Fig. 1
From: The gut–liver axis in sepsis: interaction mechanisms and therapeutic potential
During sepsis, several mechanisms contribute to disruption of the gut barrier, including IEC apoptosis, alteration of the mucus layer, and disruption of intercellular junctions, resulting in translocation of intestinal PAMPs into the liver via the lymphatic vessels, portal circulation, or biliary tract. The liver is essential to the regulation of immune defense, with effector cells such as LSECs, macrophages, stellate cells, and hepatocytes immediately identifying and engaging pathogens, clearing bacteria, and releasing cytokines. When an inappropriate immune response or overwhelming inflammation occurs with high levels of DAMPs and proinflammatory cytokine production in the liver, the normal structure of the hepatic sinus is disrupted, and such cells are damaged through apoptosis and autophagy, leading to bacterial clearance dysfunction and metabolic disorders. As a result, the gut barrier is further damaged, gut microbiota dysbiosis is exacerbated, and distal organs are injured due to the spread of PAMPs and DAMPs and systemic inflammation. IECs, intestinal epithelial cells; DAMPs, damage-associated molecular patterns; LSECs, liver sinusoidal endothelium; PAMPs, pathogen-associated molecular patterns