Immune Netw.  2006 Mar;6(1):20-26. 10.4110/in.2006.6.1.20.

Induction of Interleukin-8 Expression in Synovial Cell by Hepatitis C Virus Core Protein

Affiliations
  • 1WHO Collaborating Center of Viral Hepatitis, College of Medicine, The Catholic University of Korea, Seoul, Korea. yoonsk@catholic.ac.kr
  • 2Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea.

Abstract

BACKGROUND: Rheumatoid arthritis (RA) is a chronic and systemic inflammatory disease that is characterized by invasive synovial hyperplasia, leading to progressive joint destruction. Recent studies have described that RA is caused by virus, bacteria or outside material. Approximately 2 to 20% of RA cases are reported to be associated with infected hepatitis C virus (HCV). However, the mechanisms underlying virus-induced RA are still unknown. Moreover, few molecular studies have addressed the inflammatory aspects of HCV-associated autoimmune RA. In this study, we aimed to determine whether or not another HCV core protein transactivates the IL-8 gene expression, prototypic chemokine, in synovial cell.
METHODS
To establish the HCV core expressing stable synovial cell line, pCI-neo-core, a plasmid encoding HCV core protein, were transfected to HIG-82 cell line that is an established cell line from rabbit periaricular soft tissue. We examined the morphological changes and cell cycle distribution of HIG-82 cells with expression of HCV core protein by inverted microscopy and flow cytometry analysis, respectively. Also, we determined the mRNA levels of Interleukin (IL)-6 and IL-8 related to the inflammation by RT-PCR and then analyzed regulation of IL-8 expression by the NF-kB pathway.
RESULTS
Our study showed no significant differences in morphology and cell cycle between HIG-82 control cell line and HIG-82 expressing HCV core protein. However, expression of HCV core protein induces the IL-8 mRNA expression in HIG-82 core cells via activated NF-kB pathway.
CONCLUSION
These results suggest that HCV core protein can lead to enhanced IL-8 expression. Such a pro-inflammatory role may contribute to the etiologic pathogenesis in RA patients with HCV infection.

Keyword

Hepatitis C virus (HCV); rheumatoid arthritis (RA); cytokine; interleukin-8

MeSH Terms

Arthritis, Rheumatoid
Bacteria
Cell Cycle
Cell Line
Flow Cytometry
Gene Expression
Hepacivirus*
Hepatitis C*
Hepatitis*
Humans
Hyperplasia
Inflammation
Interleukin-8*
Interleukins
Joints
Microscopy
NF-kappa B
Plasmids
RNA, Messenger
Interleukin-8
Interleukins
NF-kappa B
RNA, Messenger
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