Fibrinogen-like protein 2 deficiency inhibits virus-induced fulminant hepatitis through abrogating inflammatory macrophage activation

Figure 5 Depletion of macrophages in fibrinogen-like protein 2 synergically attenuated liver damage after viral infection. A: H&E staining on liver sections from mice administered with either clodronate liposomes (CL) (b and d on the right) or PBS-liposomes (PBS) (a and c on the left) at 48 h post murine hepatitis virus strain 3 (MHV-3) infection; e-f, liver sections from bone marrow-derived macrophages (BMDMs) adoptive transferred mice at 48 h post MHV-3 infection (e: WT BMDM donor; f: Fibrinogen-like protein 2 (Fgl2-/-) BMDM donor); B: Serum ALT and AST levels from clodronate liposomes-treated WT and Fgl2-/- mice at 48 h post MHV-3 infection; C: Serum AST and ALT levels from WT and Fgl2-/- BMDM chimeric mice; D: representative F4/80+ iNOS+ and F4/80+ CD206+ donor macrophages from WT and Fgl2-/- BMDM chimeric mice at 48 h post infection; E: statistical analysis of iNOS+ and CD206+ donor macrophages in chimeric mice at 48 h post infection; F: H&E-stained liver section from mice which were treated with Cenicriviroc (CVC) in advance and subjected to MHV-3 infection for 48 h. Arrows represented necrotic cells, circles represent areas of hepatocyte necrosis. Image magnificence: 200×; G: aminotransferase levels of CVC treated viral fulminant hepatitis mice and its control. Data were presented as mean ± SD (n = 5). These experiments were repeated at least three times. BMDM: Bone marrow derived macrophages.