Evidence map›Paper›PMID 26245757›Full record

ArticleAnnals of the rheumatic diseases2016

Neutrophil microvesicles resolve gout by inhibiting C5a-mediated priming of the inflammasome.

Arun Cumpelik, Barbara Ankli, Daniel Zecher, Jürg A Schifferli

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of the rheumatic diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 3 countries.

Arun CumpelikDepartment of Biomedicine, University Hospital Basel, Basel, Switzerland Department of Medicine, University Hospital Basel, Basel, Switzerland.
Barbara AnkliDepartment of Rheumatology, University Hospital Basel, Basel, Switzerland.
Daniel ZecherDepartment of Biomedicine, University Hospital Basel, Basel, Switzerland Department of Medicine, University Hospital Basel, Basel, Switzerland Department of Nephrology, University Hospital Regensburg, Regensburg, Germany.
Jürg A SchifferliDepartment of Biomedicine, University Hospital Basel, Basel, Switzerland Department of Medicine, University Hospital Basel, Basel, Switzerland.
Hospital Base · CLUniversity Hospital of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesGout is a highly inflammatory but self-limiting joint disease induced by the precipitation of monosodium urate (MSU) crystals. While it is well established that inflammasome activation by MSU mediates acute inflammation, little is known about the mechanism controlling its spontaneous resolution. The aim of this study was to analyse the role of neutrophil-derived microvesicles (PMN-Ecto) in the resolution of acute gout.

methodsPMN-Ecto were studied in a murine model of MSU-induced peritonitis using C57BL/6, MerTK(-/-) and C5aR(-/-) mice. The peritoneal compartment was assessed for the number of infiltrating neutrophils (PMN), neutrophil microvesicles (PMN-Ecto), cytokines (interleukin-1β, TGFβ) and complement factors (C5a). Human PMN-Ecto were isolated from exudates of patients undergoing an acute gouty attack and functionally tested in vitro.

resultsC5a generated after the injection of MSU primed the inflammasome for IL-1β release. Neutrophils infiltrating the peritoneum in response to C5a released phosphatidylserine (PS)-positive PMN-Ecto early on in the course of inflammation. These PMN-Ecto in turn suppressed C5a priming of the inflammasome and consequently inhibited IL-1β release and neutrophil influx. PMN-Ecto-mediated suppression required surface expression of the PS-receptor MerTK and could be reproduced using PS-expressing liposomes. In addition, ectosomes triggered the release of TGFβ independent of MerTK. TGFβ, however, was not sufficient to control acute MSU-driven inflammation in vivo. Finally, PMN-Ecto from joint aspirates of patients with gouty arthritis had similar anti-inflammatory properties.

conclusionsPMN-Ecto-mediated control of inflammasome-driven inflammation is a compelling concept of autoregulation initiated early on during PMN activation in gout.

Indexed as

Acute DiseaseAnimalsCell-Derived MicroparticlesCells, CulturedComplement C5aCytokinesGoutHumansInflammasomesLiposomesMice, Inbred C57BLNeutrophil ActivationNeutrophil InfiltrationNeutrophilsPeritonitisPhosphatidylserinesComplement C5aCytokinesInflammasomesLiposomesPhosphatidylserinesCytokinesGoutInflammation

Identifiers

PMID26245757
PMCPMC4893114
OpenAlexW1955483733

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.