Buß, Claudia;
Opitz, Bastian;
Hocke, Andreas C.;
Lippmann, Juliane;
van Laak, Vincent;
Hippenstiel, Stefan;
Krüll, Matthias;
Suttorp, Norbert;
Eitel, Julia
Essential Role of Mitochondrial Antiviral Signaling, IFN Regulatory Factor (IRF)3, and IRF7 in Chlamydophila pneumoniae-Mediated IFN-β Response and Control of Bacterial Replication in Human Endothelial Cells
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Media type:
E-Article
Title:
Essential Role of Mitochondrial Antiviral Signaling, IFN Regulatory Factor (IRF)3, and IRF7 in Chlamydophila pneumoniae-Mediated IFN-β Response and Control of Bacterial Replication in Human Endothelial Cells
Contributor:
Buß, Claudia;
Opitz, Bastian;
Hocke, Andreas C.;
Lippmann, Juliane;
van Laak, Vincent;
Hippenstiel, Stefan;
Krüll, Matthias;
Suttorp, Norbert;
Eitel, Julia
imprint:
The American Association of Immunologists, 2010
Published in:The Journal of Immunology
Language:
English
DOI:
10.4049/jimmunol.0902947
ISSN:
1550-6606;
0022-1767
Origination:
Footnote:
Description:
<jats:title>Abstract</jats:title>
<jats:p>Chlamydophila pneumoniae infection of the vascular wall as well as activation of the transcription factor IFN regulatory factor (IRF)3 have been linked to development of chronic vascular lesions and atherosclerosis. The innate immune system detects invading pathogens by use of pattern recognition receptors, some of which are able to stimulate IRF3/7 activation and subsequent type I IFN production (e. g., IFN-β). In this study, we show that infection of human endothelial cells with C. pneumoniae-induced production of IFN-β, a cytokine that so far has been mainly associated with antiviral immunity. Moreover, C. pneumoniae infection led to IRF3 and IRF7 nuclear translocation in HUVECs and RNA interference experiments showed that IRF3 and IRF7 as well as the mitochondrial antiviral signaling (MAVS) were essential for IFN-β induction. Finally, C. pneumoniae replication was enhanced in endothelial cells in which IRF3, IRF7, or MAVS expression was inhibited by small interfering RNA and attenuated by IFN-β treatment. In conclusion, C. pneumoniae infection of endothelial cells activates an MAVS-, IRF3-, and IRF7-dependent signaling, which controls bacterial growth and might modulate development of vascular lesions.</jats:p>