In the IBD model, the leakage of the intestinal tract may cause excessive lipopolysaccharide (LPS) shifting into the liver through the portal vein circulation and promoting a series of proinflammatory cytokines to release, thereby inducing chronic inflammatory response via activating the proinflammatory signaling pathway such as the TLR4/MyD88/NF-κB pathway, and a long-term continuous chronic inflammation can trigger secondary liver injury and hepatitis [31]. Here, TLR4 is linked to hepatitis A virus infection.