Published online Aug 28, 2017. doi: 10.3748/wjg.v23.i32.5895
Peer-review started: January 6, 2017
First decision: March 16, 2017
Revised: March 30, 2017
Accepted: July 22, 2017
Article in press: July 24, 2017
Published online: August 28, 2017
Processing time: 235 Days and 14.4 Hours
To investigate the effect of (-)-epigallocatechin-3-gallate (EGCG) on polyinosinic-polycytidylic acid (poly I:C)-triggered intracellular innate immunity against hepatitis C virus (HCV) in hepatocytes.
A cell culture model of HCV infection was generated by infecting a hepatoma cell line, Huh7, with HCV JFH-1 strain (JFH-1-Huh7). Poly I:C with a high molecular weight and EGCG were used to stimulate the JFH-1-Huh7 cells. Real-time reverse transcription-polymerase chain reaction was used to detect the expression levels of intracellular mRNAs and of intracellular and extracellular HCV RNA. Enzyme-linked immunosorbent assay was used to evaluate the interferon (IFN)-λ1 protein level in the cell culture supernatant. Immunostaining was used to examine HCV core protein expression in Huh7 cells.
Our recent study showed that HCV replication could impair poly I:C-triggered intracellular innate immune responses in hepatocytes. In the current study, we showed that EGCG treatment significantly increased the poly I:C-induced expression of Toll-like receptor 3 (TLR3), retinoic acid-inducible gene I, and IFN-λ1 in JFH-1-Huh7 cells. In addition, supplementation with EGCG increased the poly I:C-mediated antiviral activity in JFH-1-Huh7 cells at the intracellular and extracellular HCV RNA and protein levels. Further investigation of the mechanisms showed that EGCG treatment significantly enhanced the poly I:C-induced expression of IFN-regulatory factor 9 and several antiviral IFN-stimulated genes, including ISG15, ISG56, myxovirus resistance A, and 2’-5’-oligoadenylate synthetase 1, which encode the key antiviral elements in the IFN signaling pathway.
Our observations provide experimental evidence that EGCG has the ability to enhance poly I:C-induced intracellular antiviral innate immunity against HCV replication in hepatocytes.
Core tip: The interactions between hepatitis C virus (HCV) and the host immune system in the liver play a key role in the immunopathogenesis of HCV-induced diseases. We showed here that (-)-epigallocatechin-3-gallate (EGCG) treatment could significantly increase the poly I:C-induced expression of TLR3, RIG-I and interferon (IFN)-λ1 in JFH-1-Huh7 cells. In addition, supplementation with EGCG enhanced poly I:C-mediated viral inhibition in JFH-1-Huh7 cells at both RNA and protein levels. Further investigation of the mechanisms showed that EGCG treatment significantly enhanced the poly I:C-induced expression of IFN-regulatory factor 9 and several IFN-stimulated genes. It would be interesting to investigate the possible use of EGCG in combination with current antiviral drugs for HCV therapy.