Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Monday, November 25, 2013

N2 Neutrophils, Novel Players in Brain Inflammation After Stroke

I'm sure reducing inflamation after stroke is a good thing. Does your doctor think so? And what is your doctor doing about that?
http://stroke.ahajournals.org/content/44/12/3498.abstract?etoc

Modulation by the PPARγ Agonist Rosiglitazone

  1. María A. Moro, PhD
+ Author Affiliations
  1. From the Unidad de Investigación Neurovascular, Departamento de Farmacología, Facultad de Medicina, Universidad Complutense, Instituto de Investigación Sanitaria Hospital Clínico San Carlos (IdISSC) and Instituto de Investigación Sanitaria Hospital 12 de Octubre (i+12), Madrid, Spain (M.I.C., I.B., A.M., I.L., M.A.M.); Servicio de Neurología and Instituto de Investigación Sanitaria del Hospital Universitario de La Princesa, Madrid, Spain (F.N., J.V.); Arthritis and Inflammation Research Centre, University of Melbourne and Department of Medicine, Royal Melbourne Hospital, Melbourne, Australia (J.A.H.); and Centro de Investigaciones Biológicas, CSIC, Madrid, Spain (A.L.C.).
  1. Correspondence to María A. Moro, PhD, Unidad de Investigación Neurovascular, Departamento de Farmacología, Facultad de Medicina, Universidad Complutense, Avenida Complutense s/n, 28040, Madrid, Spain. E-mail neurona@med.ucm.es
  1. * Drs Cuartero and Ballesteros contributed equally.

Abstract

Background 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.
Methods—Brain 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.

No comments:

Post a Comment