Evidence map›Paper›PMID 28630905›Full record

ArticleScience advances2017

Mechanical deformation induces depolarization of neutrophils.

Andrew E Ekpenyong, Nicole Toepfner, Christine Fiddler, Maik Herbig, Wenhong Li, Gheorghe Cojoc, Charlotte Summers, Jochen Guck, Edwin R Chilvers

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

Article in Science advances, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

52 citing papers in PubMed, 94 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

9 authors at 4 institutions in 3 countries.

Andrew E EkpenyongCavendish Laboratory, Department of Physics, University of Cambridge, Cambridge CB3 0HE, UK.ORCID 0000-0003-0191-8393
Nicole ToepfnerKlinik und Poliklinik für Kinder-und Jugendmedizin, Universitätsklinikum Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Christine FiddlerDepartment of Medicine, Addenbrooke's and Papworth Hospitals, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK.
Maik HerbigBiotechnology Center for Molecular and Cellular Bioengineering, Technische Universität Dresden, 01307 Dresden, Germany.
Wenhong LiBiotechnology Center for Molecular and Cellular Bioengineering, Technische Universität Dresden, 01307 Dresden, Germany.
Gheorghe CojocBiotechnology Center for Molecular and Cellular Bioengineering, Technische Universität Dresden, 01307 Dresden, Germany.
Charlotte SummersDepartment of Medicine, Addenbrooke's and Papworth Hospitals, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK.
Jochen GuckCavendish Laboratory, Department of Physics, University of Cambridge, Cambridge CB3 0HE, UK.
Edwin R ChilversDepartment of Medicine, Addenbrooke's and Papworth Hospitals, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK.ORCID 0000-0002-4230-9677
Papworth Hospital · GBCenter for Systems Biology Dresden · DECreighton University · USUniversity of Cambridge · GB

Funding

European Research Council 282060Wellcome Trust
6 · The paper itself

Abstract

The transition of neutrophils from a resting state to a primed state is an essential requirement for their function as competent immune cells. This transition can be caused not only by chemical signals but also by mechanical perturbation. After cessation of either, these cells gradually revert to a quiescent state over 40 to 120 min. We use two biophysical tools, an optical stretcher and a novel microcirculation mimetic, to effect physiologically relevant mechanical deformations of single nonadherent human neutrophils. We establish quantitative morphological analysis and mechanical phenotyping as label-free markers of neutrophil priming. We show that continued mechanical deformation of primed cells can cause active depolarization, which occurs two orders of magnitude faster than by spontaneous depriming. This work provides a cellular-level mechanism that potentially explains recent clinical studies demonstrating the potential importance, and physiological role, of neutrophil depriming in vivo and the pathophysiological implications when this deactivation is impaired, especially in disorders such as acute lung injury.

Indexed as

Mechanical PhenomenaCell ShapeHumansNeutrophil ActivationNeutrophil InfiltrationNeutrophilsacute lung injurycell mechanicschronic occlusive pulmonary disorderde-priminginflammationLeukocytemicrofluidicsNeutrophiloptical stretcherpriming

Identifiers

PMID28630905
PMCPMC5470826
OpenAlexW2625213887

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.