通風発作の病態 --好中球の役割--

Abstract

Gouty attack is a well-recognized sequela of the deposition of monosodium urate (MSU) crystals in joints. The deposition of MSU crystals in synovial cells and macrophages in an inflammed joint induces the secretion of several chemical mediators such as TNFα, IL-8 and IL-1β that trigger neutrophil chemotaxis. The contribution of neutrophils to the pathogenesis of acute gouty inflammation is believed to be caused by events that follow the physical interaction of MSU crystals and neutrophils. The stimulation of neutrophils by MSU crystals leads to the production and release of several inflammatory mediators such as lysosomal enzymes, oxygen-derived free radicals and inflammatory cytokines. We demonstrated that MSU crystals also induce the release of nitric oxide from neutrophils. This may indicate that nitric oxide interacts with oxygen-derived free radicals and induces more intense inflammatory reaction. Furthermore, monocytes, macrophages, lymphocytes, platelets and humoral factors including complement and cytokines take part in this reaction, and lead to consecutive reactions. The analysis of the pathophysiology of gouty attack will lead to the understanding of neutrophil physiology and potentially to more efficient strategies to control the inflammatory reactions.