Evidence map›Paper›PMID 28579778›Full record

ArticleInternational journal of nanomedicine2017

Iron oxide nanoparticles induce cytokine secretion in a complement-dependent manner in a human whole blood model.

Susann Wolf-Grosse, Anne Mari Rokstad, Syed Ali, John D Lambris, Tom E Mollnes, Asbjørn M Nilsen, Jørgen Stenvik

Open access · goldAbstract read
In one paragraph

Article in International journal of nanomedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Frontiers in immunology · 2023
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Effects of Iron Oxide Nanoparticles (γ-FeInternational journal of molecular sciences · 2019
    Article
  15. Towards a nanoparticle-based prophylactic for maternal autoantibody-related autism.Nanomedicine : nanotechnology, biology, and medicine · 2019
    Article
  16. Article
  17. Plasma protein adsorption on FeInternational journal of nanomedicine · 2019
    Article
  18. Article
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

7 authors at 4 institutions in 2 countries.

Susann Wolf-GrosseDepartment of Cancer Research and Molecular Medicine.
Anne Mari RokstadDepartment of Cancer Research and Molecular Medicine.
Syed AliDivision of Neurotoxicology, US FDA/National Center for Toxicological Research, Jefferson, AR.
John D LambrisDepartment of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Tom E MollnesCentre of Molecular Inflammation Research (CEMIR), Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim.
Asbjørn M NilsenDepartment of Cancer Research and Molecular Medicine.
Jørgen StenvikDepartment of Cancer Research and Molecular Medicine.
Central Norway Regional Health Authority · NONorwegian University of Science and Technology · NOOslo University Hospital · NOUniversity of Pennsylvania · US

Funding

Role of complement in kidney disorders: from hemodialysis to transportationP01AI068730 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI LAMBRIS, JOHN D · 2007 to 2018
$16.0M
STRUCTURE-FUNCTION ANALYSIS OF DIFFERENT C3 SPECIESR01AI030040 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI LAMBRIS, JOHN D · 1993 to 2016
$4.1M
NIAID NIH HHS P01 AI068730NIAID NIH HHS R01 AI030040
6 · The paper itself

Abstract

Iron oxide nanoparticles (IONPs) are promising nanomaterials for biomedical applications. However, their inflammatory potential has not been fully established. Here, we used a lepirudin anti-coagulated human whole blood model to evaluate the potential of 10 nm IONPs to activate the complement system and induce cytokine production. Reactive oxygen species and cell death were also assessed. The IONPs activated complement, as measured by C3a, C5a and sC5b-9, and induced the production of pro-inflammatory cytokines in a particle-dose dependent manner, with the strongest response at 10 µg/mL IONPs. Complement inhibitors at C3 (compstatin analog Cp40) and C5 (eculizumab) levels completely inhibited complement activation and secretion of inflammatory mediators induced by the IONPs. Additionally, blockade of complement receptors C3aR and C5aR1 significantly reduced the levels of various cytokines, indicating that the particle-induced secretion of inflammatory mediators is mainly C5a and C3a mediated. The IONPs did not induce cell death or reactive oxygen species, which further suggests that complement activation alone was responsible for most of the particle-induced cytokines. These data suggest that the lepirudin anti-coagulated human whole blood model is a valuable ex vivo system to study the inflammatory potential of IONPs. We conclude that IONPs induce complement-mediated cytokine secretion in human whole blood.

Indexed as

Complement ActivationAnticoagulantsAnti-Inflammatory AgentsCell SurvivalComplement C3aComplement C5aComplement C5bComplement Inactivating AgentsCytokinesFerric CompoundsHirudinsHumansMetal NanoparticlesParticle SizeReactive Oxygen SpeciesReceptors, ComplementAnticoagulantsAnti-Inflammatory AgentsComplement C3aComplement C5aComplement C5bComplement Inactivating AgentsCytokinesFerric Compoundsferric oxideHirudinslepirudinReactive Oxygen SpeciesReceptors, ComplementRecombinant Proteinscomplement activationcomplement inhibitorscytokineshuman whole bloodiron oxide nanoparticlesreactive oxygen species

Identifiers

PMID28579778
PMCPMC5449102
OpenAlexW2618797029

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.