CD300a contributes to the resolution of articular inflammation triggered by MSU crystals by controlling neutrophil apoptosis

Immunology ◽  
2021 ◽  
Author(s):  
Bruno V.S. Valiate ◽  
Celso M. Queiroz‐Junior ◽  
Francesca Levi‐Schaffer ◽  
Izabela Galvão ◽  
Mauro M. Teixeira
Keyword(s):  
Neutrophil Apoptosis ◽  
Msu Crystals

Nitric Oxide in Life and Death of Neutrophils

2019 ◽  
Vol 26 (31) ◽  
pp. 5764-5780 ◽  
Author(s):  
Svetlana I. Galkina ◽  
Ekaterina A. Golenkina ◽  
Galina M. Viryasova ◽  
Yulia M. Romanova ◽  
Galina F. Sud’ina
Keyword(s):  
Nitric Oxide ◽  
Cell Damage ◽  
Protective Role ◽  
Neutrophil Apoptosis ◽  
High Biological Activity ◽  
Life And Death ◽  
Signalling Molecule ◽  
Activated Neutrophils ◽  
Cell Death Mechanisms ◽  
Prostacyclin Synthase

Background: Nitric Oxide (NO) is a key signalling molecule that has an important role in inflammation. It can be secreted by endothelial cells, neutrophils, and other cells, and once in circulation, NO plays important roles in regulating various neutrophil cellular activities and fate. Objective: To describe neutrophil cellular responses influenced by NO and its concomitant compound peroxynitrite and signalling mechanisms for neutrophil apoptosis. Methods: Literature was reviewed to assess the effects of NO on neutrophils. Results: NO plays an important role in various neutrophil cellular activities and interaction with other cells. The characteristic cellular activities of neutrophils are adhesion and phagocytosis. NO plays a protective role in neutrophil-endothelial interaction by preventing neutrophil adhesion and endothelial cell damage by activated neutrophils. NO suppresses neutrophil phagocytic activity but stimulates longdistance contact interactions through tubulovesicular extensions or cytonemes. Neutrophils are the main source of superoxide, but NO flow results in the formation of peroxynitrite, a compound with high biological activity. Peroxynitrite is involved in the regulation of eicosanoid biosynthesis and inhibits endothelial prostacyclin synthase. NO and peroxynitrite modulate cellular 5-lipoxygenase activity and leukotriene synthesis. Long-term exposure of neutrophils to NO results in the activation of cell death mechanisms and neutrophil apoptosis. Conclusion: Nitric oxide and the NO/superoxide interplay fine-tune mechanisms regulating life and death in neutrophils.

scholarly journals THU0406 IDENTIFICATION OF INTRACELLULAR VACUOLES IN SYNOVIAL FLUID WITH CALCIUM PYROPHOSPHATE AND MONOSODIUM URATE CRYSTALS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 440.1-441
Author(s):  
M. L. Peral ◽  
I. Calabuig ◽  
A. Martín-Carratalá ◽  
M. Andrés ◽  
E. Pascual
Keyword(s):  
Clinical Practice ◽  
Synovial Fluid ◽  
Phase Contrast ◽  
Calcium Pyrophosphate ◽  
Monosodium Urate ◽  
Fluid Analysis ◽  
Cytoplasmic Vacuoles ◽  
Contrast Microscopy ◽  
Ordinary Light ◽  
Msu Crystals

