IRF7 Modulates Inflammatory Pain through upregulating IFNß in mice

Interferon regulatory factors (IRFs) are a family of transcription factors and function primarily in the immune system, which also play critical roles in other biological processes, such as pain. To date little is known about the functions of the interferon regulatory factor 7 (IRF7) involving in pain. Here we investigate the role of IRF7 signaling in nociceptive processing, using RNA interference strategies or pharmacological approaches. We show that the expression level of IRF7 and interferon (IFN) ß is upregulated in primary sensory neurons in a mouse model of inflammatory pain.IRF7-IFNß signal is involved in regulating neuronal hypersensitivity and pro-inflammatory cytokines production. The results identify IRF7-IFNß signaling as a critical mediator of neuroinflammation that involve in pain development at the level of the primary sensory ganglion. This pathway may be suggested as a potential target for pain management, particularly in orofacial inflammatory pain. Overall design: High-throughput sequencing was performed on TG tissues from mice injected with either CFA or saline (n = 3) at 3 dpi. Tissue collection followed the protocol described above, and samples were immediately processed for sequencing. Library preparation for Illumina sequencing was conducted using KAPA Stranded RNA-Seq Library Prep Kit (Illumina). Stranded-mRNA was performed sequenced on Illumina Platform NovaSeq 6000.