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

Figure 8 Fibrinogen-like protein 2 deficiency impaired inflammatory cascade in response to lipopolysaccharide treatment of viral infection. A: Immunoblot for fibrinogen-like protein 2 (Fgl2) and β-actin expression in wild-type (WT) BMDMs in response lipopolysaccharide (LPS) stimulation and murine hepatitis virus strain 3 (MHV-3) infection. B-E: Immunoblot for proteins panels from lysates of WT and Fgl2-/- BMDMs in response to LPS treatment and MHV-3 infection; B: MyD88, TRIF, IκBα, phosphorylated IκBα, phosphorylated p65 (S468) and IRF3, phosphorylated IRF3, and IRF7; C: p38, JNK, ERK and phosphorylated p38, JNK, ERK; D: Phosphorylated c-Raf, phosphorylated p65 (S276), acetyl p65 (lys310); E: BTK, and phosphorylated BTK (Y223), BTK (Tyr550). These experiments were repeated at least three times.