About: Interferon-beta expression and type I interferon receptor signaling of hepatocytes prevent hepatic necrosis and virus dissemination in Coxsackievirus B3-infected mice

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About: Interferon-beta expression and type I interferon receptor signaling of hepatocytes prevent hepatic necrosis and virus dissemination in Coxsackievirus B3-infected mice Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Interferon-beta expression and type I interferon receptor signaling of hepatocytes prevent hepatic necrosis and virus dissemination in Coxsackievirus B3-infected mice
Creator	Borst, Katharina Kalinke, Ulrich Staeheli, Peter Baumgärtner, Wolfgang Herder, Vanessa Steinmann, Eike Todt, Daniel Lienenklaus, Stefan Gerhauser, Ingo Langereis, Martijn Ott, Michael Becker, Jennifer Geffers, Robert Klause, Tanja Koestner, Wolfgang Wacker, Frank Yuan, Qinggong Detje, Claudia Van Kuppeveld, Frank Vondran, Florian Spanier, Tegtmeyer, Pia-K
Source	PMC
abstract	During Coxsackievirus B3 (CVB3) infection hepatitis is a potentially life threatening complication, particularly in newborns. Studies with type I interferon (IFN-I) receptor (IFNAR)-deficient mice revealed a key role of the IFN-I axis in the protection against CVB3 infection, whereas the source of IFN-I and cell types that have to be IFNAR triggered in order to promote survival are still unknown. We found that CVB3 infected IFN-β reporter mice showed effective reporter induction, especially in hepatocytes and only to a minor extent in liver-resident macrophages. Accordingly, upon in vitro CVB3 infection of primary hepatocytes from murine or human origin abundant IFN-β responses were induced. To identify sites of IFNAR-triggering we performed experiments with Mx reporter mice, which upon CVB3 infection showed massive luciferase induction in the liver. Immunohistological studies revealed that during CVB3 infection MX1 expression of hepatocytes was induced primarily by IFNAR-, and not by IFN-III receptor (IFNLR)-triggering. CVB3 infection studies with primary human hepatocytes, in which either the IFN-I or the IFN-III axis was inhibited, also indicated that primarily IFNAR-, and to a lesser extent IFNLR-triggering was needed for ISG induction. Interestingly, CVB3 infected mice with a hepatocyte-specific IFNAR ablation showed severe liver cell necrosis and ubiquitous viral dissemination that resulted in lethal disease, as similarly detected in classical IFNAR(-/-) mice. In conclusion, we found that during CVB3 infection hepatocytes are major IFN-I producers and that the liver is also the organ that shows strong IFNAR-triggering. Importantly, hepatocytes need to be IFNAR-triggered in order to prevent virus dissemination and to assure survival. These data are compatible with the hypothesis that during CVB3 infection hepatocytes serve as important IFN-I producers and sensors not only in the murine, but also in the human system.
has issue date	2018-08-03(xsd:dateTime)
bibo:doi	10.1371/journal.ppat.1007235
bibo:pmid	30075026
has license	cc-by
sha1sum (hex)	1c7c9d9c03f404119c5cc1dd98e0ebe17ea3bb3e
schema:url	https://doi.org/10.1371/journal.ppat.1007235
resource representing a document's title	Interferon-beta expression and type I interferon receptor signaling of hepatocytes prevent hepatic necrosis and virus dissemination in Coxsackievirus B3-infected mice
has PubMed Central identifier	PMC6107283
has PubMed identifier	30075026
schema:publication	PLoS Pathog
resource representing a document's body	covid:1c7c9d9c03f404119c5cc1dd98e0ebe17ea3bb3e#body_text
is schema:about of	named entity 'hepatocytes' named entity 'PLOS Pathogens' named entity 'mice' named entity 'infection' named entity 'IFNAR' named entity 'expression' named entity 'massive' named entity 'infection' named entity 'hepatocytes' named entity 'murine' named entity 'necrosis' named entity 'type I interferon' named entity 'hepatic' named entity 'expression' covid:arg/1c7c9d9c03f404119c5cc1dd98e0ebe17ea3bb3e named entity 'mice' named entity 'mice' named entity 'infection' named entity '2018' named entity 'promote' named entity '2018' named entity 'liver' named entity 'mice' named entity 'MX1' named entity 'Inflammation' named entity 'IFNAR' named entity 'Interferon-beta' named entity 'infection' named entity 'infection' named entity 'hepatocytes' named entity 'Inflammation' named entity 'liver' named entity 'IFNAR' named entity 'IFNLR' named entity 'IFNAR' named entity 'murine' named entity 'infection' named entity 'hepatic necrosis' named entity 'Interferon-beta' named entity 'Coxsackievirus B3' named entity 'cardiomyocyte' named entity 'infection' named entity 'One-Way ANOVA' named entity 'c2J' named entity 'hepatocytes' named entity 'necrosis' named entity 'effector cells' named entity 'liver' named entity 'lipase' named entity 'LCMV' named entity 'infection' named entity 'epithelial cells' named entity 'bioluminescent' named entity 'GraphPad Prism' named entity 'hepatocytes' named entity 'mice' named entity 'VSV' named entity 'TCA' named entity 'infection' named entity 'clinical symptoms'

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