Litcius/Paper detail

Neutrophil extracellular traps promote M1 macrophage polarization in gouty inflammation via targeting hexokinase-2

Haibo Tan, Shan Zhang, Zhihao Zhang, Jianyong Zhang, Ziyu Wang, Junlan Liao, Xia Qiu, Ertao Jia

2024Free Radical Biology and Medicine43 citationsDOIOpen Access PDF

Abstract

macrophage infiltration were observed in human gouty arthritis (GA). In vitro, MSU crystal-induced NETs or NET-associated histone H3 treatments modulated nod-like receptor protein 3 (NLRP3) inflammasome activation, M1 polarization, and metabolic changes in macrophages. These effects were eliminated by hexokinase-2 (HK-2) silencing. Moreover, NET formation and inflammation were significantly reduced in PAD4-/- GA mice. Pharmacological inhibition of NET formation with Cl-Amidine or NET degradation with DNase Ⅰ significantly reduced M1 polarization of macrophages and ameliorated inflammation in GA mice. In sum, MSU crystal-induced NETs promote M1 polarization and NLRP3 activation in macrophages via targeting HK-2. Cell-free DNA and histone H3 may be the driving elements behind the NET-induced M1 macrophage polarization, NLRP3 activation, and metabolic changes. Targeting NETs could be a potential therapeutic strategy for gout flare.

Topics & Concepts

InflammationMacrophage polarizationMacrophageExtracellularChemistryNeutrophil extracellular trapsImmunologyMedicineBiochemistryIn vitroGout, Hyperuricemia, Uric AcidNeutrophil, Myeloperoxidase and Oxidative MechanismsInflammasome and immune disorders