Abstract

Aims. This study aimed to investigate miR-106a expression in peripheral blood mononuclear cells (PBMCs) of chronic hepatitis B (CHB) patients and to analyze the function of miR-106a. Materials and Methods. miR-106a expression levels in PBMCs from 40 healthy controls and 56 CHB patients were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). The luciferase activity assays were used to determine whether miR-106a binds to 3′UTR of IL-8. miR-106a mimics and inhibitors were transfected into healthy PBMCs. IL-8 mRNA and protein levels were detected and determined by qRT-PCR and ELISA, respectively. Results. The qRT-PCR results suggested that the PBMC miR-106a levels were decreased in CHB patients. IL-8 was augmented in CHB patients and was inversely correlated with miR-106a levels. The luciferase activity assays indicated that IL-8 is a target of miR-106a. Exogenous expression of miR-106a could significantly repress IL-8 expression at both mRNA and protein levels in PBMCs, whereas miR-106a inhibitor had the opposite effects. Conclusions. This study suggested that miR-106a is downregulated in PBMCs of CHB patients and that miR-106a may play an important role in CHB by targeting IL-8.

Highlights

  • Hepatitis B virus (HBV) infection is a significant public health problem with approximately 350 million infections worldwide [1]

  • To identify the miRNAs potentially associated with HBV infection, the expression levels of miR-106a from 56 chronic hepatitis B (CHB) patients and 40 healthy controls were determined by quantitative real-time polymerase chain reaction (qRT-PCR)

  • Discussion miRNAs play an important role in HBV infection and HBV-related disease, such as hepatocellular carcinoma (HCC), and changes in miRNA

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Summary

Introduction

Hepatitis B virus (HBV) infection is a significant public health problem with approximately 350 million infections worldwide [1]. HBV is not directly cytopathogenic for infected hepatocytes and the pathogenesis of liver diseases results from complicated interactions between the HBV replication and host immune responses [4, 5]. Exploring the mechanisms of immune responses in chronic hepatitis B (CHB) patients has been the focus of intense research. Proinflammatory cytokines such as TNF-α, MCP-1, IL-1a, and IL-6 play a central role in the induction of immune responses in the pathogenesis of various infectious diseases [6,7,8,9,10]. Numerous proinflammatory mediators produced and released in association with human RSV challenge, including MCP-1 and IL-6, may promote a viral pathology [8]

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