Changes in the proteins coating monosodium urate crystals during active and subsiding inflammation. immunogold studies of synovial fluid from patients with gout and of fluid obtained using the rat subcutaneous air pouch model

Abstract

Objective. In this in vivo study, we investigated changes in the proteins that coat monosodium urate (MSU) crystals in human synovial fluid samples and rat air pouch fluid samples obtained sequentially during periods of active and resolving inflammation, in order to evaluate whether in vivo findings are consistent with hypotheses on roles of protein coating based on in vitro findings.Methods. Crystals from patients with gout were isolated from joint fluids with acute inflammation, and subsequently from the same joints at the time inflammation was resolving. Crystals were also obtained using the rat subcutaneous air pouch model. Immunogold was used to label proteins coating MSU crystals, for light microscopy (LM) and transmission electron microscopy (TEM) studies.Results. Dense immunogold-silver labeling for IgG was observed under LM on crystals from fluid with acute inflammation, whereas other proteins (apolipoproteins [Apo], fibronectin, fibrinogen, albumin) were not labeled significantly. Apo B became strongly positive on crystals as the inflammation subsided,

Role of S100A8 and S100A9 in neutrophil recruitment in response to monosodium urate monohydrate crystals in the air‐pouch model of acute gouty arthritis

“…All of these chemokines had previously been shown to play a role in neutrophil migration in the air-pouch model in response to both TNF␣ and SEA (39,40). The air-pouch model was selected since it has been used extensively in the past as a model of the synovial environment to study the mechanism of inflammation induced by different proinflammatory factors, including MSU (45)(46)(47)(48)(49)(50)(51). Designed to replicate the synovial lining, this model allows for the identification and study of emigrated leukocytes and molecules produced during an inflammatory response, although several features of the synovial environment are missing in air-pouch fibroblasts (52,53).…”

Safe disposal of inflammatory monosodium urate monohydrate crystals by differentiated macrophages

“…However, other factors besides the presence of crystals must be involved, because crystals can be detected in asymptomatic joints (2)(3)(4)(5) and at sites of experimental intracutaneous crystal injection after erythema has resolved (12). One possibility is that crystals are coated with protective proteins, such as apolipoproteins, that reduce the inflammatory potential of crystals following uptake by polymorphonuclear cells (18)(19)(20). Dyslipidemia may therefore be another variable affecting the inflammatory response of given individuals to urate crystals.…”

The interaction of monoclinic calcium pyrophosphate dihydrate crystals with neutrophils

“…The major inhibitory species in these studies has been found to be the apolipoprotein B (Apo B) component of low density lipoproteins, which, when adsorbed to monosodium urate crystals, interferes with the initial crystal neutrophil interaction and inhibits phagocytosis [36]. Ortiz-Bravo et al [37] have observed that during the initial stages of monosodium urate crystal induced inflammation, IgG is adsorbed on the crystal surface, but over time Apo B displaces the IgG on the surface and the inflammation subsides. The ability of hydroxyapatite crystals to stimulate neutrophil superoxide release and chemiluminescence was significantly decreased in the presence of serum and plasma.…”