Interferon induces interleukin 8 and bone marrow stromal cell antigen 2 expression, inhibiting the production of hepatitis B virus surface antigen from human hepatocytes

被引:8
作者
Haga, Yuki [1 ]
Kanda, Tatsuo [1 ]
Nakamoto, Shingo [1 ,2 ]
Nakamura, Masato [1 ]
Sasaki, Reina [1 ]
Wu, Shuang [1 ]
Yokosuka, Osamu [1 ]
机构
[1] Chiba Univ, Grad Sch Med, Dept Gastroenterol & Nephrol, Chuo Ku, 1-8-1 Inohana, Chiba 2608670, Japan
[2] Chiba Univ, Grad Sch Med, Dept Mol Virol, Chiba 2608670, Japan
关键词
BST2; HBV; HBsAg; Interleukin; 8; MESSENGER-RNA EXPRESSION; RESTRICTION FACTOR; INFECTION; TETHERIN; THERAPY; LINES; HBV; DNA; BST2/TETHERIN; CYTOKINES;
D O I
10.1016/j.bbrc.2017.03.150
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Hepatitis B virus (HBV) surface antigen (HBsAg) loss is one of the treatment goals of chronic HBV infection. Bone marrow stromal cell antigen 2 (BST2) is one of the interferon (IFN)-stimulated genes (ISGs) and inhibits the release of various enveloped viruses. Here we examined the effects of antiviral treatment on HBsAg levels and its intracellular mechanism in HBsAg-producing hepatocytes. In PLC/PRF/ 5 and Huhl, IFNoc-2a treatment decreased HBsAg levels in their conditioned media. Upregulation of interleukin 8 (IL8), toll-like receptor 2 (TLR2) and interferon gamma -induced protein 10 (IP10) mRNAs was associated with the reduction of HBsAg in both PLC/PRF/5 and Huhl. The HBsAg level was upregulated by knockdown of IL8, TLR2 or IP10. Exogenous addition of IL8 enhanced BST2 promoter activity and BST2 mRNA expression. Additionally, knockdown of IL8 could lead to the downregulation of BST2 mRNA. Transfection of poly(I-C) enhanced IL8 and BST2 mRNA expression and inhibited HBsAg secretion from PLC/PRF/5 cells. In conclusion, IL8 might play an important role in the enhancement of BST2 and be involved in HBsAg eradication. (C) 2017 Elsevier Inc. All rights reserved.
引用
收藏
页码:858 / 863
页数:6
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