Mercury (Macrae et al., 2008); software program used to prepare material for publication

Mercury (Macrae et al., 2008); computer software applied to prepare material for publication: SHELXTL.This work was supported by the Scientific Study Foundation of Nanjing College of Chemical Technologies (grant No. NHKY-2013?0).Supplementary information and figures for this paper are obtainable from the IUCr electronic archives (Reference: LH5664).oKai-Long Zhongdoi:10.1107/SActa Cryst. (2013). E69, o1782organic compounds
Gagn?et al. Arthritis Research Therapy 2013, 15:R73 http://arthritis-research/content/15/4/RRESEARCH ARTICLEOpen AccessModulation of monosodium urate crystal-induced responses in neutrophils by the myeloid inhibitory C-type lectin-like receptor: potential therapeutic implicationsVal ie Gagn?, Louis Marois1, Jean-Michel Levesque1, Hugo Galarneau1, Mireille H Lahoud2, Irina Caminschi2, Paul H Naccache1, Philippe Tessier1 and Maria JG Fernandes1*AbstractIntroduction: Monosodium urate crystals (MSU), the etiological agent of gout, are probably the most potent proinflammatory stimuli for neutrophils.261768-25-6 supplier 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 numerous proinflammatory stimuli, suggestive of a function for this receptor in neutrophil function.1-Chloro-6-iodohexane In stock We therefore investigated the possible role of MICL in MSU-induced neutrophil activation. Approaches: The expression of MICL was monitored in human neutrophils by flow cytometry and Western blot analysis right after stimulation with MSU. Protein tyrosine phosphorylation was also assessed by Western blot analysis plus the production of IL-1 and IL-8 by enzyme-linked immunosorbent assay. Alterations inside the concentration of cytoplasmic free of charge calcium have been monitored using the Fura-2-acetoxymethyl ester calcium indicator. MICL expression was modulated with an anti-MICL antibody in neutrophils and siRNA within the PLB-985 neutrophil-like cell line. Results: MSU 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 enhance in cytoplasmic calcium levels, protein tyrosine phosphorylation and IL-8 but not IL-1 production.PMID:23341580 Pretreatment of neutrophils with colchicine inhibited the MSU-induced downregulation of MICL expression. Conclusions: Our findings strongly suggest that MICL acts as an inhibitory receptor in human neutrophils because the downregulation of MICL expression enhances MSU-induced neutrophil activation. Considering the fact that MSU downregulates the expression of MICL, MICL could play a pathogenic role in gout by enhancing neutrophil effector functions. In assistance of this notion, colchicine counteracts the MSU-induced loss of MICL expression. Our findings as a result also give further insight in to the prospective molecular mechanisms behind the anti-inflammatory properties of this drug. Key phrases: Cytokine production, out, Immunoreceptor tyrosine-based inhibitory motif, Monosodium urate crystals, Neutrophil, Signaling* Correspondence: [email protected] Contributed equally 1 Department of Microbiology, Infectious Diseases, and Immunology, Faculty of Medicine, Laval University, Centre for Study in Immunology and Rheumatology, Investigation Centre CHUQ-CHUL, Bloc T1-49, 2705 boulevard Laurier, Quebec, QC, G1V 4G2, Canada Full list of author details is out there at the finish with the post?2013 Gagn?et al.; licensee BioMed Central Ltd. This really is an Open Access art.