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J Cell Physiol. 2015 Oct;230(10):2382-9. doi: 10.1002/jcp.24967.

Autophagy Mediates HBx-Induced Nuclear Factor-κB Activation and Release of IL-6, IL-8, and CXCL2 in Hepatocytes.

Author information

1
State Key Laboratory of Digestive Diseases, Institute of Digestive Diseases, LKS Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, China.
2
Department of Anaesthesia & Intensive Care, The Chinese University of Hong Kong, Hong Kong, China.
3
School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, China.
4
School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China.
5
Department of Surgery, The Chinese University of Hong Kong, Hong Kong, China.

Abstract

Hepatitis B virus (HBV) and one of its encoded proteins, HBV X protein (HBx), have been shown to induce autophagy in hepatoma cells. Substantial evidence indicates that autophagy is a potent suppressor of inflammation. However, sporadic reports suggest that autophagy could promote pro-inflammatory cytokine expression and inflammation in some biological contexts. Here, we show that overexpression of HBx induces LC3B-positive autophagosome formation, increases autophagic flux and enhances the expression of ATG5, ATG7, and LC3B-II in normal hepatocytes. Abrogation of autophagy by small interfering RNA against ATG5 and ATG7 prevents HBx-induced formation of autophagosomes. Autophagy inhibition also abrogates HBx-induced activation of nuclear factor-κB (NF-κB) and production of interleukin-6 (IL-6), IL-8, and CXCL2. These findings suggest that autophagy is required for HBx-induced NF-κB activation and pro-inflammatory cytokine production and could shed new light on the complex role of autophagy in the modulation of inflammation.

PMID:
25708728
DOI:
10.1002/jcp.24967
[Indexed for MEDLINE]

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