The crosstalk of neutrophil extracellular trap-inflammasome and their roles in disease progression.

Neutrophil extracellular traps (NETs) are a network of fibrous structures composed of DNA, histones, and antimicrobial proteins released by neutrophils, which play a crucial role in the innate immune system's defense against infection. When neutrophils encounter pathogens, they can release NETs to capture and neutralize these invaders, preventing their spread and prompting other immune cells to destroy them. The classical inflammasome is a cytoplasmic polyprotein complex activated by infectious and/or non-infectious stimuli that activates the protease caspase-1 to induce pyroptosis and promotes the maturation and release of interleukin (IL)-1β and IL-18, while the non-classical inflammasome activates cysteinyl aspartate specific proteinase (caspase)-4/11 to induce pyroptosis. Inflammasome activation is also an important component of the innate immune response. This review elaborates on the constituent proteins and molecular regulation of NETs and inflammasomes, summarizes the crosstalk between NETs and inflammasomes and its negative effects in the disease process, and also discusses the therapeutic effects of drugs targeting NETs and/or inflammasomes on related diseases.