These findings identify an unrecognized crosstalk between chemokine signaling and crystal-driven NETosis, providing mechanistic insight into sterile inflammatory diseases including gout, pseudogout, atherosclerosis, and pancreatitis, and supporting the concept that antagonists of CXCL8 receptors (CXCR1/2) could limit pathological NET formation. Here, CXCR1 is linked to atherosclerosis.