Background:Synovial fluid analysis using polarized microscopy is the gold standard for the diagnosis of crystal-related arthritis. In our experience, we have noted that, when calcium pyrophosphate (CPP) crystals are observed, they sometimes appear within intracellular vacuoles. However, this phenomenon is not seen in those samples containing monosodium urate (MSU) crystals. This finding has been scantly reported in the literature, but may be useful in clinical practice to ensure accurate crystal identification.Objectives:Our study aims to assess whether the presence of vacuoles contributes to identifying the type of crystal, and also to gauge the frequency of their presentation.Methods:We conducted an observational study in a rheumatology unit between February and June of 2019. Synovial fluids containing CPP or MSU crystals, obtained in daily clinical practice, were consecutively included for analysis. Two observers simultaneously analyzed the presence of vacuoles by ordinary light and phase contrast microscopy in less than 24 hours after their extraction, using a microscope equipped with two viewing stations. The primary study variable was to determine whether CPP and MSU crystals are seen inside intracellular vacuoles, and to calculate the frequency of this finding for each type of crystal, estimating their 95% confidence interval (95% CI) and comparing rates using Fisher’s exact test.Results:Twenty-one samples were obtained. Data is given in the Table. MSU crystals were present in 7 (33.3%) and CPP crystals in 14 (66.6%). Interestingly, none of the MSU samples showed crystal-containing vacuoles (95% CI 0-35.4%). On the contrary, cytoplasmic vacuoles containing crystals were present in all of the CPP samples (95% CI 78.5-100%). The findings were confirmed by phase-contrast microscopy. Differences were statistically significant (p<0.001).Table.SAMPLES ACCORDING TO TYPE OF MICROCRYSTAL(n=21)SAMPLES WITH VACUOLS(UNDER ORDINARY LIGHT)SAMPLES WITH VACUOLS(UNDER PHASE CONTRAST)CPP (14; 66.6%)14 (100%)(95%CI 78.5-100%)14 (100%)(95%CI 78.5-100%)MSU (7; 33.3%)0 (0%)(95%CI 0-35.4%)0 (0%)(95%CI 0-35.4%)Conclusion:The presence of vacuoles may be a useful and easy way to differentiate MSU and CPP crystals when performing synovial fluid microscopy in clinical practice, since it appears to be a distinctive feature in CPP crystal fluids.References:[1]Kohn NN, Hughes RE, McCarty DJ Jr, Faires JS. The significance of calcium phosphate crystals in the synovial fluid of arthritic patients: the «pseudogout syndrome». II. Identification of crystals. Ann InternMed. 1962 May;56:738-45.[2]Pascual E, Sivera F, Andrés M. Synovial Fluid Analysis for Crystals. CurrOpRheumatol 2011;23:161-169.[3]McCarty DJ, Koopman WJ. Arthritis and allied conditions: A textbook of rheumatology, volumen 1. Lea &amp;Febiger. 1993.[4]Pascual E, Sivera F. Synovial fluid crystal Analysis. En Gout and other crystal arthropathies. Terkeltaub R ed. Elsevier; 2012: p.20-34.[5]Hwang HS, Yang CM, Park SJ, Kim HA. Monosodium Urate Crystal-Induced Chondrocyte Death via Autophagic Process. Int J Mol Sci. 2015 Dec 8;16(12):29265-77.Image 1. Microscopy with ordinary light. Cells with cytoplasmic vacuoles are observed, as well as abundant intra and extracellular CPP crystals.Image 2. Microscopy with phase contrast technique. Cells with intracellular vacuoles are observed inside which have microcrystals with parallelepiped morphology, compatible with CPP.Disclosure of Interests: :None declared

scholarly journals Human Cytomegalovirus Delays Neutrophil Apoptosis and Stimulates the Release of a Prosurvival Secretome

2017 ◽  
Vol 8 ◽  
Author(s):  
Joanna M. Pocock ◽  
Daniel M. L. Storisteanu ◽  
Matthew B. Reeves ◽  
Jatinder K. Juss ◽  
Mark R. Wills ◽  
...  
Keyword(s):  
Human Cytomegalovirus ◽  
Neutrophil Apoptosis

scholarly journals Lower Temperatures Exacerbate NLRP3 Inflammasome Activation by Promoting Monosodium Urate Crystallization, Causing Gout

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1919
Author(s):  
Huijeong Ahn ◽  
Gilyoung Lee ◽  
Geun-Shik Lee
Keyword(s):  
Environmental Factor ◽  
Nlrp3 Inflammasome ◽  
Inflammasome Activation ◽  
Optimal Temperature ◽  
Monosodium Urate ◽  
Nlrp3 Inflammasome Activation ◽  
Hyperthermia Therapy ◽  
Effects Of Temperature ◽  
Lower Temperature ◽  
Msu Crystals

