Evidence map›Paper›PMID 33482848›Full record

ArticleJournal of neuroinflammation2021

Chronic exposure to IL-6 induces a desensitized phenotype of the microglia.

Mireia Recasens, Beatriz Almolda, Jeús Pérez-Clausell, Iain L Campbell, Berta González, Bernardo Castellano

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
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  7. The volatile oil ofFrontiers in pharmacology · 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

6 authors at 3 institutions in 2 countries.

Mireia RecasensDepartment of Cell Biology, Physiology and Immunology, Institute of Neuroscience, Universitat Autònoma de Barcelona, 08193, Bellaterra, Barcelona, Spain.
Beatriz AlmoldaDepartment of Cell Biology, Physiology and Immunology, Institute of Neuroscience, Universitat Autònoma de Barcelona, 08193, Bellaterra, Barcelona, Spain. beatriz.almolda@uab.cat.ORCID http://orcid.org/0000-0001-6631-4385
Jeús Pérez-ClausellDepartment of Cell Biology, Physiology and Immunology, Universitat de Barcelona, 08028, Barcelona, Spain.
Iain L CampbellSchool of Life and Environmental Sciences and Charles Perkins Centre, University of Sydney, Sydney, NSW, 2006, Australia.
Berta GonzálezDepartment of Cell Biology, Physiology and Immunology, Institute of Neuroscience, Universitat Autònoma de Barcelona, 08193, Bellaterra, Barcelona, Spain.
Bernardo CastellanoDepartment of Cell Biology, Physiology and Immunology, Institute of Neuroscience, Universitat Autònoma de Barcelona, 08193, Bellaterra, Barcelona, Spain.
Universitat Autònoma de Barcelona · ESThe University of Sydney · AUUniversitat de Barcelona · ES

Funding

Ministry of Science and Innovation BFU2014-55459Ministry of Science and Innovation BFU2017-87843-R
6 · The paper itself

Abstract

backgroundWhen the homeostasis of the central nervous system (CNS) is altered, microglial cells become activated displaying a wide range of phenotypes that depend on the specific site, the nature of the activator, and particularly the microenvironment generated by the lesion. Cytokines are important signals involved in the modulation of the molecular microenvironment and hence play a pivotal role in orchestrating microglial activation. Among them, interleukin-6 (IL-6) is a pleiotropic cytokine described in a wide range of pathological conditions as a potent inducer and modulator of microglial activation, but with contradictory results regarding its detrimental or beneficial functions. The objective of the present study was to evaluate the effects of chronic IL-6 production on the immune response associated with CNS-axonal anterograde degeneration.

methodsThe perforant pathway transection (PPT) paradigm was used in transgenic mice with astrocyte-targeted IL6-production (GFAP-IL6Tg). At 2, 3, 7, 14, and 21 days post-lesion, the hippocampal areas were processed for immunohistochemistry, flow cytometry, and protein microarray.

resultsAn increase in the microglia/macrophage density was observed in GFAP-IL6Tg animals in non-lesion conditions and at later time-points after PPT, associated with higher microglial proliferation and a major monocyte/macrophage cell infiltration. Besides, in homeostasis, GFAP-IL6Tg showed an environment usually linked with an innate immune response, with more perivascular CD11b

conclusionsChronic exposure to IL-6 induces a desensitized phenotype of the microglia.

Indexed as

MicrogliaAnimalsFemaleInterleukin-6MaleMiceMice, TransgenicNerve DegenerationPerforant PathwayPhenotypeInterleukin-6Axonal sproutingMHCIIMonocytePrimed microgliaT cell

Identifiers

PMID33482848
PMCPMC7821504
OpenAlexW3121970547

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.