Intestinal barrier dysfunction, a hallmark of colitis, is characterized by reduced mucin and tight junction protein expression, which facilitates paracellular translocation of luminal bacteria, endotoxins, and LPS into systemic circulation through the activation of TLR4/MyD88/NF-κB signaling pathway, which is linked to the development of liver injury [24,25]. Here, TLR4 is linked to colitis.