IL1B and Sepsis: It causes a large number of inflammatory mediators such as interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α) to pass through the BBB and induces damage to central neurons and synapses.[23] Disruption of the BBB is thought to cause neuroinflammation.[24] According to a murine tibial fracture surgery model, activation of T cells increases the levels of IL-17A, and disruption of the BBB is thought to be associated with POD-like behavior.[25] Sometimes, the body has a systemic inflammatory response such as sepsis.