Evidence map›Paper›PMID 26226941›Full record

ArticleScientific reports2015

E-cadherin expression in macrophages dampens their inflammatory responsiveness in vitro, but does not modulate M2-regulated pathologies in vivo.

Jan Van den Bossche, Damya Laoui, Thomas Naessens, Hermelijn H Smits, Cornelis H Hokke, Benoît Stijlemans, Johan Grooten, Patrick De Baetselier, Jo A Van Ginderachter

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Frontiers in immunology · 2026
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  9. Immunonutritional Protease Inhibitors fromInternational journal of molecular sciences · 2021
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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

9 authors at 4 institutions in 2 countries.

Jan Van den Bossche1] Laboratory of Myeloid Cell Immunology, VIB, Brussels, Belgium [2] Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium.
Damya Laoui1] Laboratory of Myeloid Cell Immunology, VIB, Brussels, Belgium [2] Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium.
Thomas NaessensDepartment of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.
Hermelijn H SmitsDepartment of Parasitology, Leiden University Medical Centre, Leiden, The Netherlands.
Cornelis H HokkeDepartment of Parasitology, Leiden University Medical Centre, Leiden, The Netherlands.
Benoît Stijlemans1] Laboratory of Myeloid Cell Immunology, VIB, Brussels, Belgium [2] Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium.
Johan GrootenDepartment of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.
Patrick De Baetselier1] Laboratory of Myeloid Cell Immunology, VIB, Brussels, Belgium [2] Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium.
Jo A Van Ginderachter1] Laboratory of Myeloid Cell Immunology, VIB, Brussels, Belgium [2] Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium.
Vrije Universiteit Brussel · BEGhent University · BELeiden University · NLVIB-VUB Laboratory Myeloid Cell Immunology · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IL-4/IL-13-induced alternatively activated macrophages (M(IL-4/IL-13), AAMs or M2) are known to express E-cadherin, enabling them to engage in heterotypic cellular interactions and IL-4-driven macrophage fusion in vitro. Here we show that E-cadherin overexpression in Raw 264.7 macrophages inhibits their inflammatory response to LPS stimulation, as demonstrated by a reduced secretion of inflammatory mediators like interleukin (IL)-6, tumor necrosis factor (TNF) and nitric oxide (NO). To study the function of E-cadherin in M(IL-4/IL-13) macrophages in vivo, we generated macrophage-specific E-cadherin-deficient C57BL/6 mice. Using this new tool, we analyzed immunological parameters during two typical AAM-associated Th2-driven diseases and assessed Th2-associated granuloma formation. Although E-cadherin is strongly induced in AAMs during Taenia crassiceps helminth infections and allergic airway inflammation, its deletion in macrophages does not affect the course of both Th2 cytokine-driven diseases. Moreover, macrophage E-cadherin expression is largely redundant for granuloma formation around Schistosoma mansoni ova. Overall, we conclude that E-cadherin is a valuable AAM marker which suppresses the inflammatory response when overexpressed. Yet E-cadherin deletion in macrophages does not affect M(LPS+IFNγ) and M(IL-4) polarization in vitro, nor in vivo macrophage function, at least in the conditions tested.

Indexed as

AnimalsB-LymphocytesBronchoalveolar LavageCadherinsCysticercosisInflammationInflammation MediatorsInterleukin-13Interleukin-4MacrophagesMice, Inbred C57BLMice, KnockoutSchistosomiasis mansoniTh2 CellsCadherinsInflammation MediatorsInterleukin-13Interleukin-4

Identifiers

PMID26226941
PMCPMC4521155
OpenAlexW944478982

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.