux, Cellules cultivées, Souris, Souris de lignée C57BL, Souris knockout.
English descriptors
- KwdEn :
- Animals, Cells, Cultured, Dendritic Cells (immunology), Dendritic Cells (metabolism), Dendritic Cells (microbiology), Down-Regulation (immunology), Interferon Type I (physiology), Mice, Mice, Inbred C57BL, Mice, Knockout, Neutrophil Infiltration (immunology), Neutrophils (pathology), Pneumonia, Bacterial (immunology), Pneumonia, Bacterial (metabolism), Pneumonia, Bacterial (microbiology), Signal Transduction (genetics), Signal Transduction (immunology), Staphylococcus aureus (immunology), Toll-Like Receptor 9 (deficiency), Toll-Like Receptor 9 (genetics), Toll-Like Receptor 9 (physiology).
- MESH :
- chemical , deficiency : Toll-Like Receptor 9.
- chemical , genetics : Toll-Like Receptor 9.
- chemical , physiology : Interferon Type I, Toll-Like Receptor 9.
- genetics : Signal Transduction.
- immunology : Dendritic Cells, Down-Regulation, Neutrophil Infiltration, Pneumonia, Bacterial, Signal Transduction, Staphylococcus aureus.
- metabolism : Dendritic Cells, Pneumonia, Bacterial.
- microbiology : Dendritic Cells, Pneumonia, Bacterial.
- pathology : Neutrophils.
- Animals, Cells, Cultured, Mice, Mice, Inbred C57BL, Mice, Knockout.
Abstract
The importance of type I IFN signaling in the innate immune response to viral and intracellular pathogens is well established, with an increasing literature implicating extracellular bacterial pathogens, including Staphylococcus aureus, in this signaling pathway. Airway epithelial cells and especially dendritic cells (DCs) contribute to the production of type I IFNs in the lung. We were interested in establishing how S. aureus activates the type I IFN cascade in DCs. In vitro studies confirmed the rapid uptake of S. aureus by DCs followed promptly by STAT1 phosphorylation and expression of IFN-β. Signaling occurred using heat-killed organisms and in the absence of PVL and α-toxin. Consistent with the participation of endosomal and not cytosolic receptors, signaling was predominantly mediated by MyD88, TLR9, and IRF1 and blocked by cytochalasin D, dynasore, and chloroquine. To determine the role of TLR9 signaling in the pathogenesis of S. aureus pneumonia, we infected WT and Tlr9(-/-) mice with MRSA USA300. Tlr9(-/-) mice had significantly improved clearance of S. aureus from the airways and lung tissue. Ifnar(-/-) mice also had improved clearance. This enhanced clearance in Tlr9(-/-) mice was not due to differences in the numbers of recruited neutrophils into the airways, but instead correlated with decreased induction of TNF. Thus, we identified TLR9 as the critical receptor mediating the induction of type I IFN signaling in DCs in response to S. aureus, illustrating an additional mechanism through which S. aureus exploits innate immune signaling to facilitate infection.
DOI: 10.4049/jimmunol.1201055
PubMed: 22962685
Affiliations:
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Le document en format XML
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Airway epithelial cells and especially dendritic cells (DCs) contribute to the production of type I IFNs in the lung. We were interested in establishing how S. aureus activates the type I IFN cascade in DCs. In vitro studies confirmed the rapid uptake of S. aureus by DCs followed promptly by STAT1 phosphorylation and expression of IFN-β. Signaling occurred using heat-killed organisms and in the absence of PVL and α-toxin. Consistent with the participation of endosomal and not cytosolic receptors, signaling was predominantly mediated by MyD88, TLR9, and IRF1 and blocked by cytochalasin D, dynasore, and chloroquine. To determine the role of TLR9 signaling in the pathogenesis of S. aureus pneumonia, we infected WT and Tlr9(-/-) mice with MRSA USA300. Tlr9(-/-) mice had significantly improved clearance of S. aureus from the airways and lung tissue. Ifnar(-/-) mice also had improved clearance. This enhanced clearance in Tlr9(-/-) mice was not due to differences in the numbers of recruited neutrophils into the airways, but instead correlated with decreased induction of TNF. Thus, we identified TLR9 as the critical receptor mediating the induction of type I IFN signaling in DCs in response to S. aureus, illustrating an additional mechanism through which S. aureus exploits innate immune signaling to facilitate infection.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>État de New York</li></region><settlement><li>New York</li></settlement><orgName><li>Université Columbia</li></orgName></list><tree><noCountry><name sortKey="Prince, Alice" sort="Prince, Alice" uniqKey="Prince A" first="Alice" last="Prince">Alice Prince</name></noCountry><country name="États-Unis"><region name="État de New York"><name sortKey="Parker, Dane" sort="Parker, Dane" uniqKey="Parker D" first="Dane" last="Parker">Dane Parker</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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