Biomedical Research

Background: Toll-Like Receptors (TLRs) play critical roles in innate immunity. HBV can modulate the expression of TLRs and/or inhibit TLR signaling cascades to escape the innate immune response. However, the mechanism of HBV in the regulation of TLRs remains unclear. In this study, we aimed to clarify whether miR-200b suppresses host innate immune response against HBV infection by targeting TLR4 signaling pathway.

Methods: First, the expression of miR-200b in HBV-infected liver tissues and HBV-producing HepG2.2.15 cells was detected using Quantitative Real-time PCR (qRT-PCR). We then examined the association between chronic HBV infection and the expression of miR-200b. ELISA assay was used to evaluate the host innate immune response. Further, the potential target genes related to innate immunity of miR-200b were also predicted. Western blot and luciferase reporter assays were performed to confirm the predicted genes.

Results: An upregulated expression of miR-200b was observed in HBV-infected liver tissues and HepG2.2.15 cells. Besides, a positive association was found between chronic HBV infection and the expression of miR-200b. A luciferase reporter assay revealed that MyD88 and IRAK4 were the downstream targets of miR-200b. Finally, knockdown of miR-200b in HepG2.2.15 cells suppressed TLR4-mediated innate response.

Conclusions: Our study revealed that miR-200b was related to HBV infection through a pathway involving the MyD88 and IRAK4 and provides new insights into the understanding of mechanisms of HBV-induced immunosuppressive strategy.

Author(s): Yazhen Niu, Ming Gao, Na Feng, Jingjing Yang
Abstract | Full-Text | PDF

Share this