Fig. 5

HBeAg induced inflammation and fibrogenesis response in vivo via TLR-2 in macrophages. Male Balb/c mice (5 mice in each group) were tail intravenous injected with recombinant HBeAg 40 μg or received the equivalent volume of PBS, then were sacrificed at 4, 8, 12, and 24 h respectively. Liver sections were stained with HE and F4/80 (A). The mRNA levels of the liver were detected via qRT-PCR (B–E). Plasma levels of ALT and AST were also examined (F, G). Male Balb/c mice (5 mice in each group) were treated with CCl₄ (1 ml/kg in olive oil) together with intravenous administration of HBeAg 40 μg or the same volume of PBS. Liver sections were stained with α-SMA, F4/80, Desmin, and ki67 (H, I). Levels of serum ALT were examined (J). Male Balb/c mice were intraperitoneal injection of 0.2 ml clodronate-liposome (7 mg/ml) or control-liposome before CCl₄ or HBeAg treatment as mentioned above. Monocyte depletion efficiency was examined at day 1 and day 4 by F4/80 staining (K). The mRNA levels in the liver of mice treated with HBeAg for 4 h were detected through qRT-PCR (L–O). The mRNA levels in the liver of mice treated with CCl₄ and HBeAg in turn were tested by qRT-PCR (P–T). TLR-2 inhibitor (C29) was injected intraperitoneally (1.3 μmol/g) 1 h before HBeAg treatment (40 μg per mouse), with the same volume of dissolving reagent as the vehicle group (5 mice in each group). The mRNA levels in the liver were tested by qRT-PCR (U–X). *p = 0.05, **P < 0.01, ***P < 0.001