2 min read

ID: 870887

Short Link: https://gregory-ms.com/articles/870887/

Discovery Date: 31 August 2022, 03:50:07 UTC

Published Date: 2022-08-29 23:00:00

Source: BioMedCentral

Link: https://fluidsbarrierscns.biomedcentral.com/articles/10.1186/s12987-022-00365-5

Manual Selection: true

Machine Learning Gaussian Naive Bayes Model: false

Abstract

jats:titleAbstract</jats:title>jats:sec jats:titleBackground</jats:title> jats:pIn 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.</jats:p> </jats:sec>jats:sec jats:titleMethods</jats:title> jats:pThe 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.</jats:p> </jats:sec>jats:sec jats:titleResults</jats:title> jats:pThe 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.</jats:p> </jats:sec>jats:sec jats:titleConclusions</jats:title> jats:pThis 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.</jats:p> </jats:sec>

Noun Phrases in Title

  • Microglia-derived CCL2
  • a prime role
  • neocortex neuroinflammation
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