Inflammation without neuronal death triggers striatal neurogenesis comparable to stroke

What is your doctor doing to mimic this in your stroke recovery? ANYTHING AT ALL?
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Inflammation without neuronal death triggers striatal neurogenesis comparable to stroke

• Katie Z. Chapman^{a, 1},
• Ruimin Ge^{a, 1},
• Emanuela Monni^a,
• Jemal Tatarishvili^a,
• Henrik Ahlenius^b,
• Andreas Arvidsson^{a, c},
• Christine T. Ekdahl^d,
• Olle Lindvall^{a, 2},
• Zaal Kokaia^{a, , 2,}

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doi:10.1016/j.nbd.2015.08.013

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Highlights

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LPS-induced inflammation without neuronal loss triggers striatal neurogenesis

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Magnitude of striatal neurogenesis is similar to that after stroke-induced injury

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Microarray on sorted microglia identifies factors potentially regulating neurogenesis

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CXCL13 is upregulated in microglia and increases neuroblast migration in vitro

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Microglia-derived CXCL13, acting through CXCR5, might be neuroprotective in stroke

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Abstract

Ischemic stroke triggers neurogenesis from neural stem/progenitor cells (NSPCs) in the subventricular zone (SVZ) and migration of newly formed neuroblasts towards the damaged striatum where they differentiate to mature neurons. Whether it is the injury per se or the associated inflammation that gives rise to this endogenous neurogenic response is unknown. Here we showed that inflammation without corresponding neuronal loss caused by intrastriatal lipopolysaccharide (LPS) injection leads to striatal neurogenesis in rats comparable to that after a 30 min middle cerebral artery occlusion, as characterized by striatal DCX + neuroblast recruitment and mature NeuN +/BrdU + neuron formation. Using global gene expression analysis, changes in several factors that could potentially regulate striatal neurogenesis were identified in microglia sorted from SVZ and striatum of LPS-injected and stroke-subjected rats. Among the upregulated factors, one chemokine, CXCL13, was found to promote neuroblast migration from neonatal mouse SVZ explants in vitro. However, neuroblast migration to the striatum was not affected in constitutive CXCL13 receptor CXCR5^−/− mice subjected to stroke. Infarct volume and pro-inflammatory M1 microglia/macrophage density were increased in CXCR5^−/− mice, suggesting that microglia-derived CXCL13, acting through CXCR5, might be involved in neuroprotection following stroke. Our findings raise the possibility that the inflammation accompanying an ischemic insult is the major inducer of striatal neurogenesis after stroke.