Neutrophil extracellular traps regulate IL-1β-mediated inflammation in familial Mediterranean fever

Apostolidou, Eirini; Skendros, Panagiotis; Kambas, Konstantinos; Mitroulis, Ioannis; Konstantinidis, Theocharis; Chrysanthopoulou, Akrivi; Nakos, Konstantinos; Tsironidou, Victoria; Koffa, Maria; Boumpas, Dimitrios T.; Ritis, Konstantinos

doi:10.1136/annrheumdis-2014-205958

Cited by 98 publications

(110 citation statements)

References 51 publications

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“…In a similar manner, an increase in the amount of proinflammatory, procoagulant platelet-derived EVs in patients with Crohn's disease compared with that in healthy subjects was observed, implicating these EVs in disease progression (80). Both neutrophil-derived and platelet-derived EVs were shown to increase in patients with an anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) compared with that in remittent AAV subjects (81)(82)(83). Furthermore, platelet-derived EVs associated with oxidized high-mobility group box 1 protein (HMGB1) were shown to increase neutrophil activation, which could be responsible for phenotypes associated with systemic sclerosis.…”

Section: Immune Regulation By Circulating Endogenous Evsmentioning

confidence: 61%

Regulation of chronic inflammatory and immune processes by extracellular vesicles

Robbins

Dorronsoro

Booker

2016

Journal of Clinical Investigation

236

195

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Section: Immune Regulation By Circulating Endogenous Evsmentioning

confidence: 61%

Regulation of chronic inflammatory and immune processes by extracellular vesicles

Robbins

Dorronsoro

Booker

2016

Journal of Clinical Investigation

236

195

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“…Indeed, bioactive IL-1β has been detected on NETs released during inflammatory attacks of familial Mediterranean fever [49]. Moreover, IL-1β can also be created outside of the cell via mechanisms involving caspase-1 or independently of the inflammasome by cleavage of pro-IL-1 β into its bioactive form by neutrophil serine protease 3 [50][51][52].…”

Section: Local Situation In Goutmentioning

confidence: 99%

How neutrophil extracellular traps orchestrate the local immune response in gout

et al. 2015

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Neutrophil granulocytes possess a large arsenal of pro-inflammatory substances and mechanisms that empower them to drive local acute immune reactions to invading microorganisms or endogenous inflammatory triggers. The use of this armory needs to be tightly controlled to avoid chronic inflammation and collateral tissue damage. In gout, inflammation arises from precipitation of uric acid in the form of needle-shaped monosodium urate crystals. Inflammasome activation by these crystals in local immune cells results in a rapid and dramatic recruitment of neutrophils. This neutrophil influx is accompanied by the infamously intense clinical symptoms of inflammation during an acute gout attack. Neutrophilic inflammation however is equipped with a built-in safeguard; activated neutrophils form neutrophil extracellular traps (NETs). At the very high neutrophil densities that occur at the site of inflammation, NETs build aggregates that densely pack the monosodium urate (MSU) crystals and trap and degrade pro-inflammatory mediators by inherent proteases. Local removal of cytokines and chemokines by aggregated NETs explains how acute inflammation can stop in the consistent presence of the inflammatory trigger. Aggregated NETs resemble early stages of the typical large MSU deposits that constitute the pathognomonic structures of gout, tophi. Although tophi contribute to muscosceletal damage and mortality in patients with chronic gout, they can therefore be considered as a payoff that is necessary to silence the intense inflammatory response during acute gout.

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“…These particles increased CD54 surface expression and IL6 and IL8 production from human vein endothelial cells (HUVECs) in vitro, suggesting that they can promote inflammation of the vessel wall [72] . ANCA induced EVs also contained tissue factor and may thus promote hypercoagulability and the increased rates of thrombosis observed in patients with ANCA disease [76,77] .…”

Section: Evs In Chronic Kidney Diseasementioning

confidence: 99%

“…However, most research on leukocyte function within the vascular wall has concentrated on neutrophils. ANCA can induce generation of EVs from preactivated, e.g., tumor necrosis factor (TNF)a primed neutrophils [72,76,77] . These particles increased CD54 surface expression and IL6 and IL8 production from human vein endothelial cells (HUVECs) in vitro, suggesting that they can promote inflammation of the vessel wall [72] .…”

Section: Evs In Chronic Kidney Diseasementioning

confidence: 99%

Extracellular vesicles as mediators of vascular inflammation in kidney disease

Helmke

Vietinghoff

2016

WJN

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Vascular inflammation is a common cause of renal impairment and a major cause of morbidity and mortality of patients with kidney disease. Current studies consistently show an increase of extracellular vesicles (EVs) in acute vasculitis and in patients with atherosclerosis. Recent research has elucidated mechanisms that mediate vascular wall leukocyte accumulation and differentiation. This review addresses the role of EVs in this process. Part one of this review addresses functional roles of EVs in renal vasculitis. Most published data address anti-neutrophil cytoplasmic antibody (ANCA) associated vasculitis and indicate that the number of EVs, mostly of platelet origin, is increased in active disease. EVs generated from neutrophils by activation by ANCA can contribute to vessel damage. While EVs are also elevated in other types of autoimmune vasculitis with renal involvement such as systemic lupus erythematodes, functional consequences beyond intravascular thrombosis remain to be established. In typical hemolytic uremic syndrome secondary to infection with shiga toxin producing Escherichia coli , EV numbers are elevated and contribute to toxin distribution into the vascular wall. Part two addresses mechanisms how EVs modulate vascular inflammation in atherosclerosis, a process that is aggravated in uremia. Elevated numbers of circulating endothelial EVs were associated with atherosclerotic complications in a number of studies in patients with and without kidney disease. Uremic endothelial EVs are defective in induction of vascular relaxation. Neutrophil adhesion and transmigration and intravascular thrombus formation are critically modulated by EVs, a process that is amenable to therapeutic interventions. EVs can enhance monocyte adhesion to the endothelium and modulate macrophage differentiation and cytokine production with major influence on the local inflammatory milieu in the plaque. They significantly influence lipid phagocytosis and antigen presentation by mononuclear phagocytes. Finally, platelet, erythrocyte and monocyte EVs cooperate in shaping adaptive T cell immunity. Future research is needed to define changes in uremic EVs and their differential effects on inflammatory leukocytes in the vessel wall.

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Neutrophil extracellular traps regulate IL-1β-mediated inflammation in familial Mediterranean fever

Cited by 98 publications

References 51 publications

Regulation of chronic inflammatory and immune processes by extracellular vesicles

Regulation of chronic inflammatory and immune processes by extracellular vesicles

How neutrophil extracellular traps orchestrate the local immune response in gout

Extracellular vesicles as mediators of vascular inflammation in kidney disease

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