Evidence map›Paper›PMID 28289157›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2017

Targeting Neutrophilic Inflammation Using Polymersome-Mediated Cellular Delivery.

James D Robertson, Jon R Ward, Milagros Avila-Olias, Giuseppe Battaglia, Stephen A Renshaw

Open access · hybridAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Roscovitine WorsensAmerican journal of respiratory cell and molecular biology · 2022
    Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Engineering Polymersomes for Diagnostics and Therapy.Advanced healthcare materials · 2018
    Review
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

5 authors at 3 institutions in 3 countries.

James D RobertsonDepartment of Biomedical Science, University College London, London WC1E 6BT, United Kingdom.ORCID 0000-0002-9961-0073
Jon R WardDivision of Infection and Immunity, University College London, London WC1E 6BT, United Kingdom.ORCID 0000-0001-9453-3147
Milagros Avila-OliasDepartment of Biomedical Science, University College London, London WC1E 6BT, United Kingdom.
Giuseppe BattagliaDepartment of Chemistry, University College London, London WC1E 6BT, United Kingdom; and s.a.renshaw@sheffield.ac.uk g.battaglia@ucl.ac.uk.ORCID 0000-0003-3349-6770
Stephen A RenshawDivision of Infection and Immunity, University College London, London WC1E 6BT, United Kingdom; s.a.renshaw@sheffield.ac.uk g.battaglia@ucl.ac.uk.ORCID 0000-0003-1790-1641
Department of Science and Technology · INInstitute of Infection and Immunity · CAMRC Laboratory for Molecular Cell Biology · GB

Funding

Medical Research Council G0700091Medical Research Council G0701932Medical Research Council G108/595Medical Research Council MR/K006312/1Medical Research Council MR/M004864/1Wellcome TrustWellcome Trust GR077544AIA
6 · The paper itself

Abstract

Neutrophils are key effector cells in inflammation and play an important role in neutralizing invading pathogens. During inflammation resolution, neutrophils undergo apoptosis before they are removed by macrophages, but if apoptosis is delayed, neutrophils can cause extensive tissue damage and chronic disease. Promotion of neutrophil apoptosis is a potential therapeutic approach for treating persistent inflammation, yet neutrophils have proven difficult cells to manipulate experimentally. In this study, we deliver therapeutic compounds to neutrophils using biocompatible, nanometer-sized synthetic vesicles, or polymersomes, which are internalized by binding to scavenger receptors and subsequently escape the early endosome through a pH-triggered disassembly mechanism. This allows polymersomes to deliver molecules into the cell cytosol of neutrophils without causing cellular activation. After optimizing polymersome size, we show that polymersomes can deliver the cyclin-dependent kinase inhibitor (R)-roscovitine into human neutrophils to promote apoptosis in vitro. Finally, using a transgenic zebrafish model, we show that encapsulated (R)-roscovitine can speed up inflammation resolution in vivo more efficiently than the free drug. These results show that polymersomes are effective intracellular carriers for drug delivery into neutrophils. This has important consequences for the study of neutrophil biology and the development of neutrophil-targeted therapeutics.

Indexed as

MicrospheresAnimalsAnimals, Genetically ModifiedApoptosisCells, CulturedCyclin-Dependent KinasesDrug Delivery SystemsFish DiseasesHumansInflammationInterleukin-8LiposomesMicroscopy, FluorescenceNeutrophil ActivationNeutrophilsPolymerizationCyclin-Dependent KinasesInterleukin-8LiposomesPurinesRoscovitine

Identifiers

PMID28289157
PMCPMC5392731
OpenAlexW2601855636

What OpenQuestion holds

Textmetadata
LicenceTDM
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.