Gout is a recurrent and chronic form of arthritis caused by the deposition of monosodium urate (MSU) crystals in the joints. Macrophages intake MSU crystals, the trigger for NLRP3 inflammasome activation, which leads to the release of interleukin (IL)-1β and results in the flaring of gout. The effects of temperature, an environmental factor for MSU crystallization, on IL-1β secretion have not been well studied. This study examined the effects of temperature on inflammasome activation. Specific triggers activated canonical inflammasomes (NLRP3, NLRC4, and AIM2) in murine macrophages at various temperatures (25, 33, 37, 39, and 42 °C). The maturation of IL-1β and caspase-1 was measured as an indicator for inflammasome activation. As expected, the optimal temperature of inflammasome activation was 37 °C. The MSU crystal-mediated activation of inflammasome increased at temperatures lower than 37 °C and decreased at higher temperatures. MSU crystals at lower temperatures enhanced IL-1β secretion via the NLRP3 inflammasome pathway. A lower temperature promoted the formation of MSU crystals without changing phagocytosis. Overall, lower temperatures form more MSU crystals and enhance NLRP3 inflammasome activation. In light of these findings, it is possible that hyperthermia therapy may reduce gout flaring.

scholarly journals Urate-induced epigenetic modifications in myeloid cells

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
M. Badii ◽  
O. I. Gaal ◽  
M. C. Cleophas ◽  
V. Klück ◽  
R. Davar ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Whole Blood ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Myeloid Cells ◽  
Cytokine Signaling ◽  
Human Monocytes ◽  
Methylation Array ◽  
Histone 3 ◽  
Msu Crystals

Abstract Objectives Hyperuricemia is a metabolic condition central to gout pathogenesis. Urate exposure primes human monocytes towards a higher capacity to produce and release IL-1β. In this study, we assessed the epigenetic processes associated to urate-mediated hyper-responsiveness. Methods Freshly isolated human peripheral blood mononuclear cells or enriched monocytes were pre-treated with solubilized urate and stimulated with LPS with or without monosodium urate (MSU) crystals. Cytokine production was determined by ELISA. Histone epigenetic marks were assessed by sequencing immunoprecipitated chromatin. Mice were injected intraarticularly with MSU crystals and palmitate after inhibition of uricase and urate administration in the presence or absence of methylthioadenosine. DNA methylation was assessed by methylation array in whole blood of 76 participants with normouricemia or hyperuricemia. Results High concentrations of urate enhanced the inflammatory response in vitro in human cells and in vivo in mice, and broad-spectrum methylation inhibitors reversed this effect. Assessment of histone 3 lysine 4 trimethylation (H3K4me3) and histone 3 lysine 27 acetylation (H3K27ac) revealed differences in urate-primed monocytes compared to controls. Differentially methylated regions (e.g. HLA-G, IFITM3, PRKAB2) were found in people with hyperuricemia compared to normouricemia in genes relevant for inflammatory cytokine signaling. Conclusion Urate alters the epigenetic landscape in selected human monocytes or whole blood of people with hyperuricemia compared to normouricemia. Both histone modifications and DNA methylation show differences depending on urate exposure. Subject to replication and validation, epigenetic changes in myeloid cells may be a therapeutic target in gout.

scholarly journals Evolution of neutrophil apoptosis in septic shock survivors and nonsurvivors

2012 ◽  
Vol 27 (4) ◽  
pp. 415.e1-415.e11 ◽  
Author(s):  
Eduardo Tamayo ◽  
Esther Gómez ◽  
Juan Bustamante ◽  
José I. Gómez-Herreras ◽  
Rosalba Fonteriz ◽  
...  
Keyword(s):  
Septic Shock ◽  
Neutrophil Apoptosis

Intravenous Immunoglobulin Therapy Induces Neutrophil Apoptosis in Kawasaki Disease

2002 ◽  
Vol 103 (2) ◽  
pp. 161-168 ◽  
Author(s):  
Hiroshi Tsujimoto ◽  
Seiichiro Takeshita ◽  
Keigo Nakatani ◽  
Youichi Kawamura ◽  
Tomoharu Tokutomi ◽  
...  
Keyword(s):  
Kawasaki Disease ◽  
Intravenous Immunoglobulin ◽  
Immunoglobulin Therapy ◽  
Neutrophil Apoptosis ◽  
Intravenous Immunoglobulin Therapy

scholarly journals Recovery of neutrophil apoptosis by ectoine: a new strategy against lung inflammation

2012 ◽  
Vol 41 (2) ◽  
pp. 433-442 ◽  
Author(s):  
Ulrich Sydlik ◽  
Henrike Peuschel ◽  
Adnana Paunel-Görgülü ◽  
Stefanie Keymel ◽  
Ursula Krämer ◽  
...  
Keyword(s):  
Lung Inflammation ◽  
Neutrophil Apoptosis ◽  
New Strategy
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