Resolution Of Gout Research Articles

Immune and inflammatory mechanisms and therapeutic targets of gout: An update.

Gout is an autoimmune disease characterized by acute or chronic inflammation and damage to bone joints induced due to the precipitation of monosodium urate (MSU) crystals. In recent years, with the continuous development of animal models and ongoing clinical investigations, more immune cells and inflammatory factors have been found to play roles in gouty inflammation. The inflammatory network involved in gout has been discovered, providing a new perspective from which to develop targeted therapy for gouty inflammation. Studies have shown that neutrophil macrophages and T lymphocytes play important roles in the pathogenesis and resolution of gout, and some inflammatory cytokines, such as those in the interleukin-1 (IL-1) family, have been shown to play anti-inflammatory or proinflammatory roles in gouty inflammation, but the mechanisms underlying their roles are unclear. In this review, we explore the roles of inflammatory cytokines, inflammasomes and immune cells in the course of gout development and the research status of therapeutic drugs used for inflammation to provide insights into future targeted therapy for gouty inflammation and the direction of gout pathogenesis research.

Cytokine levels in human synovial fluid during the different stages of acute gout: role of transforming growth factor β1 in the resolution phase

ObjectivesTo determine the most relevant parameters in synovial fluid (SF) during the various stages of acute gout.MethodsSFs from 38 gouty patients were analysed for white blood cell (WBC) count, percentage...

Characterization of E-selectin expression, leucocyte traffic and clinical sequelae in urate crystal-induced inflammation: an insight into gout.

The self-limiting response to urate crystals allows the exploration of events involved in both the onset and resolution of gout. Using i.v. injected radiolabelled anti-E-selectin monoclonal antibody 1.2b6 together with differentially radiolabelled neutrophils, mononuclear cells and albumin, we have characterized the expression of E-selectin in relation to leucocyte traffic, microvascular permeability and clinical sequelae following intracutaneous injection of monosodium urate crystals. We found that the inflammatory response in this model involved several distinct phases. First, E-selectin expression increased over 2-6 h in the context of increases in neutrophil and mononuclear cell accumulation, and albumin leakage. Secondly, leucocyte accumulation rapidly declined despite persisting E-selectin expression. Thirdly, E-selectin expression peaked at approximately 8 h and then fell despite an increase in clinically detectable erythema and induration. Lastly, these clinical manifestations of inflammation resolved despite the continued presence of urate crystals in the tissues. The further dissection of mechanisms regulating these phases will lead to a better understanding of events in both the pathogenesis and resolution of gout. Of broader significance, this inflammatory model may yield information about the protective events that underly resolution of inflammation, and provide insights into factors which determine chronicity.