Modulation of monosodium urate crystal-induced responses in neutrophils by the myeloid inhibitory C-type lectin-like receptor: potential therapeutic implications View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2013-07-09

AUTHORS

Valérie Gagné, Louis Marois, Jean-Michel Levesque, Hugo Galarneau, Mireille H Lahoud, Irina Caminschi, Paul H Naccache, Philippe Tessier, Maria JG Fernandes

ABSTRACT

IntroductionMonosodium urate crystals (MSU), the etiological agent of gout, are one of the most potent proinflammatory stimuli for neutrophils. The modulation of MSU-induced neutrophil activation by inhibitory receptors remains poorly characterized. The expression of the myeloid inhibitory C-type lectin-like receptor (MICL) in neutrophils is downregulated by several proinflammatory stimuli, suggestive of a role for this receptor in neutrophil function. We thus investigated the potential role of MICL in MSU-induced neutrophil activation.MethodsThe expression of MICL was monitored in human neutrophils by flow cytometry and Western blot analysis after stimulation with MSU. Protein tyrosine phosphorylation was also assessed by Western blot analysis and the production of IL-1 and IL-8 by enzyme-linked immunosorbent assay. Changes in the concentration of cytoplasmic free calcium were monitored with the Fura-2-acetoxymethyl ester calcium indicator. MICL expression was modulated with an anti-MICL antibody in neutrophils and siRNA in the PLB-985 neutrophil-like cell line.ResultsMSU induced the downregulation of MICL expression in neutrophils. A diminution in the expression of MICL induced by antibody cross-linking or siRNA enhanced the MSU-dependent increase in cytoplasmic calcium levels, protein tyrosine phosphorylation and IL-8 but not IL-1 production. Pretreatment of neutrophils with colchicine inhibited the MSU-induced downregulation of MICL expression.ConclusionsOur findings strongly suggest that MICL acts as an inhibitory receptor in human neutrophils since the downregulation of MICL expression enhances MSU-induced neutrophil activation. Since MSU downregulates the expression of MICL, MICL may play a pathogenic role in gout by enhancing neutrophil effector functions. In support of this notion, colchicine counteracts the MSU-induced loss of MICL expression. Our findings thus also provide further insight into the potential molecular mechanisms behind the anti-inflammatory properties of this drug. More... »

PAGES

r73

References to SciGraph publications

  • 2010-04-26. Gout. Mechanisms of inflammation in gout in ARTHRITIS RESEARCH & THERAPY
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    http://scigraph.springernature.com/pub.10.1186/ar4250

    DOI

    http://dx.doi.org/10.1186/ar4250

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1046635930

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/23837669


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