2. Academic Validation
  3. IL-10 upregulates SOCS3 to inhibit type I interferon signaling to promote PoRVA replication in intestinal epithelial cells

IL-10 upregulates SOCS3 to inhibit type I interferon signaling to promote PoRVA replication in intestinal epithelial cells

  • Vet Microbiol. 2024 Sep 23:298:110259. doi: 10.1016/j.vetmic.2024.110259.
Haixin Liu 1,  Yongpan Zhao 2,  Huimin Du 1,  Pengcheng Hao 1,  Haolun Tian 1,  Kun Wang 1,  Yudong Qiu 1,  Haiying Dong 1,  Qian Du 3,  Dewen Tong 4,  Yong Huang 5
Affiliations

Affiliations

  • 1 College of Veterinary Medicine, Northwest A&F University, Yangling, China.
  • 2 College of Veterinary Medicine, Northwest A&F University, Yangling, China; Shaanxi Animal Husbandry Experimental and Demonstration Center, China.
  • 3 College of Veterinary Medicine, Northwest A&F University, Yangling, China; Engineering Research Center of Efficient New Vaccines for Animals, Ministry of Education, Yangling, China; Key Laboratory of Ruminant Disease Prevention and Control (West), Ministry of Agriculture and Rural Affairs, Yangling, China; Engineering Research Center of Efficient New Vaccines for Animals, Universities of Shaanxi Province, Yangling, China.
  • 4 College of Veterinary Medicine, Northwest A&F University, Yangling, China; Engineering Research Center of Efficient New Vaccines for Animals, Ministry of Education, Yangling, China; Key Laboratory of Ruminant Disease Prevention and Control (West), Ministry of Agriculture and Rural Affairs, Yangling, China; Engineering Research Center of Efficient New Vaccines for Animals, Universities of Shaanxi Province, Yangling, China. Electronic address: dwtong@nwsuaf.edu.cn.
  • 5 College of Veterinary Medicine, Northwest A&F University, Yangling, China; Engineering Research Center of Efficient New Vaccines for Animals, Ministry of Education, Yangling, China; Key Laboratory of Ruminant Disease Prevention and Control (West), Ministry of Agriculture and Rural Affairs, Yangling, China; Engineering Research Center of Efficient New Vaccines for Animals, Universities of Shaanxi Province, Yangling, China. Electronic address: Yonghuang@nwsuaf.edu.cn.
PMID: 39332165 DOI: 10.1016/j.vetmic.2024.110259
Abstract

Porcine group A rotavirus (PoRVA) is one of the common enteric viruses causing severe diarrhea in piglets. Although PoRVA Infection has been identified to promote IL-10 production, the role of IL-10 during viral Infection remains unclear. In this study, we found that elevated IL-10 levels during PoRVA Infection promote viral replication by inhibiting type I interferon production and response. IL-10 treatment upregulated the expression of SOCS3 in PoRVA-infected IPEC-J2 cells, which inhibited IFN-I production by preventing the degradation of IκB and nuclear translocation of NF-κB, thereby significantly promoting PoRVA replication. Furthermore, we determined that SOCS3 also inhibited type Ⅰ interferon signaling pathway, which led to a significantly reduced ISGs after IFN-α stimulation. In PoRVA-infected cells, overexpression of SOCS3 significantly inhibits phosphorylation and heterodimerization of STAT1, thereby promoting viral replication. Finally, we demonstrated the effect of IL-10 on PoRVA replication in vivo by murine models of PoRVA Infection. PoRVA replication levels were lower in the ileum of IL-10 knockout (IL-10-/-) mice than that in PoRVA-infected wild-type mice, but PoRVA replication levels were higher in the ileum of IFNAR knockout (IFNAR-/-) mice than that in PoRVA-infected wild-type mice. Taken together, our findings provide information to understand the strategies of PoRVA to evade host innate Antiviral immunity.

Keywords

IFN-I; IL-10; PoRVA; SOCS3.

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