About: Microglial cell loss after ischemic stroke favors brain neutrophil accumulation

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An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Microglial cell loss after ischemic stroke favors brain neutrophil accumulation
Creator	Bosch, Anna Calvo, Maria Gaja-Capdevila, Núria Gallizioli, Mattia Gunzer, Matthias Justicia, Carles Miró-Mur, Francesc Ruíz-Jaen, Francisca Salas-Perdomo, Angélica Denes, · Leonardo Márquez-Kisinousky, · Otxoa-De-Amezaga, Amaia Pedragosa, · Planas, Anna
Source	PMC
abstract	Stroke attracts neutrophils to the injured brain tissue where they can damage the integrity of the blood–brain barrier and exacerbate the lesion. However, the mechanisms involved in neutrophil transmigration, location and accumulation in the ischemic brain are not fully elucidated. Neutrophils can reach the perivascular spaces of brain vessels after crossing the endothelial cell layer and endothelial basal lamina of post-capillary venules, or migrating from the leptomeninges following pial vessel extravasation and/or a suggested translocation from the skull bone marrow. Based on previous observations of microglia phagocytosing neutrophils recruited to the ischemic brain lesion, we hypothesized that microglial cells might control neutrophil accumulation in the injured brain. We studied a model of permanent occlusion of the middle cerebral artery in mice, including microglia- and neutrophil-reporter mice. Using various in vitro and in vivo strategies to impair microglial function or to eliminate microglia by targeting colony stimulating factor 1 receptor (CSF1R), this study demonstrates that microglial phagocytosis of neutrophils has fundamental consequences for the ischemic tissue. We found that reactive microglia engulf neutrophils at the periphery of the ischemic lesion, whereas local microglial cell loss and dystrophy occurring in the ischemic core are associated with the accumulation of neutrophils first in perivascular spaces and later in the parenchyma. Accordingly, microglia depletion by long-term treatment with a CSF1R inhibitor increased the numbers of neutrophils and enlarged the ischemic lesion. Hence, microglial phagocytic function sets a critical line of defense against the vascular and tissue damaging capacity of neutrophils in brain ischemia. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1007/s00401-018-1954-4) contains supplementary material, which is available to authorized users.
has issue date	2018-12-22(xsd:dateTime)
bibo:doi	10.1007/s00401-018-1954-4
bibo:pmid	30580383
has license	cc-by
sha1sum (hex)	dcd269e34e588ed3ce743184f98ed65229b84fdd
schema:url	https://doi.org/10.1007/s00401-018-1954-4
resource representing a document's title	Microglial cell loss after ischemic stroke favors brain neutrophil accumulation
has PubMed Central identifier	PMC6513908
has PubMed identifier	30580383
schema:publication	Acta Neuropathol
resource representing a document's body	covid:dcd269e34e588ed3ce743184f98ed65229b84fdd#body_text
is schema:about of	named entity 'accumulation' named entity 'brain ischemia' covid:arg/dcd269e34e588ed3ce743184f98ed65229b84fdd named entity 'stimulating' named entity 'crossing' named entity 'perivascular spaces' named entity 'microglia' named entity 'brain lesion' named entity 'ischemic' named entity 'involved' named entity 'brain tissue' named entity 'brain' named entity 'blood-brain barrier' named entity 'leptomeninges' named entity 'layer' named entity 'targeting' named entity 'ischemic' named entity 'sets' named entity 'receptor' named entity 'neutrophils' named entity 'location' named entity 'neutrophils' named entity 'brain ischemia' named entity 'bone marrow' named entity 'parenchyma' named entity 'leptomeninges' named entity 'endothelial' named entity 'Neutrophils' named entity 'microglial cell' named entity 'ischemic' named entity 'brain lesion' named entity 'neutrophils' named entity 'capillary' named entity 'ischemic' named entity 'phagocytic' named entity 'lesion' named entity 'microglial' named entity 'ischemic stroke' named entity 'extravasation' named entity 'Stroke' named entity 'CSF1R inhibitor' named entity 'phagocytosing' named entity 'skull' named entity 'perivascular spaces' named entity 'microglia' named entity 'lesion' named entity 'ischemic' named entity 'neutrophils' named entity 'neutrophils' named entity 'neutrophils' named entity 'CSF1R' named entity 'ischemic tissue' named entity 'venules' named entity 'brain tissue' named entity 'microglia' named entity 'microglial cells' named entity 'neutrophil' named entity 'basal lamina' named entity 'studied' named entity 'tissue' named entity 'endothelial cell layer' named entity 'neutrophils' named entity 'microglia' named entity 'microglia' named entity 'extravasation' named entity 'long-term' named entity 'neutrophils' named entity 'pial'

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