期刊連結：http://www.gouthyperuricemia.com

Purpose: Gout is a common inflammatory joint disease with an incompletely understood etiology. A considerable number of cytokines have shown to be elevated in synovial fluid and surrounding tissues, and the serum concentrations of a subset of these also relate to gout severity. The combined effects of the cytokines found in gouty arthritis likely explain most of the clinical features of gout inflammation. Here we review several key cytokines implicated in the pathogenesis of gout.
Findings: Gout has a complex genetic background and has a hereditary character. Genome-wide association studies (GWAS) have identified polymorphisms within or near a number of genes encoding cytokines, cytokine receptors or elements of their signal transduction pathways, further affecting these cytokines in the gout pathomechanism. There have been several findings identifying cytokines such as interleukin-1 (IL-1) and IL-8, pivotal mediators commonly involved in tissue repair and resolution, as important cytokines in monosodium urate (MSU) crystal–induced inflammation and resolution. They also account for most of the neutrophil chemotactic activity released from cultured human monocytes incubated with MSU crystals though specific signaling pathways like mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK1/2) pathways. Additionally, modulation of cytokines such as granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-2, IL-17A, IL-17F, IL-23 and IL-22 may affect neutrophils recruitment in MSU-induced inflammation.
Conclusion: Thus, understanding which cytokines play a pivotal role in the gout process can suggest potential therapeutic targets. It is likely that as our understanding of the cytokine networks in gout increase, so will the number of potential targets.