Abstract
Only primates suffer from hyperuricemia and gout. Acute gouty attack with fulminate inflammation may recover within 7-10 days. The pathogenesis of monosodium urate monohydrate (MSU) crystal-induced acute gouty inflammation has been gradually elucidated. It is conceivable that MSU crystals possess both danger-associated pathological pattern (DAMP) and physical microcrystal properties that may activate innate immune cells IL-1 production and subsequent IL-6, IL-8 and TNF-α release from neighborhood cells. By contrast, the molecular basis of acute gouty inflammation resolution mostly remains unclear. Previous studiesdemonstrated that intracellular negative cytokine regulators CIS and SOCS-3 involved in the resolution of acute gouty inflammation in synergism with anti-inflammatory cytokine molecules (TGF-β1, IL-10 and soluble TNF-α receptors type 1 and 2). This commentary aims to dissect the potential mechanisms of induction and resolution of acute gouty attack. Besides, the unsolved problems in these issues are discussed.
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