Evidence map›Paper›PMID 33766057›Full record

ArticleJournal of nanobiotechnology2021

Therapies with CCL25 require controlled release via microparticles to avoid strong inflammatory reactions.

J Spinnen, K Fröhlich, N Sinner, M Stolk, J Ringe, L Shopperly, M Sittinger, T Dehne, M Seifert

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

Article in Journal of nanobiotechnology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

3 citing papers in PubMed, 9 citations in OpenAlex.

  1. Triple-Combination Therapy with a Multifunctional Yolk-Shell Nanozyme Au@CeOAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  2. Article
  3. 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

9 authors at 2 institutions in 1 country.

J SpinnenTissue Engineering Laboratory, BIH Center for Regenerative Therapies, Department for Rheumatology and Clinical Immunology & Berlin Institute of Health at Charité-Universitätsmedizin Berli, BCRT, Charitéplatz 1, 10117, Berlin, Germany. jacob.spinnen@charite.de.ORCID http://orcid.org/0000-0002-6726-2860
K FröhlichTissue Engineering Laboratory, BIH Center for Regenerative Therapies, Department for Rheumatology and Clinical Immunology & Berlin Institute of Health at Charité-Universitätsmedizin Berli, BCRT, Charitéplatz 1, 10117, Berlin, Germany.
N SinnerTissue Engineering Laboratory, BIH Center for Regenerative Therapies, Department for Rheumatology and Clinical Immunology & Berlin Institute of Health at Charité-Universitätsmedizin Berli, BCRT, Charitéplatz 1, 10117, Berlin, Germany.
M StolkTissue Engineering Laboratory, BIH Center for Regenerative Therapies, Department for Rheumatology and Clinical Immunology & Berlin Institute of Health at Charité-Universitätsmedizin Berli, BCRT, Charitéplatz 1, 10117, Berlin, Germany.
J RingeTissue Engineering Laboratory, BIH Center for Regenerative Therapies, Department for Rheumatology and Clinical Immunology & Berlin Institute of Health at Charité-Universitätsmedizin Berli, BCRT, Charitéplatz 1, 10117, Berlin, Germany.
L ShopperlyTissue Engineering Laboratory, BIH Center for Regenerative Therapies, Department for Rheumatology and Clinical Immunology & Berlin Institute of Health at Charité-Universitätsmedizin Berli, BCRT, Charitéplatz 1, 10117, Berlin, Germany.
M SittingerTissue Engineering Laboratory, BIH Center for Regenerative Therapies, Department for Rheumatology and Clinical Immunology & Berlin Institute of Health at Charité-Universitätsmedizin Berli, BCRT, Charitéplatz 1, 10117, Berlin, Germany.
T DehneTissue Engineering Laboratory, BIH Center for Regenerative Therapies, Department for Rheumatology and Clinical Immunology & Berlin Institute of Health at Charité-Universitätsmedizin Berli, BCRT, Charitéplatz 1, 10117, Berlin, Germany.
M SeifertInstitute of Medical Immunology and Berlin Institute of Health Center for Regenerative Therapies, Institute of Medical Immunology, Charité-Universitaetsmedizin Berlin, corporate member of Freie Universitaet Berlin and Humboldt-Universitaet Zu Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.ORCID http://orcid.org/0000-0002-6372-9769
Berlin Institute of Health at Charité - Universitätsmedizin Berlin · DEHumboldt-Universität zu Berlin · DE

Funding

Bundesministerium für Bildung und Forschung #13GW0099
6 · The paper itself

Abstract

backgroundChemokine therapy with C-C motif chemokine ligand 25 (CCL25) is currently under investigation as a promising approach to treat articular cartilage degeneration. We developed a delayed release mechanism based on Poly (lactic-co-glycolic acid) (PLGA) microparticle encapsulation for intraarticular injections to ensure prolonged release of therapeutic dosages. However, CCL25 plays an important role in immune cell regulation and inflammatory processes like T-cell homing and chronic tissue inflammation. Therefore, the potential of CCL25 to activate immune cells must be assessed more thoroughly before further translation into clinical practice. The aim of this study was to evaluate the reaction of different immune cell subsets upon stimulation with different dosages of CCL25 in comparison to CCL25 released from PLGA particles.

resultsImmune cell subsets were treated for up to 5 days with CCL25 and subsequently analyzed regarding their cytokine secretion, surface marker expression, polarization, and migratory behavior. The CCL25 receptor C-C chemokine receptor type 9 (CCR9) was expressed to a different extent on all immune cell subsets. Direct stimulation of peripheral blood mononuclear cells (PBMCs) with high dosages of CCL25 resulted in strong increases in the secretion of monocyte chemoattractant protein-1 (MCP-1), interleukin-8 (IL-8), interleukin-1β (IL-1β), tumor-necrosis-factor-α (TNF-α) and interferon-γ (IFN-γ), upregulation of human leukocyte antigen-DR (HLA-DR) on monocytes and CD4

conclusionsWhile supernatants of CCL25 loaded PLGA microparticles did not provoke strong inflammatory reactions, direct stimulation with CCL25 shows the critical potential to induce global inflammatory activation of human leukocytes at certain concentrations. These findings underline the importance of a safe and reliable release system in a therapeutic setup. Failure of the delivery system could result in strong local and systemic inflammatory reactions that could potentially negate the benefits of chemokine therapy.

Indexed as

Chemokine CCL2ChemokinesChemokines, CCDelayed-Action PreparationsHumansInflammationInterferon-gammaInterleukin-1betaInterleukin-8Leukocytes, MononuclearLigandsMacrophagesMonocytesPolylactic Acid-Polyglycolic Acid CopolymerReceptors, CCRTumor Necrosis Factor-alphaCC chemokine receptor 9CCL25 protein, humanCCL2 protein, humanChemokine CCL2ChemokinesChemokines, CCCXCL8 protein, humanDelayed-Action PreparationsInterferon-gammaInterleukin-1betaInterleukin-8LigandsPolylactic Acid-Polyglycolic Acid CopolymerReceptors, CCRTNF protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID33766057
PMCPMC7992824
OpenAlexW3137083495

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.