The IL-17 receptor IL-17RE mediates polyIC-induced exacerbation of experimental allergic asthma.

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  • Additional Information
    • Affiliation:
      Department of Internal Medicine V – Pulmonology, Allergology and Critical Care Medicine, Saarland University, D-66421, Homburg, Germany
      Division of Asthma Exacerbation & Regulation, Priority Area Asthma and Allergy, Leibniz Lung Center Borstel, Airway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Germany
    • Abstract:
      Background: The interleukin 17 receptor E (IL-17RE) is specific for the epithelial cytokine interleukin-17C (IL-17C). Asthma exacerbations are frequently caused by viral infections. Polyinosinic:polycytidylic acid (pIC) mimics viral infections through binding to pattern recognition receptors (e.g. TLR-3). We and others have shown that pIC induces the expression of IL-17C in airway epithelial cells. Using different mouse models, we aimed to investigate the function of IL-17RE in the development of experimental allergic asthma and acute exacerbation thereof.Methods: Wild-type (WT) and IL-17RE deficient (Il-17re-/-) mice were sensitized and challenged with OVA to induce allergic airway inflammation. pIC or PBS were applied intranasally when allergic airway inflammation had been established. Pulmonary expression of inflammatory mediators, numbers of inflammatory cells, and airway hyperresponsiveness (AHR) were analyzed.Results: Ablation of IL-17RE did not affect the development of OVA-induced allergic airway inflammation and AHR. pIC induced inflammation independent of IL-17RE in the absence of allergic airway inflammation. Treatment of mice with pIC exacerbated pulmonary inflammation in sensitized and OVA-challenged mice in an IL-17RE-dependent manner. The pIC-induced expression of cytokines (e.g. keratinocyte-derived chemokine (KC), granulocyte-colony stimulating factor (G-CSF)) and recruitment of neutrophils were decreased in Il-17re-/- mice. pIC-exacerbated AHR was partially decreased in Il-17re-/- mice.Conclusions: Our results indicate that IL-17RE mediates virus-triggered exacerbations but does not have a function in the development of allergic lung disease.
    • Journal Subset:
      Biomedical; Europe; UK & Ireland
    • ISSN:
      1465-9921
    • MEDLINE Info:
      PMID: NLM32641167 NLM UID: 101090633
    • Publication Date:
      In Process
    • Publication Date:
      20200716
    • DOI:
      http://dx.doi.org/10.1186/s12931-020-01434-9
    • Accession Number:
      144456519
  • Citations
    • ABNT:
      VELLA, G. et al. The IL-17 receptor IL-17RE mediates polyIC-induced exacerbation of experimental allergic asthma. Respiratory Research, [s. l.], v. 21, n. 1, p. 1–8, 2020. DOI 10.1186/s12931-020-01434-9. Disponível em: http://search.ebscohost.com/login.aspx?direct=true&site=eds-live&db=rzh&AN=144456519. Acesso em: 4 ago. 2020.
    • AMA:
      Vella G, Lunding L, Ritzmann F, et al. The IL-17 receptor IL-17RE mediates polyIC-induced exacerbation of experimental allergic asthma. Respiratory Research. 2020;21(1):1-8. doi:10.1186/s12931-020-01434-9.
    • AMA11:
      Vella G, Lunding L, Ritzmann F, et al. The IL-17 receptor IL-17RE mediates polyIC-induced exacerbation of experimental allergic asthma. Respiratory Research. 2020;21(1):1-8. doi:10.1186/s12931-020-01434-9
    • APA:
      Vella, G., Lunding, L., Ritzmann, F., Honecker, A., Herr, C., Wegmann, M., Bals, R., & Beisswenger, C. (2020). The IL-17 receptor IL-17RE mediates polyIC-induced exacerbation of experimental allergic asthma. Respiratory Research, 21(1), 1–8. https://doi.org/10.1186/s12931-020-01434-9
    • Chicago/Turabian: Author-Date:
      Vella, Giovanna, Lars Lunding, Felix Ritzmann, Anja Honecker, Christian Herr, Michael Wegmann, Robert Bals, and Christoph Beisswenger. 2020. “The IL-17 Receptor IL-17RE Mediates PolyIC-Induced Exacerbation of Experimental Allergic Asthma.” Respiratory Research 21 (1): 1–8. doi:10.1186/s12931-020-01434-9.
    • Harvard:
      Vella, G. et al. (2020) ‘The IL-17 receptor IL-17RE mediates polyIC-induced exacerbation of experimental allergic asthma’, Respiratory Research, 21(1), pp. 1–8. doi: 10.1186/s12931-020-01434-9.
    • Harvard: Australian:
      Vella, G, Lunding, L, Ritzmann, F, Honecker, A, Herr, C, Wegmann, M, Bals, R & Beisswenger, C 2020, ‘The IL-17 receptor IL-17RE mediates polyIC-induced exacerbation of experimental allergic asthma’, Respiratory Research, vol. 21, no. 1, pp. 1–8, viewed 4 August 2020, .
    • MLA:
      Vella, Giovanna, et al. “The IL-17 Receptor IL-17RE Mediates PolyIC-Induced Exacerbation of Experimental Allergic Asthma.” Respiratory Research, vol. 21, no. 1, July 2020, pp. 1–8. EBSCOhost, doi:10.1186/s12931-020-01434-9.
    • Chicago/Turabian: Humanities:
      Vella, Giovanna, Lars Lunding, Felix Ritzmann, Anja Honecker, Christian Herr, Michael Wegmann, Robert Bals, and Christoph Beisswenger. “The IL-17 Receptor IL-17RE Mediates PolyIC-Induced Exacerbation of Experimental Allergic Asthma.” Respiratory Research 21, no. 1 (July 8, 2020): 1–8. doi:10.1186/s12931-020-01434-9.
    • Vancouver/ICMJE:
      Vella G, Lunding L, Ritzmann F, Honecker A, Herr C, Wegmann M, et al. The IL-17 receptor IL-17RE mediates polyIC-induced exacerbation of experimental allergic asthma. Respiratory Research [Internet]. 2020 Jul 8 [cited 2020 Aug 4];21(1):1–8. Available from: http://search.ebscohost.com/login.aspx?direct=true&site=eds-live&db=rzh&AN=144456519