Mechanisms that lead to the regulation of NLRP3 inflammasome expression and activation in human dental pulp fibroblasts

Abstract

Our results demonstrated that the NLRP3 inflammasome in HDPFs is crucial for IL-1β secretion in response to LPS plus ATP. LPS engaged the TLR4/MyD88/NF-κB pathway to enhance NLRP3 and pro-IL-1β expression in HDPFs. ATP promoted the generation of ROS and activated the NLRP3 inflammasome in a ROS-dependent manner.