IL1B and infection: Once brain injury or infection occurs, microglia turn into the activated state and secrete a series of proinflammatory and neurotoxic mediators, such as interleukin-1 beta (IL-1β), nitric oxide (NO), tumor necrosis factor alpha (TNF-α), and reactive oxygen species (ROS), which not only regulate neuronal function and synaptic transmission but also give rise to neuronal oxidative stress and degeneration associated with deficits in a variety of cognitive and memory tasks [8–10].