NLRP3 and bacterial infectious disease: Corroborating the genetic evidence that BTK is a positive regulator of NLRP3 signaling, treatment with ibrutinib or acalabrutinib suppresses NLRP3- but not AIM2-induced inflammasome activation and blocks IL-1β processing in human and mouse macrophages or TAMs in vitro as well as in vivo in mouse models of ischemic brain injury, polymicrobial sepsis and bacterial infection (Ito et al., 2015; Liu et al., 2017; Benner et al., 2019; de Porto et al., 2019; O’Riordan et al., 2019; Weber, 2021).