Related Experiment Video
Updated: Nov 5, 2025

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
Published on: May 21, 2018
NLRP3 inflammasome in sepsis (Review)
Xueyan Shi1, Sichuang Tan2, Sipin Tan1
1Department of Sepsis Translational Medicine, Key Laboratory of Hunan Province, Xiangya School of Medicine, Central South University, Changsha, Hunan 410008, P.R. China.
Abstract:
Sepsis is an imbalanced response to infection that leads to life-threatening organ dysfunction. Although an increasing number of anti-inflammatory drugs are available, the options for treating sepsis remain limited. Therefore, it is imperative to understand the pathogenesis and pathophysiology of sepsis and develop novel therapeutic targets to treat this state. The Nod-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is a cytoplasmic high-molecular weight protein complex composed of the sensor NLRP3, adapter protein apoptosis-related speck-like protein and pro-caspase-1. It functions by cleaving pro-caspase-1 to become active caspase-1, resulting in the maturation and release of IL-1β and IL-18. Activation of the NLRP3 inflammasome is necessary for innate immune defense and also serves an important role in adaptive immune responses. Studies have shown that the NLRP3 inflammasome is involved in the occurrence and evolution of sepsis and other immune inflammatory diseases. The present paper reviews the activation pathways and biological function of the NLRP3 inflammasome in sepsis, with the aim to provide a basis for further research.

