English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/92096
Share/Impact:
Statistics
logo share SHARE   Add this article to your Mendeley library MendeleyBASE
Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:

DC FieldValueLanguage
dc.contributor.authorPlanas, Anna M.-
dc.date.accessioned2014-02-20T08:55:50Z-
dc.date.available2014-02-20T08:55:50Z-
dc.date.issued2010-07-
dc.identifier.citation7th FENS (2010)-
dc.identifier.urihttp://hdl.handle.net/10261/92096-
dc.descriptionTrabajo presentado al 7th Forum of European Neuroscience (FENS) celebrado en Amsterdam del 3 al 7 de julio de 2010.-
dc.description.abstractIn spite of noticeable advances in understanding immune responses to acute brain injury after stroke, we are far from figuring out how the immune system affects infarction and injury progression. The chain of cellular and molecular reactions set by acute cell damage after stroke involves releasing proinflammatory mediators, upregulating chemokines and cytokines, glial reactivity, blood-brain barrier breakdown, and leukocyte adhesion/infiltration, which globally are assumed to exacerbate brain tissue damage. Acute brain damage alerts the innate immune system, the front line of defence against invading pathogens, and this leads to the massive release of proinflammatory mediators. This phenomenon occurs in the absence of pathogens by the generation of >danger signals> after cell injury. Neuronal necrotic cell death liberates normally intracellular molecules to the extracellular environment where they can activate pattern recognition receptors, such as toll-like receptors (TLR), in surrounding cells. Also, disruption of the extracellular matrix after protease-mediated cleavage might unveil epitopes that could activate TLRs. Signalling though TLRs triggers a complex network of molecular responses and release of proinflammatory mediators that exacerbate acute brain damage. Furthermore, the complement system, including the lectin pathway, also contributes to brain damage after stroke. Our findings show that genetic deficiency in mannose binding lectin (MBL) is associated to a better stroke outcome in animals and in humans. However, inhibition of innate immune responses might have risks, as increasing the already high susceptibility of stroke patients to infection. Although this did not occur in the MBL-deficient stroke patients of our study, putative adverse effects associated with inhibition of innate immunity should not be neglected. Finally, TLRs, the complement, and certain proinflammatory cytokines might have some beneficial effects under particular situations, as in preconditioning, and also by acting upon stem cells and favouring neurogenesis and regeneration. Better knowledge of the relevant molecular players should help designing strategies aimed to improve the neurological outcome after stroke through modulation of innate immunity.-
dc.language.isoeng-
dc.rightsclosedAccess-
dc.titleActivation of innate immune response after stroke-
dc.typecomunicación de congreso-
dc.date.updated2014-02-20T08:55:50Z-
dc.description.versionPeer Reviewed-
Appears in Collections:(IIBB) Comunicaciones congresos
Files in This Item:
File Description SizeFormat 
accesoRestringido.pdf15,38 kBAdobe PDFThumbnail
View/Open
Show simple item record
 


WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.