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

Figure 4 Fibrinogen-like protein 2 promotes pro-inflammatory macrophage polarization following murine hepatitis virus strain 3 infection. A: H&E staining on liver sections from wild type (WT) and fibrinogen-like protein 2 (Fgl2-/-) mice at 48 and 72 h post viral infection. Circled field represented bulk necrosis. Arrows point to necrotic cells; B: Serum alanine transaminase and aspartate transaminase levels at 0, 24, 48, and 72 h post viral infection in WT and Fgl2-/- mice; C: Flow cytometry of KCs and MoMFs in hepatic CD45+ leukocytes at steady condition and 48 h following viral fulminant hepatitis in WT and Fgl2-/- mice (left); and respective frequency at 48 h post infection; D: Frequency of polarized M1 (iNOS+), M2 (CD206+) KCs at 0 and 24 h post murine hepatitis virus strain 3 (MHV-3) infection; E: Frequency of Ly6Chi and Ly6Clow MoMFs at 0 and 48 h post MHV-3 infection. Data are presented as mean ± SD (n = 5). These experiments were repeated at least three times.