Activation and manipulation of inflammasomes and pyroptosis during bacterial infections

Abstract

Following detection of pathogen infection and disrupted cellular homeostasis, cells can activate a range of cell death pathways, such as apoptosis, necroptosis and pyroptosis, as part of their defence strategy. The initiation of pro-inflammatory, lytic pyroptosis is controlled by inflammasomes, which respond to a range of cellular perturbations. As is true for many host defence pathways, pathogens have evolved multiple mechanisms to subvert this pathway, many of which have only recently been described. Herein, we will discuss the mechanisms by which inflammasomes sense pathogen invasion and initiate pyroptosis and the effector mechanisms used by pathogens to suppress this pathway and preserve their niche.

Engineered Extracellular Vesicles Driven by Erythrocytes Ameliorate Bacterial Sepsis by Iron Recycling, Toxin Clearing and Inflammation Regulation

“…Pathogen‐triggered cell death has important consequences on sepsis progression. [ 7 , 12 ] We first determined the occurrence of apoptosis of host cells in response to Staphylococcus aureus ( S. aureus ) infection. Since bacterial components trigger apoptosis in macrophages during an innate defense process, [ 13 ] we evaluated apoptosis of macrophages in a S. aureus infection model ( Figure 1 a ).…”

“…It has been suggested that host uses programmed immune cell death to fight infections. [ 7 , 15 ] Given that we found the production of apoEVs is a feature of host response to infection, we evaluated the therapeutic potential of apoEVs and tested their effects on S. aureus ‐induced sepsis model. ApoEVs derived from in vitro cultured apoptotic BMDMs were intravenously administered after disease onset (Figure 2i ).…”

“…[ 6 ] Previous studies have unveiled the utility of pyroptosis or necrosis during infection to destroy intracellular niches, and subsequently coordinate an appropriate innate immune response, which leads to bacteria elimination via pore‐induced intracellular trap or neutrophil extracellular traps. [ 7 ] However, further research is needed to fully understand how apoptosis contributed to the defense against infection in vivo. Apoptosis converts cells into apoptotic extracellular vesicles (apoEVs), [ 8 ] yet it remains unknown whether apoEVs released during bacterial infection could generate anti‐bacterial response.…”

Expression and significance of effector proteins NLRP3 and gasdermin D N-terminal protein in the pyrolysis pathway in breast cancer

“…Mature IL-18 and IL-1β are secreted from the membrane pores to the cellular exterior and gather vast quantities of the inflammatory cells outside the cell to expand the inflammatory response. [12][13][14][15][16][17] The nonclassic pyrolysis pathway is mainly directly recognized by caspase-4/5/11 and combined with the endotoxin lipopolysaccharide of gram-negative bacteria. After being activated by oligomerization, it shows the corresponding protease activity.…”

The Clinical Chameleon of Autoinflammatory Diseases in Children

“…Genes associated with these diseases have been sequentially identified since 1997 onwards, and with the exception of MKD, the majority of them encode for proteins involved in the inflammasome architecture or in programmed cell death [ 11 ]. In particular, inflammasomes, structured with a central sensor protein, an adaptor protein and CASPASE-1, modulate IL-1β release and work as platforms to protect the human body from the outnumber of pathogenic organisms [ 12 ].…”