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|Public on Apr 09, 2020
|Transcriptional response to IFN-κ and IFN-κDual in A549 cell line
|Expression profiling by array
|Type I interferon (IFN) is the first line of defense against virus infection. By using both in vivo and in vitro influenza infection models, we found that type I IFN-κ, limited the replication of influenza viruses by stimulating a IFNAR-MAPK-cFos-CHD6 axis. Similarly, Zika virus (ZIKV) was also highly sensitive to IFN-κ-mediated suppression. With an IAV infected mouse model, we found that IFN-κ was the earliest responding type I interferon among all known members in mice after H9N2 infection, a low-pathogenic Avian Influenza, whereas this early induction did not occur upon highly pathogenic H7N9 infection. IFN-κ can efficiently contain both low- and high-pathogenic influenza replication in cultured human lung cells, and CHD6 was the major effector responsive molecule for IFN-κ, but not for IFN-α/β. Furthermore, we discovered that both IFNAR1 and IFNAR2 subunits of type I interferon receptor and their downstream axis of p38-cFos are engaged in IFN-κ signaling cascade to acti vate CHD6, which didn`t require STAT1 activity. In addition, we showed that the pre-treatment with IFN-κ before IAV challenge protected mice from high mortality. Altogether, our study identified an IFN-κ-specific pathway that suppressed influenza A virus in vitro and in vivo. Thus, IFN-κ may have potential as a new prevention and treatment agents against emerging viruses
|RNAseq of A549 cells transfected with plasmids encoding WT IFN-κ, IFN-κ Dual, or pSV1.0 empty vector
RNA was isolated 24 hours after transfected. Samples were collected in biological triplicate and pSV1.0 empty vector was control.
|Dec 29, 2019
|Last update date
|Aug 31, 2022
|No.2901 Caolang Road
|Agilent-039494 SurePrint G3 Human GE v2 8x60K Microarray 039381 (Probe Name version)
|This SubSeries is part of SuperSeries:
|IFN-kappa Suppresses the Replication of Influenza A Virus through IFNAR-MAPK-Fos-CHD6 Axis
|TAR (of TXT)