Evidence map›Paper›PMID 31297055›Full record

ArticleFrontiers in pharmacology2019

Targeting the Eph/Ephrin System as Anti-Inflammatory Strategy in IBD.

Andrea Grandi, Irene Zini, Simone Palese, Carmine Giorgio, Massimiliano Tognolini, Francesco Marchesani, Stefano Bruno, Lisa Flammini, Anna Maria Cantoni, Riccardo Castelli and 4 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

16 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  8. Article
  9. Article
  10. The EPH/Ephrin System in Colorectal Cancer.International journal of molecular sciences · 2022
    Review
  11. Review
  12. Article
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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

14 authors at 1 institution in 1 country.

Andrea GrandiFood and Drug Department, University of Parma, Parma, Italy.
Irene ZiniFood and Drug Department, University of Parma, Parma, Italy.
Simone PaleseFood and Drug Department, University of Parma, Parma, Italy.
Carmine GiorgioFood and Drug Department, University of Parma, Parma, Italy.
Massimiliano TognoliniFood and Drug Department, University of Parma, Parma, Italy.
Francesco MarchesaniFood and Drug Department, University of Parma, Parma, Italy.
Stefano BrunoFood and Drug Department, University of Parma, Parma, Italy.
Lisa FlamminiFood and Drug Department, University of Parma, Parma, Italy.
Anna Maria CantoniDepartment of Veterinary Sciences, University of Parma, Parma, Italy.
Riccardo CastelliFood and Drug Department, University of Parma, Parma, Italy.
Alessio LodolaFood and Drug Department, University of Parma, Parma, Italy.
Antonella FusariDepartment of Veterinary Sciences, University of Parma, Parma, Italy.
Elisabetta BarocelliFood and Drug Department, University of Parma, Parma, Italy.
Simona BertoniFood and Drug Department, University of Parma, Parma, Italy.
University of Parma · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Besides their long-known critical role in embryonic growth and in cancer development and progression, erythropoietin-producing hepatocellular carcinoma type B (EphB) receptor tyrosine kinases and their ephrin-B ligands are involved in the modulation of immune responses and in remodeling and maintaining the integrity of the intestinal epithelial layer. These processes are critically involved in the pathogenesis of inflammatory-based disorders of the gut, like inflammatory bowel diseases (IBDs). Accordingly, our aim was to investigate the role of the EphB/ephrin-B system in intestinal inflammation by assessing the local and systemic effects produced by its pharmacological manipulation in 2,4,6-trinitrobenzenesulfonic acid (TNBS)- (Th1-dependent model) and dextran sulphate sodium (DSS)- (innate response model) induced colitis in mice. To this purpose, we administered chimeric Fc-conjugated proteins, allegedly able to uni-directionally activate either forward (ephrin-B1-Fc) or reverse (EphB1-Fc) signaling, and the soluble monomeric EphB4 extracellular domain protein, that, simultaneously interfering with both signaling pathways, acts as EphB/ephrin-B antagonist.The blockade of the EphB/ephrin-B forward signaling by EphB4 and EphB1-Fc was ineffective against DSS-induced colitis while it evoked remarkable beneficial effects against TNBS colitis: it counteracted all the evaluated inflammatory responses and the changes elicited on splenic T lymphocytes subpopulations, without preventing the appearance of a splice variant of ephrin-B2 gene elicited by the haptenating agent in the colon. Interestingly, EphB4, preferentially displacing EphB4/ephrin-B2 interaction over EphB1/ephrin-B1 binding, was able to promote Tumor Necrosis Factor alpha (TNFα) release by splenic mononuclear cells

Indexed as

DSS experimental colitisEphB1-FcEphB4ephrin-B2splenocytes cultureTNBS-induced colitis

Identifiers

PMID31297055
PMCPMC6606944
OpenAlexW2949678753

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.