Human and mouse NAIP/NLRC4 inflammasome responses to bacterial infection

Intracellular immune complexes known as inflammasomes sense breaches of cytosolic sanctity. Inflammasomes promote downstream proinflammatory events, including interleukin-1 (IL-1) family cytokine release and pyroptotic cell death. The nucleotide-binding leucine-rich repeat family, apoptosis inhibitory protein/nucleotide-binding leucine-rich repeat family, caspase recruitment domain (CARD) domain-containing protein 4 (NAIP/NLRC4) inflammasome is involved in a range of pathogenic and protective inflammatory processes in mammalian hosts. In particular, the NAIP/NLRC4 inflammasome responds to flagellin and components of the virulence-associated type III secretion (T3SS) apparatus in the host cytosol, thereby allowing it to be a critical mediator of host defense during bacterial infection. Notable species- and cell type-specific differences exist in NAIP/NLRC4 inflammasome responses to bacterial pathogens. With a focus on Salmonella enterica serovar Typhimurium as a model pathogen, we review differences between murine and human NAIP/NLRC4 inflammasome responses. Differences in NAIP/NLRC4 inflammasome responses across species and cell types may have arisen in part due to evolutionary pressures.

Automated summary

Inflammasomes are intracellular immune complexes that detect disruptions in cellular integrity and promote proinflammatory responses. The NAIP/NLRC4 inflammasome plays a crucial role in mediating host defense during bacterial infection by responding to flagellin and components of the T3SS apparatus. There are notable species-specific and cell type-specific differences in NAIP/NLRC4 inflammasome responses to bacterial pathogens, which may have arisen due to evolutionary pressures.