Evidence map›Paper›PMID 36042496›Full record

ArticleFluids and barriers of the CNS2022

Microglia-derived CCL2 has a prime role in neocortex neuroinflammation.

Mariella Errede, Tiziana Annese, Valentina Petrosino, Giovanna Longo, Francesco Girolamo, Ignazio de Trizio, Antonio d'Amati, Antonio Uccelli, Nicole Kerlero de Rosbo, Daniela Virgintino

Open access · goldAbstract read
In one paragraph

Article in Fluids and barriers of the CNS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
3.1field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 41 citations in OpenAlex.

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  8. Neuroinflammation and Disease: Pathways and Opportunities.Annual review of pharmacology and toxicology · 2026
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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

10 authors at 3 institutions in 1 country.

Mariella Errede *Department of Basic Medical Sciences, Neuroscience, and Sensory Organs, University of Bari School of Medicine, Piazza Giulio Cesare, Policlinics, 70124, Bari, Italy.
Tiziana Annese *Department of Basic Medical Sciences, Neuroscience, and Sensory Organs, University of Bari School of Medicine, Piazza Giulio Cesare, Policlinics, 70124, Bari, Italy.
Valentina PetrosinoDepartment of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa, Italy.
Giovanna LongoDepartment of Basic Medical Sciences, Neuroscience, and Sensory Organs, University of Bari School of Medicine, Piazza Giulio Cesare, Policlinics, 70124, Bari, Italy.
Francesco GirolamoDepartment of Basic Medical Sciences, Neuroscience, and Sensory Organs, University of Bari School of Medicine, Piazza Giulio Cesare, Policlinics, 70124, Bari, Italy.
Ignazio de TrizioDepartment of Basic Medical Sciences, Neuroscience, and Sensory Organs, University of Bari School of Medicine, Piazza Giulio Cesare, Policlinics, 70124, Bari, Italy.
Antonio d'AmatiDepartment of Basic Medical Sciences, Neuroscience, and Sensory Organs, University of Bari School of Medicine, Piazza Giulio Cesare, Policlinics, 70124, Bari, Italy.
Antonio UccelliDepartment of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa, Italy.
Nicole Kerlero de Rosbo *IRCCS Ospedale Policlinico San Martino, Genoa, Italy.
Daniela Virgintino *Department of Basic Medical Sciences, Neuroscience, and Sensory Organs, University of Bari School of Medicine, Piazza Giulio Cesare, Policlinics, 70124, Bari, Italy. daniela.virgintino@uniba.it.
University of Bari Aldo Moro · ITUniversity of Genoa · ITOspedale Policlinico San Martino · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), several areas of demyelination are detectable in mouse cerebral cortex, where neuroinflammation events are associated with scarce inflammatory infiltrates and blood-brain barrier (BBB) impairment. In this condition, the administration of mesenchymal stem cells (MSCs) controls neuroinflammation, attenuating astrogliosis and promoting the acquisition of stem cell traits by astrocytes. To contribute to the understanding of the mechanisms involved in the pathogenesis of EAE in gray matter and in the reverting effects of MSC treatment, the neocortex of EAE-affected mice was investigated by analyzing the cellular source(s) of chemokine CCL2, a molecule involved in immune cell recruitment and BBB-microvessel leakage.

methodsThe study was carried out by immunohistochemistry (IHC) and dual RNAscope IHC/in situ hybridization methods, using astrocyte, NG2-glia, macrophage/microglia, and microglia elective markers combined with CCL2.

resultsThe results showed that in EAE-affected mice, hypertrophic microglia are the primary source of CCL2, surround the cortex neurons and the damaged BBB microvessels. In EAE-affected mice treated with MSCs, microgliosis appeared diminished very soon (6 h) after treatment, an observation that was long-lasting (tested after 10 days). This was associated with a reduced CCL2 expression and with apparently preserved/restored BBB features. In conclusion, the hallmark of EAE in the mouse neocortex is a condition of microgliosis characterized by high levels of CCL2 expression.

conclusionsThis finding supports relevant pathogenetic and clinical aspects of the human disease, while the demonstrated early control of neuroinflammation and BBB permeability exerted by treatment with MSCs may have important therapeutic implications.

Indexed as

Chemokine CCL2Encephalomyelitis, Autoimmune, ExperimentalNeocortexAnimalsDisease Models, AnimalHumansMiceMice, Inbred C57BLMicrogliaNeuroinflammatory DiseasesCcl2 protein, mouseChemokine CCL2CCL2Experimental autoimmune encephalomyelitisMesenchymal stem cellsMicrogliaNeocortex

Identifiers

PMID36042496
PMCPMC9429625
OpenAlexW4293697921

What OpenQuestion holds

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LicenceCC BY
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.