Evidence map›Paper›PMID 30672109›Full record

ArticleJournal of biomedical materials research. Part A2019

Modulation of macrophage phenotype via phagocytosis of drug-loaded microparticles.

Kathryn L Wofford, D Kacy Cullen, Kara L Spiller

Abstract read
In one paragraph

Article in Journal of biomedical materials research. Part A, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Article
  2. Article
  3. Targeting macrophages in liver fibrosis.Frontiers in immunology · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Clickable Biomaterials for Modulating Neuroinflammation.International journal of molecular sciences · 2022
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. 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

3 authors.

Kathryn L WoffordSchool of Biomedical Engineering, Science and Health Systems, Drexel University, Philadelphia, Pennsylvania.
D Kacy CullenCenter for Neurotrauma, Neurodegeneration and Restoration, CMC VA Medical Center, Philadelphia, Pennsylvania.
Kara L SpillerSchool of Biomedical Engineering, Science and Health Systems, Drexel University, Philadelphia, Pennsylvania.

Funding

Understanding and Controlling Macrophage Behavior in AngiogenesisR01HL130037 · NHLBI · DREXEL UNIVERSITY · PI SPILLER, KARA LORRAINE · 2016 to 2024
$4.7M
Chronic neurodegenerative and neurophysiological sequela of closed-head TBII01RX001097 · VA · PHILADELPHIA VA MEDICAL CENTER · PI DUDA, JOHN ERIC · 2015 to 2018
–
Department of Education GAANN iCARE FellowshipDepartment of Veteran's Affairs I01-RX001097NHLBI NIH HHS R01 HL130037NHLBI NIH HHS R01-HL130037RRD VA I01 RX001097
6 · The paper itself

Abstract

Monocyte-derived macrophages play a critical role in directing wound pathology following injury. Depending on their phenotype, macrophages also promote tissue regeneration. However, the therapeutic administration of macrophages with a controlled phenotype is challenging because macrophages are highly plastic and quickly revert to a detrimental, inflammatory phenotype in response to the environment of a damaged tissue. To address this issue, we developed a novel strategy to modulate macrophage phenotype intracellularly through phagocytosis of drug-loaded microparticles. Poly(lactic-co-glycolic acid) microparticles loaded with the anti-inflammatory drug dexamethasone (Dex) were phagocytosed by monocytes and stored intracellularly for at least 5 days. After differentiation into macrophages, cell phenotype was characterized over time with high-throughput gene expression analysis via NanoString. We found that the microparticles modulated macrophage phenotype for up to 7 days after microparticle uptake, with decreases in inflammation-related genes at early timepoints and upregulation of homing- and phagocytosis-related genes at multiple timepoints in a manner similar to cells treated with continuous free Dex. These data suggest that intracellularly loading macrophages with Dex microparticles via phagocytosis could be a unique methodology to selectively modulate macrophage phenotype over time. This strategy would allow therapeutic administration of macrophages for the treatment of a number of inflammatory disease and disorders. © 2019 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 107A: 1213-1224, 2019.

Indexed as

DexamethasoneDrug CarriersHumansMacrophagesMonocytesPhagocytosisDexamethasoneDrug Carrierscell-microparticle interactionsdexamethasonegene expressionintracellular particlesmacrophage

Identifiers

PMID30672109
PMCPMC6499658

What OpenQuestion holds

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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.