Staphylococcus aureus induces type I IFN signaling in dendritic cells via TLR9.
Staphylococcus aureus induces type I IFN signaling in dendritic cells via TLR9.
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DOI：
10.4049/jimmunol.1201055
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发表时间：
2012-10-15
期刊：
影响因子：
--
通讯作者：
Prince A
中科院分区：
文献类型：
--
作者：
Parker D;Prince A
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 (DC) 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 DC. In vitro studies confirmed the rapid uptake of S. aureus by DC followed promptly by STAT1 phosphorylation and expression of IFN-β. Signaling occurred using heat-killed organism 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 dendritic cells in response to S. aureus, illustrating an additional mechanism through which S. aureus exploits innate immune signaling to facilitate infection.
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DOI：
10.1086/650204
发表时间：
2010-02-15
期刊：
The Journal of infectious diseases
影响因子：
--
作者：
Lee MH;Arrecubieta C;Martin FJ;Prince A;Borczuk AC;Lowy FD
通讯作者：
Lowy FD
DOI：
10.1073/pnas.0631696100
发表时间：
2003-05-27
影响因子：
11.1
作者：
Lee, J;Chuang, TH;Cottam, HB
通讯作者：
Cottam, HB
影响因子：
6.4
作者：
Iverson, Amy R.;Boyd, Kelli L.;McCullers, Jonathan A.
通讯作者：
McCullers, Jonathan A.
影响因子：
3.9
作者：
Haller, Otto;Staeheli, Peter;Kochs, Georg
通讯作者：
Kochs, Georg
影响因子：
5.8
作者：
Kapetanovic, Ronan;Jouvion, Gregory;Adib-Conquy, Minou
通讯作者：
Adib-Conquy, Minou