Mechanisms of inflammation in gout

Abstract

An acute attack of gout is a paradigm of acute sterile inflammation, as opposed to pyogenic inflammation. Recent studies suggest that the triggering of IL-1β release from leucocytes lies at the heart of a cascade of processes that involves multiple cytokines and mediators. The NLRP3 inflammasome appears to have a specific role in this regard, but the biochemical events leading to its activation are still not well understood. We review the known mechanisms that underlie the inflammatory process triggered by urate crystals and suggest areas that require further research.

Impact of obesity and hypertriglyceridemia on gout development with or without hyperuricemia: A prospective study

“…The relationship between hyperuricemia and gouty arthritis is initiated from phagocytosis of MSU crystals by white cells. MSU crystals trigger Toll-like receptors or interleukin-1 (IL-1) receptors on the surface of macrophages to activate NLRP3 inflammasome to release IL-1␤ and subsequently induce neutrophil and macrophage influx (18). According to previous research, soluble urate can be a danger signal to trigger NLRP3 inflammasome (19) and play an adjuvant role as an alum to activate inflammation (18).…”

“…MSU crystals trigger Toll-like receptors or interleukin-1 (IL-1) receptors on the surface of macrophages to activate NLRP3 inflammasome to release IL-1␤ and subsequently induce neutrophil and macrophage influx (18). According to previous research, soluble urate can be a danger signal to trigger NLRP3 inflammasome (19) and play an adjuvant role as an alum to activate inflammation (18). Antigen presentation by B cells to CD4ϩ and CD8ϩ T cells further contributes to a pathogenic role of IgM/IgG antibodies to facilitate crystallization of urate and leads to the phagocytosis of MSU crystals and sensing of NLRP3 inflammasome (20).…”

Neutrophil: Lymphocyte Ratio and Mean Platelet Volume in Patients with Gout

“…The NLR value was significantly higher in patients with gout during the active phase compared to healthy controls. In the current [3,9]. MSU crystals stimulate release of C5a, bradykinin, and kallikrein.…”

“…MPV is indirectly linked to platelet activity. Larger platelets are more active than smaller ones in terms of metabolic and enzymatic activity [4][5][6][7][8][9]. Neutrophillymphocyte ratio (NLR) is a marker that can be estimated by using leukocyte subtypes from the complete blood count.…”

Gout – a guide for the general and acute physicians

“…6 Once activated, monocytes and macrophages release chemokines (eg CXCL-1, IL-8, C-GSF) that promote neutrophil chemotaxis, survival and proliferation. 6 Other chemokines, such as CCL-2, recruit additional macrophages and monocytes, 6 resulting in secretion of TNF-α (promoting cellular activation, endothelial adhesion and phagocytosis) and further IL-1β (promoting endothelial adhesion, endogenous pyrogen) causing a self-propagating intense inflammatory response in which neutrophils release lysozymes on phagocytosing MSU crystals. Components of the innate immune system, eg tolllike receptors and complement pathways, are also activated by MSU crystals.…”