Superoxide Dismutase 1 Protects Hepatocytes from Type I Interferon-Driven Oxidative Damage

نویسندگان

  • Anannya Bhattacharya
  • Ahmed N. Hegazy
  • Nikolaus Deigendesch
  • Lindsay Kosack
  • Jovana Cupovic
  • Richard K. Kandasamy
  • Andrea Hildebrandt
  • Doron Merkler
  • Anja A. Kühl
  • Bojan Vilagos
  • Christopher Schliehe
  • Isabel Panse
  • Kseniya Khamina
  • Hatoon Baazim
  • Isabelle Arnold
  • Lukas Flatz
  • Haifeng C. Xu
  • Philipp A. Lang
  • Alan Aderem
  • Akinori Takaoka
  • Giulio Superti-Furga
  • Jacques Colinge
  • Burkhard Ludewig
  • Max Löhning
  • Andreas Bergthaler
چکیده

Tissue damage caused by viral hepatitis is a major cause of morbidity and mortality worldwide. Using a mouse model of viral hepatitis, we identified virus-induced early transcriptional changes in the redox pathways in the liver, including downregulation of superoxide dismutase 1 (Sod1). Sod1(-/-) mice exhibited increased inflammation and aggravated liver damage upon viral infection, which was independent of T and NK cells and could be ameliorated by antioxidant treatment. Type I interferon (IFN-I) led to a downregulation of Sod1 and caused oxidative liver damage in Sod1(-/-) and wild-type mice. Genetic and pharmacological ablation of the IFN-I signaling pathway protected against virus-induced liver damage. These results delineate IFN-I mediated oxidative stress as a key mediator of virus-induced liver damage and describe a mechanism of innate-immunity-driven pathology, linking IFN-I signaling with antioxidant host defense and infection-associated tissue damage. VIDEO ABSTRACT.

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عنوان ژورنال:

دوره 43  شماره 

صفحات  -

تاریخ انتشار 2015