Objective   To explore the different expression of Toll-like receptor 7 (TLR7) between HepG2.2.15 cells

which were stably transfected HBV gene

and HepG2 cells

and then analyze the expressions of the TLR7-induced inflammation factors in HepG2.2.15 cell line.    Methods   Real-time PCR was used to analyze the different expressions of TLR7

IL-6 and TNF-α between in HepG2 and HepG2.2.15 cells. After the cells were treated with Gardiquimod

a TLR ligand

at 0

1

3 and 10 μg/ml for 6 h

the messenger ribonucleic acid (mRNA) expressions of IL-6 and TNF-α were measured by real-time PCR

and the protein secretion of the 2 cytokines was determined by ELISA after 48 hours’ treatment. Western blot analysis was used to analyze the activation of NF-κB in HepG2.2.15 cells after Gardiquimod stimulation for 20 min.    Results   The expression of TLR7 in HepG2.2.15 cells was about 30-fold higher than that in the HepG2 cells. The mRNA levels of IL-6 and TNF-α were higher in HepG2.2.15 cells than in HepG2 cells (about 7.5 and 9.3 folds respectively)

even without Gardiquimod stimulation. After the cells were stimulated by Gardiquimod for 6 h

although the mRNA of IL-6 and TNF-α in HepG2 cells were slightly increased (compared with the control

P0.05)

the increase of IL-6 and TNF-α mRNA levels was more significant in HepG2.2.15 cells than in HepG2 cells (compared with the control

P0.01

and with HepG2 cells

P0.01). The cells were treated with Gardiquimod for 48 h

the induced expressions of the 2 cytokines protein levels had a consistent changes with the mRNAs level at a dose-dependent manner (compared with control P0.01). While HepG2.2.15 cells were stimulated by Gardiquimod for 20 min

the nuclear immigration of NF-κB p65 subunit was significantly increased.    Conclusion   The activation of TLR7 upregulates the expressions of the IL-6 and TNF-α

suggesting that the TLR7 might be involved in the pathogenesis of the viral hepatitis.