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N2 Neutrophils, Novel Players in Brain Inflammation After Stroke

dc.contributor.authorCuartero Desviat, María Isabel
dc.contributor.authorBallesteros Martín, Iván
dc.contributor.authorMoraga Yébenes, Ana
dc.contributor.authorNombela, Florentino
dc.contributor.authorVivancos Mora, José
dc.contributor.authorHamilton, John A.
dc.contributor.authorCorbí, Ángel L.
dc.contributor.authorLizasoaín Hernández, Ignacio
dc.contributor.authorMoro Sánchez, María Ángeles
dc.date.accessioned2024-01-29T08:10:01Z
dc.date.available2024-01-29T08:10:01Z
dc.date.issued2013-12
dc.description.abstractBackground and Purpose—Neutrophils have been traditionally recognized as major mediators of a deleterious inflammatory response in acute ischemic stroke, but their potential as a therapeutic target remains unexplored. Recent evidence indicates that neutrophils may acquire different phenotypes and contribute to resolution of inflammation through the release of anti-inflammatory mediators. Thus, similar to M2 macrophages, neutrophils have been proposed to shift toward an N2 phenotype, a polarization that is peroxisome proliferator-activated receptor-γ dependent in macrophages. We hypothesize that peroxisome proliferator-activated receptor-γ activation with rosiglitazone induces changes in neutrophilic mobilization and phenotype that might influence stroke outcome. MethoBrain sections and cell suspensions were prepared from mice exposed to permanent distal middle cerebral artery occlusion. Double immunostaining with stereological counting of brain sections and flow-cytometry analysis of brain cell suspensions were performed. Results—Rosiglitazone accelerated neutrophil infiltration to the ischemic core, concomitantly to neuroprotection. Some neutrophils (≈31%) expressed M2 markers, namely Ym1 and CD206 (mannose receptor). After treatment with the peroxisome proliferator-activated receptor-γ agonist rosiglitazone, most neutrophils (≈77%) acquired an N2 phenotype. Interestingly, rosiglitazone increased neutrophil engulfment by microglia/macrophages, a clearance that preferentially affected the N2 subset. Conclusions—We present the first evidence of neutrophil reprogramming toward an N2 phenotype in brain inflammation, which can be modulated by activation of the peroxisome proliferator-activated receptor-γ nuclear receptor. We also show that N2 polarization is associated with an increased neutrophil clearance, thus suggesting that this switch is a crucial event for resolution of inflammation that may participate in neuroprotection.
dc.description.departmentDepto. de Farmacología y Toxicología
dc.description.facultyFac. de Medicina
dc.description.refereedTRUE
dc.description.sponsorshipUnión Europea
dc.description.sponsorshipMinisterio de Economía y Competitividad
dc.description.sponsorshipComunidad de Madrid
dc.description.statuspub
dc.identifier.citationCuartero MI, Ballesteros I, Moraga A, Nombela F, Vivancos J, Hamilton JA, Corbí ÁL, Lizasoain I, Moro MA. N2 neutrophils, novel players in brain inflammation after stroke: modulation by the PPARγ agonist rosiglitazone. Stroke. 2013 Dec;44(12):3498-508. doi: 10.1161/STROKEAHA.113.002470.
dc.identifier.doi10.1161/strokeaha.113.002470
dc.identifier.essn1524-4628
dc.identifier.issn0039-2499
dc.identifier.officialurlhttps://www.ahajournals.org/journal/str
dc.identifier.urihttps://hdl.handle.net/20.500.14352/95717
dc.issue.number12
dc.journal.titleStroke
dc.language.isoeng
dc.page.final3508
dc.page.initial3498
dc.publisherLippincott, Williams & Wilkins [Commercial Publisher]
dc.relation.projectIDSAF2009-08145
dc.relation.projectIDSAF2012-33216
dc.relation.projectIDSAF2011-23354
dc.relation.projectIDCSD2010-00045
dc.relation.projectIDFEDER RETICS-RD12/0014/0003
dc.relation.projectIDS2010/BMD-2336
dc.relation.projectIDS2010/BMD-2349
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internationalen
dc.rights.accessRightsopen access
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subject.cdu615.01/.03
dc.subject.keywordImmunomodulation
dc.subject.keywordInflammation
dc.subject.keywordPhagocytosisN2
dc.subject.ucmCiencias Biomédicas
dc.subject.unesco32 Ciencias Médicas
dc.titleN2 Neutrophils, Novel Players in Brain Inflammation After Stroke
dc.typejournal article
dc.volume.number44
dspace.entity.typePublication
relation.isAuthorOfPublication8df1e280-f5ce-4745-8d33-8c3ae0573875
relation.isAuthorOfPublication6c931648-bca4-4958-9413-18d378ca9645
relation.isAuthorOfPublication22bd5da1-89a4-434c-8dca-7c2f8db2b710
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relation.isAuthorOfPublication.latestForDiscovery8df1e280-f5ce-4745-8d33-8c3ae0573875

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