The NLRP3 Inflammasome and IL-1β Accelerate Immunologically Mediated Pathology in Experimental Viral Fulminant Hepatitis
Fig 2
IL-1R1 deficiency attenuates MHV-3-induced hepatitis.
IL-1R1-/- mice and their C57BL/6 wild-type (WT) littermates were infected with MHV-3 (100 PFU), (A) The survival rate was monitored for a total of 20 days. One representative of three experiments with similar results is shown. *p<0.05. (B) The liver architecture was analyzed by H&E staining (left), and serum ALT/AST levels were determined with an AU5400 automatic biochemistry analyzer (right). Scale bar 20 μm, n = 5 per group, *p<0.05 and **p<0.001, NS: no significant difference. (C) The expression of Bgp1 in MHV-3-infected livers was compared by western-blotting. Three representative samples per group are shown. (D) The virus titers in livers at 72h post-infection were analyzed by plaque assay (up), and results were compared by statistical analysis (down). *p<0.05. (E) Peritoneal exudative macrophages (PEMs) were isolated from virus infected mice at 24h and the virions were detected by electron microscopy. Arrows indicate spherical virions. (F) The expression of Bgp1 in PEMs and RAW264.7 cells that treated with IL-1β (20 ng/ml) at the indicated time points was detected by western-blotting (up panel). RAW264.7 cells were treated with IL-1β (20 ng/ml) and PBS for a total 48h firstly, cells were further infected with MHV-3 and virus titers were detected by plaque assay at the indicated time points (down panel). *p<0.05 compared to PBS-treated counterparts.