Activation status of circulating neutrophils in gout patients

The causative agent behind gouty inflammation, monosodium urate (MSU) crystals, triggers neutrophils to produce reactive oxygen species (ROS) and cast out neutrophil extracellular traps (NETs). We have previously demonstrated that when neutrophils encounter MSU crystals in vitro, they produce ROS that are strictly intracellular, and this response is highly primed in in vivo transmigrated neutrophils. Since neutrophil activation markers in blood have been linked to active gout and cardiovascular events during long-term follow-up, we wanted to further investigate neutrophil activation in gout.

Blood neutrophils from patients with polyarticular gout and healthy controls were tested for activation status, including ROS production, NET formation, and receptor expression. The majority of patients in our study were treated with urate-lowering drugs and some were also treated with colchicine and/or prednisolone. CRP (as a marker of disease activity) and plasma urate levels were measured. Statistical significance was calculated using the Wilcoxon rank-sum test.

Peripheral blood neutrophils from gout patients, similarly to those from healthy controls, displayed a resting phenotype with regard to surface receptor expression, and neither NET formation nor ROS production was primed compared to neutrophils from healthy controls. Levels of ROS production did not correlate with CRP or plasma urate levels, but a trend towards lower intracellular ROS production in colchicine-treated patients was noted.

Blood neutrophils from patients with polyarticular gout do not display an activated phenotype, and respond in a functionally similar way to neutrophils from healthy controls.