Interleukin-22 facilitates the interferon-λ-mediated production of tripartite motif protein 25 to inhibit replication of duck viral hepatitis A virus type 1

• Published in: Veterinary research (Paris) 2023-06, Vol.54 (1), p.53-53, Article 53
• Main Authors: An, Hao, Liu, Yumei, Shu, Ming, Chen, Junhao
• Format: Article
• Language: English
• Subjects: Animals; Antibodies; Chromatography; Cytokines; Ducks; Hepatitis; Hepatitis A virus; Hepatitis Virus, Duck; IFN-λ; IL-22; Infections; Interferon; Interferon Lambda; Interleukin-22; Interleukins; Kinases; Phosphorylation; Plasmids; Proteins; Signal transduction; STAT3; TRIM25; Viruses
• ISSN: 1297-9716; 0928-4249; 1297-9716
• DOI: 10.1186/s13567-023-01188-4

The innate immune system provides a defense against invading pathogens by inducing various interferon (IFN)-stimulated genes (ISGs). We recently reported that tripartite motif protein 25 (TRIM25), an important ISG, was highly upregulated in duck embryo hepatocyte cells (DEFs) after infection with duck viral hepatitis A virus type 1 (DHAV-1). However, the mechanism of upregulation of TRIM25 remains unknown. Here we reported that interleukin-22 (IL-22), whose expression was highly facilitated in DEFs and various organs of 1-day-old ducklings after DHAV-1 infection, highly enhanced the IFN-λ-induced production of TRIM25. The treatment with IL-22 neutralizing antibody or the overexpression of IL-22 highly suppressed or facilitated TRIM25 expression, respectively. The phosphorylation of signal transducer and activator of transcription 3 (STAT3) was crucial for the process of IL-22 enhancing IFN-λ-induced TRIM25 production, which was suppressed by WP1066, a novel inhibitor of STAT3 phosphorylation. The overexpression of TRIM25 in DEFs resulted in a high production of IFNs and reduced DHAV-1 replication, whereas the attenuated expression of IFNs and facilitated replication of DHAV-1 were observed in the RNAi group, implying that TRIM25 defended the organism against DHAV-1 propagation by inducing the production of IFNs. In summary, we reported that IL-22 activated the phosphorylation of STAT3 to enhance the IFN-λ-mediated TRIM25 expression and provide a defense against DHAV-1 by inducing IFN production.