The common cold is one of the most frequent human inflammatory diseases caused by viruses and can facilitate bacterial superinfections, resulting in sinusitis or pneumonia. The active ingredient of the drug Soledum, 1,8-cineole, is commonly applied for treating inflammatory diseases of the respiratory tract. However, the potential for 1,8-cineole to treat primary viral infections of the respiratory tract remains unclear. In the present study, we demonstrate for the first time that 1,8-cineole potentiates poly(I:C)-induced activity of the antiviral transcription factor interferon regulatory factor 3 (IRF3), while simultaneously reducing proinflammatory nuclear factor (NF)-κB activity in human cell lines, inferior turbinate stem cells (ITSCs) and in ex vivo cultivated human nasal mucosa. Co-treatment of cell lines with poly(I:C) and 1,8-cineole resulted in significantly increased IRF3 reporter gene activity compared with poly(I:C) alone, whereas NF-κB activity was reduced. Accordingly, 1,8-cineole- and poly(I:C) treatment led to increased nuclear translocation of IRF3 in ITSCs and a human ex vivo model of rhinosinusitis compared with the poly(I:C) treatment approach. Nuclear translocation of IRF3 was significantly increased in ITSCs and slice cultures treated with lipopolysaccharide (LPS) and 1,8-cineole compared with the LPS-treated cells mimicking bacterial infection. Our findings strongly suggest that 1,8-cineole potentiates the antiviral activity of IRF3 in addition to its inhibitory effect on proinflammatory NF-κB signalling, and may thus broaden its field of application.
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GABAB receptor-mediated hypertension via hyperpolarization of solitary tract nucleus neurons that receive and integrate baroreceptor afferent inputs. See pp. 1417-1434 for further details. Image kindly provided by Omar Logue
Research Article|
June 29 2016
1,8-Cineole potentiates IRF3-mediated antiviral response in human stem cells and in an ex vivo model of rhinosinusitis
Janine Müller;
Janine Müller
*Department of Otolaryngology, Head and Neck Surgery, Klinikum Bielefeld, D-33604 Bielefeld, Germany
†Department of Cell Biology, University of Bielefeld, 33619 Bielefeld, Germany
‡AG Molecular Neurobiology, University of Bielefeld, 33619 Bielefeld, Germany
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Johannes F.W. Greiner;
Johannes F.W. Greiner
*Department of Otolaryngology, Head and Neck Surgery, Klinikum Bielefeld, D-33604 Bielefeld, Germany
†Department of Cell Biology, University of Bielefeld, 33619 Bielefeld, Germany
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Marie Zeuner;
Marie Zeuner
†Department of Cell Biology, University of Bielefeld, 33619 Bielefeld, Germany
§Reading School of Pharmacy, University of Reading, PO Box 226, Whiteknights, Reading, Berkshire RG6 6AP, UK
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Viktoria Brotzmann;
Viktoria Brotzmann
*Department of Otolaryngology, Head and Neck Surgery, Klinikum Bielefeld, D-33604 Bielefeld, Germany
†Department of Cell Biology, University of Bielefeld, 33619 Bielefeld, Germany
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Johanna Schäfermann;
Johanna Schäfermann
*Department of Otolaryngology, Head and Neck Surgery, Klinikum Bielefeld, D-33604 Bielefeld, Germany
†Department of Cell Biology, University of Bielefeld, 33619 Bielefeld, Germany
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Frederique Wieters;
Frederique Wieters
*Department of Otolaryngology, Head and Neck Surgery, Klinikum Bielefeld, D-33604 Bielefeld, Germany
†Department of Cell Biology, University of Bielefeld, 33619 Bielefeld, Germany
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Darius Widera;
Darius Widera
†Department of Cell Biology, University of Bielefeld, 33619 Bielefeld, Germany
§Reading School of Pharmacy, University of Reading, PO Box 226, Whiteknights, Reading, Berkshire RG6 6AP, UK
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Holger Sudhoff;
Holger Sudhoff
*Department of Otolaryngology, Head and Neck Surgery, Klinikum Bielefeld, D-33604 Bielefeld, Germany
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Barbara Kaltschmidt;
Barbara Kaltschmidt
†Department of Cell Biology, University of Bielefeld, 33619 Bielefeld, Germany
‡AG Molecular Neurobiology, University of Bielefeld, 33619 Bielefeld, Germany
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Christian Kaltschmidt
†Department of Cell Biology, University of Bielefeld, 33619 Bielefeld, Germany
Correspondence: C. Kaltschmidt ([email protected]).
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Publisher: Portland Press Ltd
Received:
November 26 2015
Revision Received:
April 20 2016
Accepted:
April 22 2016
Accepted Manuscript online:
April 25 2016
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© 2016 The Author(s). published by Portland Press Limited on behalf of the Biochemical Society
2016
Clin Sci (Lond) (2016) 130 (15): 1339–1352.
Article history
Received:
November 26 2015
Revision Received:
April 20 2016
Accepted:
April 22 2016
Accepted Manuscript online:
April 25 2016
Citation
Janine Müller, Johannes F.W. Greiner, Marie Zeuner, Viktoria Brotzmann, Johanna Schäfermann, Frederique Wieters, Darius Widera, Holger Sudhoff, Barbara Kaltschmidt, Christian Kaltschmidt; 1,8-Cineole potentiates IRF3-mediated antiviral response in human stem cells and in an ex vivo model of rhinosinusitis. Clin Sci (Lond) 1 August 2016; 130 (15): 1339–1352. doi: https://doi.org/10.1042/CS20160218
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