Inflammasomes and host defenses against bacterial infections

The inflammasome has emerged as an important molecular protein complex which initiates proteolytic processing of pro-IL-1β and pro-IL-18 into mature inflammatory cytokines. In addition, inflammasomes initiate pyroptotic cell death that may be independent of those cytokines. Inflammasomes are central to elicit innate immune responses against many pathogens, and are key components in the induction of host defenses following bacterial infection. Here, we review recent discoveries related to NLRP1, NLRP3, NLRC4, NLRP6, NLRP7, NLRP12 and AIM2-mediated recognition of bacteria. Mechanisms for inflammasome activation and regulation are now suggested to involve kinases such as PKR and PKCδ, ligand binding proteins such as the NAIPs, and caspase-11 and caspase-8 in addition to caspase-1. Future research will determine how specific inflammasome components pair up in optimal responses to specific bacteria.

► The inflammasomes are central for many anti-bacterial host defenses. ► In addition to caspase-1, caspase-11 and caspase-8 are emerging as important players in pro-inflammatory signaling. ► NLRP1, NLRP3, NLRC4, NLRP6, NLRP7, NLRP12, AIM2, ASC and NAIPs are inflammasome components. ► Kinases may control both NLRP3 and NLRC4 inflammasomes. ► Cooperation between different inflammasomes may be necessary for optimal responses.