Abstract
Gout is one of the most common and painful forms of arthritis in humans with a growing incidence and prevalence over the last decades. Recent studies into the pathophysiology of acute gout have revealed that MSU (monosodium urate), the crystalline form of uric acid, is recognized by immune cells as a danger signal and can initiate an inflammatory response. This response is orchestrated by the intracellular pattern-recognition receptor NLRP3, which upon exposure to MSU, forms a cytosolic multiprotein-complex called the inflammasome, leading to the activation of caspase- 1. Caspase-1 then cleaves the highly pro-inflammatory cytokines interleukin (IL)-1β and IL-18, leading to the secretion of their biologically active forms and culminating in an acute gout attack. This newfound molecular understanding of the pathology of gout has seen the introduction of IL-1 inhibitors as an improved treatment for acute gout with reduced side effects compared to conventional gout therapies.
Keywords: Uric acid, inflammasome, IL-1β, caspase-1, monosodium urate, hyperuricemia, leukemias, polycythemia, Lesch-Nyhan-Syndrome, SLC2A9, Xenopus oocytes
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