UNASSIGNED: Neutrophil granulocytes possess a large arsenal of pro-inflammatory substances and mechanisms that empower them to drive local acute immune reactions to invading microorganisms or endogenous inflammatory triggers. The use of this armory needs to be tightly controlled to avoid chronic @entity32 and collateral tissue damage. In @entity210 , @entity32 arises from precipitation of uric acid in the form of needle-shaped monosodium urate crystals. Inflammasome activation by these crystals in local immune cells results in a rapid and dramatic recruitment of neutrophils. This neutrophil influx is accompanied by the infamously intense clinical symptoms of @entity32 during an @entity697 . Neutrophilic @entity32 however is equipped with a built-in safeguard; activated neutrophils form neutrophil extracellular traps (NETs). At the very high neutrophil densities that occur at the site of @entity32 , NETs build aggregates that densely pack the monosodium urate (MSU) crystals and trap and degrade pro-inflammatory mediators by inherent proteases. Local removal of cytokines and chemokines by aggregated NETs explains how acute @entity32 can stop in the consistent presence of the inflammatory trigger. Aggregated NETs resemble early stages of the typical large MSU deposits that constitute the pathognomonic structures of @entity210 , tophi. Although tophi contribute to muscosceletal damage and mortality in @entity1 with @entity102 , they can therefore be considered as a payoff that is necessary to silence the intense inflammatory response during @entity697 .

How neutrophil extracellular traps orchestrate the local immune response in XXXX .

@entity1 :: ('9606', 'Species') :: ['patients'] @entity32 :: ('MESH:D007249', 'Disease') :: ['inflammation'] @entity697 :: ('MESH:D000208', 'Disease') :: ['acute gout', 'acute gout attack'] @entity102 :: ('MESH:D002908', 'Disease') :: ['chronic gout'] @entity210 :: ('MESH:D006073', 'Disease') :: ['gout']
@entity210 :: (MESH:D006073,Disease) :: ['gout']
