Lipopolysaccharide/adenosine triphosphate induces IL‑1β and IL-18 secretion through the NLRP3 inflammasome in RAW264.7 murine macrophage cells

Abstract The NOD-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome plays pivotal roles in inflammation and autoimmunity. The NLRP3 inflammasome is activated in response to various signals, including pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs). However, its role in inflammation remains unclear. In this study, we used lipopolysaccharide (LPS) and adenosine triphosphate (ATP) to simulate an inflammatory environment as the testing model. We found that the exposure of RAW264.7 cells to LPS/ATP triggered the activation of caspase-1 (P 0.05). In addition, the silencing of NLRP3 with small interfering RNA (siRNA) suppressed the generation of proinflammatory cytokines, such as IL-1β (P 0.05), along with the decreased mRNA and protein expression of NLRP3 and caspase-1 (P 0.05). Our results suggest that the NLRP3/ASC/caspase-1 axis participates in the regulation of pro-imflammatory cytokine secretion in RAW264.7 cells, particularly the generation of IL-1β and IL-18.