Sepsis is recognized as the systemic host response to invasive infection, in which hyper-immunological reactions highlighted by elevated blood cytokine levels occur. Sepsis is clinically defined as systemic inflammatory response syndrome (SIRS) caused by infection (Table 34.1) [1]. In 2016, the diagnostic criteria for sepsis were revised, and it was newly defined as “life-threatening organ dysfunction caused by a dysregulated host response to infection” [2]; however, there is no fundamental difference from the previous definition. Endotoxin (lipopolysaccharide; LPS) plays a crucial role in triggering the overreaction of the immunological defense system. In addition, sepsis induces changes of systemic hemodynamics that evolve from an early hyperdynamic (“warm shock”) state to a late hypodynamic (“cold shock”) state. Similar hemodynamic changes were reportedly observed after a large LPS injection [3]. This supports the view that it is not the bacterial infection itself, but rather the LPS that directly contributes to the pathophysiology of septic shock.