Overexpression of A20 inhibits the inflammatory response during dengue fever infection

Abstract

Aim: Dengue hemorrhagic fever is a devastating disease. This study aimed to investigate the role of A20 in dengue fever infection. Materials & methods: DENV2-infected human umbilical vein endothelial cells were transfected with shRNA-A20/CD14 and A20/CD14-mimics, respectively. The expressions of inflammatory and anti-inflammatory factors, A20 and downstream proteins of the NF-κB signaling pathway were detected. Results: A20 knockdown increased the expression of IL-6, IL-10, IL-8 and CD14 during dengue virus infection, whereas overexpression of A20 had the opposite effect. FACS revealed that A20 negatively regulated the expression of CD14. Conclusion: In DENV2-infected human umbilical vein endothelial cells overexpressing A20, TNF-α stimulation inhibited NF-κB-mediated inflammatory response by negative feedback. Furthermore, A20 could affect the release of inflammatory factors via negative regulation of CD14, thus affecting the entire inflammatory response.