Evidence map›Paper›PMID 24830384›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014

Stimulation of mesenchymal stromal cells (MSCs) via TLR3 reveals a novel mechanism of autocrine priming.

Claudia A Dumitru, Hatim Hemeda, Mark Jakob, Stephan Lang, Sven Brandau

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Stem Cell Therapy in Ischemic Heart Failure.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2025
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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

5 authors at 2 institutions in 1 country.

Claudia A DumitruDepartment of Otorhinolaryngology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Hatim HemedaDepartment of Otorhinolaryngology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Mark JakobDepartment of Otorhinolaryngology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Stephan LangDepartment of Otorhinolaryngology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Sven BrandauDepartment of Otorhinolaryngology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany sven.brandau@uk-essen.de.
University of Duisburg-Essen · DEEssen University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesenchymal stem/stromal cells (MSCs) are emerging as important regulators of innate and adaptive immunity. In this context, both proinflammatory and anti-inflammatory effects have been described for MSCs. The mechanisms mediating this functional plasticity are poorly characterized at present. Here, we investigated the inflammatory responses of MSCs isolated from human nasal mucosa (nmMSCs) upon challenge with different Toll-like receptor (TLR) ligands. We found that TLR3 ligands induced the strongest release of both proinflammatory cytokines [interleukin (IL)-6 and IL-8] and type I interferon by nmMSCs compared with other TLR ligands. Notably, TLR3 ligands triggered a biphasic cytokine response, with an early peak of type I interferon at 4 h poststimulation and a late release of proinflammatory cytokines at 24 h poststimulation. While the early interferon response was subject to direct stimulation, the proinflammatory response was regulated by factors released during the early cytokine response, which subsequently enhanced sensitivity to TLR3 ligation and amplified the production of IL-6 and IL-8 but not that of interferon. Taken together, our findings indicate that TLR3 ligands polarize the inflammatory phenotype of MSCs in a time-dependent manner. Thus, our study proposes a novel model that helps to explain the strikingly dichotomous functionality of MSCs in inflammation and immunoregulation.

Indexed as

Autocrine CommunicationAdultAgedBlotting, WesternCells, CulturedEnzyme-Linked Immunosorbent AssayFemaleFluorescent Antibody TechniqueHumansInflammationInflammation MediatorsInterferon-gammaInterleukin-6Interleukin-8LipopolysaccharidesMaleInflammation MediatorsInterferon-gammaInterleukin-6Interleukin-8LipopolysaccharidesRNA, MessengerToll-Like Receptor 3biphasic cytokine responsefunctional polarizationinterferon type IPoly I:Cproinflammatory cytokines

Identifiers

PMID24830384
PMCPMC5395723
OpenAlexW2106185445

What OpenQuestion holds

Textmetadata
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.