English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/206352
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:


Role of MBL in neutrophil infiltration after TBI

AuthorsPedragosa, Jordi; Planas, Anna M.
Issue Date21-Jan-2019
CitationERA-NET NEURON Cofund Meeting (2019)
AbstractQuestions: Traumatic Brain Injury (TBI) is a leading cause of death and permanent disability worldwide. Following the primary biomechanical damage, leukocyte infiltration and the complement cascade are recognized as critical mechanisms involved in secondary brain damage. Several studies show that the Lectin Pathway (LP) is activated in brain ischemia and pharmacological targeting of mannose-binding lectin (MBL) is protective. Stroke patients carrying genetic MBL deficiency present smaller infarctions and better outcomes. The objective of this study is to investigate the involvement of LP in the inflammatory response in a mouse model of TBI. For comparative purposes we used a model of cerebral ischemia. We focused on the innate immune response leaded by neutrophil infiltration to the damaged brain tissue. Methods: Wild-type mice and MBL-deficient were subjected to controlled cortical impact as a model of TBI, or permanent middle cerebral artery occlusion for induction of ischemia. Paraffin and cryostat brain sections were obtained and specific staining for neutrophils was carried out at different time points after brain injury. Cell counting was performed with a stereological microscope. We studied neutrophil infiltration, specific location in vascular or parenchymal compartments, and studied signs of formation of neutrophil extracellular traps. Results: MBL-deficient mice show reduced tromboinflammation and better outcomes after ischemia. Both stroke and TBI caused neutrophil infiltration to the injured brain tissue. Neutrophil infiltration was reduced in MBL-deficient mice versus wild-type mice after ischemia, and we are evaluating the results for TBI. The results support that MBL promotes neutrophil infiltration after acute brain injury.
DescriptionTrabajo presentado en ERA-NET NEURON Cofund Meeting: Network of European Funding for Neuroscience Research, celebrado en Bonn (Alemania), del 21 al 23 de enero de 2019
Appears in Collections:(IIBB) Comunicaciones congresos
Files in This Item:
File Description SizeFormat 
accesoRestringido.pdf15,38 kBAdobe PDFThumbnail
Show full item record
Review this work

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