Cellular markers of neuroinflammation and neurogen

Authors: Vera Sekeljic Danijela Bataveljic Stefan Stamenkovic Marzena Ułamek Mirosław Jabłoński Lidija Radenovic Ryszard Pluta Pavle R Andjus

Publish Date: 2011/06/26

Volume: 217, Issue: 2, Pages: 411-420

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Abstract

MRI was employed to follow the neurodegenerative foci and the localization of inflammatory cells by magnetically labeled CD4+ or CD8+ lymphocytes in the ischemia/reperfusion longlived rats 9 and 13 months after 10 min of cardiac arrest MRI of ischemic rats showed 1 blood–brain barrier BBB leakage in the area of the dorsal hippocampus and brainstemhindbrain level in basal cerebellum 2 unlike antiCD8 magnetic antibodies antiCD4 ultra small paramagnetic iron oxide particles USPIO antibodies revealed hypointense areas in the brainsteminterbrain region and caudoputamen not found in animals that were not injected with USPIO antibodies and 3 dilation in the retrosplenial area Immunocytochemistry revealed microglial activation in the hippocampus and striatum with indications of activation in thalamic lateral dorsal nuclei and the subventricular zone In the CA1 and CA3 regions it was noted that OX42 and ED1positive granules appear in neuronal somata Immunostaining of lymphocytes with TCR confirmed the Tcell presence in ischemic brain parenchyma of the hippocampus and striatum The above observations thus point to a persistent dysfunction of BBB that in longterm may still lead to infiltration of T cells that are predominantly of helper CD4+ type Such inflammatory processes are backed by microglial activity even up to 1 year after ischemia/reperfusion Moreover in these animals an augmented expression of neurogenesis markers and neuroblast migration was also revealed in the subventricular zone Thus a balance of degenerative processes and inflammatory surveillance with neurogenesis could determine the longterm outcome of global ischemia survival or the previously proposed formation of amyloid plaques and Alzheimer’stype dementia

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