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

Figure 6 Fibrinogen-like protein 2 promoted bone marrow-derived macrophages M1 polarization in vitro. A: Supernatant concentration of NO2-, IL-1β, TNF-α, IL -6, IL-12 and MCP-1 released by bone marrow-derived macrophages (BMDMs) after LPS (100 ng/mL) treatment or murine hepatitis virus strain 3 (MHV-3) infection for 24 h; B: Relative transcriptional level of M1 markers (NOS2, IL-6, IL-12, IL-1β, TNF-α and marco) of WT and fibrinogen-like protein 2 (Fgl2-/-) BMDMs after the stimulation of LPS for 6 hours; C: Relative transcriptional level of M1 markers of WT and Fgl2-/- BMDMs after MHV-3 infection for 8 hours; D: Supernatant IL-10 concentration of BMDMs culture after the IL-4 stimulation (20 ng/mL) for 72 h; E: mRNA expression of M2 markers (Fizz1, ARG1, YM-1, MRC1, IL-10 and TGF-β) of WT and Fgl2 -/- BMDMs after of IL-4 treatment for 72 h. All data are presented as mean ± SD (n > 3). These experiments were repeated at least three times.