[TLR9 expression and its relationship with MCP-1 and TNF-α in HCV-stimulated BV2 cells]

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2011 Oct;27(10):1083-5.
[Article in Chinese]

Abstract

Aim: To detect TLR9 expression and its effect on the secretion of MCP-1 and TNF-α after mouse microglia (BV2) were infected by hepatitis C virus (HCV), and to explore the mechanism of HCV-induced central nervous system (CNS) infection.

Methods: BV2 cells were cultured in vitro and divided into a HCV-positive serum group, a normal serum group (negative control) and a blank control group, with each group of 20 samples. The cells and the supernatants were collected at 12 h, detected for TLR9 expression by flow cytometry (FCM), and determined for the levels of TNF-α and MCP-1 by ELISA. Then the data was statistically analyzed by SPSS11.0.

Results: (1) FCM showed TLR9 expression in all three groups, with the strongest expression in the HCV-positive serum group (P<0.01), while there was no statistical significance between the normal serum group and the blank control group (P>0.05). (2) The levels of TNF-α and MCP-1 in the HCV-positive serum group were higher than those in the other groups (P<0.01), which correlated with enhanced TLR9 expression in the HCV-positive serum group.

Conclusion: HCV-positive serum causes enhanced TLR9 expression and the secretion of MCP-1 and TNF-α. in BV2 cells, suggesting the involvement of TLR9 in the early inherent immune response triggered by HCV-induced CNS infection.

Publication types

  • English Abstract

MeSH terms

  • Animals
  • Cell Line
  • Chemokine CCL2 / blood
  • Chemokine CCL2 / metabolism*
  • Hepacivirus*
  • Humans
  • Mice
  • Microglia / metabolism*
  • Microglia / virology*
  • Toll-Like Receptor 9 / metabolism*
  • Tumor Necrosis Factor-alpha / blood
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Chemokine CCL2
  • Toll-Like Receptor 9
  • Tumor Necrosis Factor-alpha