The defective expression of hepatocyte aquaporin-8, a water channel involved in bile secretion, also contributes to the development of bile secretory dysfunction in sepsis.[26] P-selectin-mediated recruitment of leukocytes plays a potential role in reduction of bile flow in sepsis-associated cholestasis.[27] Moreover, epithelial tight junctions in the hepatobiliary system are important in maintaining the osmotic gradient for bile production. Here, SELP is linked to Sepsis.