Literature DB >> 20395644

Differences in MSU-induced superoxide responses by neutrophils from gout subjects compared to healthy controls and a role for environmental inflammatory cytokines and hyperuricemia in neutrophil function and survival.

William John Martin1, Rebecca Grainger, Andrew Harrison, Jacquie L Harper.   

Abstract

OBJECTIVE: To determine whether monosodium urate (MSU) crystal-induced superoxide production is greater for neutrophils from patients with gout compared to asymptomatic hyperuricemic and healthy controls, and whether neutrophil functions are altered by an MSU crystal-induced inflammatory environment.
METHODS: Neutrophils were purified from the whole blood of study participants, restimulated with 500 mg MSU crystals ex vivo, and superoxide production measured using the colorimetric dye WST-1. Purified neutrophils were exposed to conditioned media from MSU crystal-activated blood monocyte cultures with and without neutralizing antibodies for interleukin 1ss (IL-1ss), IL-8 (CXCL8), IL-6, and tumor necrosis factor-alpha (TNF-alpha). Neutrophil superoxide production was measured and neutrophil apoptosis and IL-8 production were determined by flow cytometry. Serum samples were collected from participants and analyzed by Lincoplex bead array for IL-1ss, IL-8, IL-6, and TNF-alpha.
RESULTS: Neutrophils from gout and asymptomatic hyperuricemic subjects produced higher levels of MSU crystal-induced superoxide, and a weak trend toward elevated serum cytokines was observed compared to healthy controls. A correlation between serum uric acid and elevated neutrophil superoxide production was also observed. Neutrophils exposed to media from MSU crystal-activated monocytes exhibited enhanced superoxide production to MSU-crystal stimulation, increased IL-8 production, and extended cell survival that was predominantly dependent on IL-8, TNF-alpha and IL-6, respectively.
CONCLUSION: Neutrophils from gout and asymptomatic hyperuricemic individuals are primed for enhanced MSU crystal-induced superoxide production that may be driven by a subclinical inflammatory cytokine environment combined with hyperuricemia. This inflammatory environment likely contributes to elevated neutrophil IL-8 production and survival in the absence of direct crystal stimulation. Asymptomatic hyperuricemia is not associated with suppressed neutrophil function.

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Year:  2010        PMID: 20395644     DOI: 10.3899/jrheum.091080

Source DB:  PubMed          Journal:  J Rheumatol        ISSN: 0315-162X            Impact factor:   4.666


  11 in total

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