NLRP3 and infection: The passive release of HMGB1 from damaged cells or activated immune cells following infection, injury, and sterile inflammation also demonstrates the regulation of inflammatory responses [33,34,35,36], which can also be mediated through inflammasomes, large caspase-1-activating protein complexes, including NLRP3 [37], and, more importantly, these cytoplasmic release of HMGB1 from activated glia or injured neurons can also act as a cytokine [38,39].