Gout is a prototype crystal-induced inflammatory disorder, characterized by neutrophil infiltration into inflamed joints. The identification of the role of NLRP3 inflammasome in the recognition of monosodium urate crystals and the subsequent release of IL-1β was a milestone in the elucidation of the pathogenesis of this disorder. IL-1β signaling is considered nowadays as the initiatory event that induces gouty inflammation and promotes the recruitment of vast numbers of neutrophils at the sites of inflammation. Crystal-induced neutrophil activation results in apoptosis inhibition, degranulation, superoxide production, cytokine release and, as recently described, formation of neutrophil extracellular traps, further amplifying the inflammatory process. Finally, neutrophil apoptosis and uptake of apoptotic material by macrophages drive the resolution of acute inflammation. In this review, we discuss the recent experimental data regarding the crosstalk between IL-1β and neutrophils in the pathogenesis of acute gout.