Colchicine suppresses neutrophil superoxide production in a murine model of gouty arthritis: a rationale for use of low‐dose colchicine

Chia, Elizabeth W.; Grainger, Rebecca; Harper, Jacquie L.

doi:10.1038/bjp.2008.20

Cited by 91 publications

(72 citation statements)

References 20 publications

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“…Mostly important, MSW, which develops based on TCM theory, clinical research, and pharmacodynamic findings (Yin and Si, 2006), is prepared with two additional agents on the basis of SM and does a more comprehensive and synergetic effect than EM and SM on gouty diseases. Acute gouty arthritis is caused by MSU crystals in and around the joints, which causes acute inflammation that manifests as intense pain, swelling, and reddening of the skin (Chia et al, 2008). TCM believes that a formula with clearing heat, eliminating dampness and promoting blood circulation is useful for treating acute gout.…”

Section: Discussionmentioning

confidence: 99%

A network pharmacology approach to determine active ingredients and rationality of herb combinations of Modified-Simiaowan for treatment of gout

Zhao

Yang³

et al. 2015

Journal of Ethnopharmacology

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Section: Discussionmentioning

confidence: 99%

A network pharmacology approach to determine active ingredients and rationality of herb combinations of Modified-Simiaowan for treatment of gout

Zhao

Yang³

et al. 2015

Journal of Ethnopharmacology

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“…Both MSU crystals and the inflammatory cytokine environment have been shown to prolong neutrophil survival and stimulate neutrophil IL-8 (CXCL8) and superoxide production, factors that can contribute to ongoing inflammation (26)(27)(28)(29)(30). In contrast, neutrophil apoptosis and clearance by phagocytic cells are recognized as playing a key part in TGF␤1 production and resolution (24,26,28,31,32).…”

Section: Discussionmentioning

confidence: 99%

Monosodium urate monohydrate crystal–recruited noninflammatory monocytes differentiate into M1‐like proinflammatory macrophages in a peritoneal murine model of gout

Martin

Shaw

Liu

et al. 2011

Arthritis & Rheumatism

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Objective. To profile monosodium urate monohydrate (MSU) crystal-recruited monocyte inflammatory function during the course of in vivo differentiation, in a murine model of peritoneal MSU crystal-induced inflammation.Methods. C57BL/6J mice were injected intraperitoneally with MSU crystals, and the peritoneal cells were harvested at different time points. The MSU crystal-recruited monocyte/macrophage population was analyzed for the expression of differentiation and activation markers, cytokine production following MSU crystal restimulation ex vivo and in vivo, expression of NLRP3-associated proteins (ASC, caspase 1) and prointerleukin-1␤ (proIL-1␤), and phagocytic capacity.Results. Monocytes recruited 8 hours after MSU crystal stimulation (F4/80 low Gr-1 int 7/4؉) exhibited poor phagocytic capacity, expressed low levels of proIL-1␤, and failed to produce proinflammatory cytokines in response to MSU crystal restimulation. In the absence of MSU crystal restimulation, differentiating monocytes produced low levels of transforming growth factor ␤1 ex vivo, and this was abrogated following MSU crystal restimulation. Over time these cells developed a proinflammatory phenotype in vivo, characterized by the production of IL-1␤, tumor necrosis factor ␣, IL-6, CCL2 (monocyte chemotactic protein 1), and CXCL1 (cytokine-induced neutrophil chemoattractant) following ex vivo MSU crystal restimulation, and leading to IL-1␤ production and cell infiltration following MSU crystal rechallenge in vivo. Proinflammatory function was associated with differentiation toward a macrophage phenotype (F4/80 high Gr-1-7/4-), an increase in phagocytic capacity, and an increase in the expression of proIL-1␤. Conclusion. MSU crystal-recruited monocytes differentiate into proinflammatory M1-like macrophages in vivo. This proinflammatory macrophage phenotype is likely to play a key role in perpetuating inflammation in gouty arthritis in the presence of ongoing deposition of fresh MSU crystals.Acute gout is an intensely painful form of inflammatory arthritis caused by the formation of monosodium urate monohydrate (MSU) crystals in the joint and connective tissues. An acute attack of gout is characterized by intense pain and swelling and reddening of the skin around the affected area. Without treatment this inflammatory response will resolve naturally over 7-10 days.Interleukin-1␤ (IL-1␤) has been identified as a pivotal cytokine in gout and MSU crystal-induced inflammation (1-3). More recently, studies have identified IL-1␤ production following activation of the NLRP3 inflammasome in resident macrophages as a key event in the initiation of an attack of acute gout (4-7). However, there is a growing body of evidence indicating that cells of the monocyte/macrophage lineage play a pivotal role not only in the initiation but also in the progression and resolution of acute gouty inflammation.It has been proposed that the self-limiting nature of an acute gout attack is linked to the differentiation state of the MSU crystal-recruited monocyte population. In...

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“…In the same manner, colchicine modulates the expression of E-selectin on membranes of endothelial cells and selectively inhibits the release of L-selectin from neutrophils, thus preventing the cascade of inflammatory pathways in the endothelium [10]. Additionally, low doses of colchicine selectively suppress monosodium urate-induced superoxide anion release from neutrophils [11].…”

Section: Mechanisms Of Action Of Colchicinementioning

confidence: 99%

“…Toxicol. (2015) 11 (11) of pericarditis [88]. These recommendations were largely based on preliminary small trials and expert opinion, considering colchicine therapy over several weeks to months as an alternative to corticosteroids and nonsteroidal anti-inflammatory drugs in acute pericarditis and post-pericardiotomy syndrome driven by inflammatory and autoimmune stimuli.…”

Section: The Use Of Colchicine In Nonrheumatic Cardiovascular Disordersmentioning

confidence: 99%

Colchicine as an anti-inflammatory and cardioprotective agent

Gasparyan

Ayvazyan

Yessirkepov

et al. 2015

Expert Opinion on Drug Metabolism & Toxicology

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Colchicine suppresses neutrophil superoxide production in a murine model of gouty arthritis: a rationale for use of low‐dose colchicine

Cited by 91 publications

References 20 publications

A network pharmacology approach to determine active ingredients and rationality of herb combinations of Modified-Simiaowan for treatment of gout

A network pharmacology approach to determine active ingredients and rationality of herb combinations of Modified-Simiaowan for treatment of gout

Monosodium urate monohydrate crystal–recruited noninflammatory monocytes differentiate into M1‐like proinflammatory macrophages in a peritoneal murine model of gout

Colchicine as an anti-inflammatory and cardioprotective agent

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