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We have studied MHC class II antigen expression and lymphocytic infiltration during dopaminergic neurone degeneration produced by intoxication with 1-methyl-4-phenyl-1,2,3,6-tetrahydropiridine (MPTP). Microglial activation was observed in the striatum and in the substantia nigra (SN) in this model. We noticed a marked increase of MHC class II antigen expression on microglia and T-cell recruitment in these regions after MPTP treatment. B-lymphocytes were not observed. T-cell infiltration predominantly consisted of CD8+ cells at every time point but CD4+ cells were present too. More than a half of the observed lymphocytes showed strong staining of CD44 antigen. Our findings suggest a possible immune system involvement in the pathological process following MPTP intoxication.
EN
Astrocytes are the main class of neuroglia, serving a wide range of adaptive functions in the mammalian nervous system. They interact with neurons, providing structural, metabolic and trophic support for them. In pathological circumstances, astrocytes have the potential to induce neuronal dysfunction, but they can also play a neuroprotective role, releasing neuronal growth factors. Here we review recent findings regarding the role of astrocytes in the biology of the brain in physiological conditions, as well as their reaction following the onset of neurodegenerative disorders.
EN
A immunohistochemical study of postnatal development of the paraclaustral reservoir of migrating cells in the rat brain was performed using anti-GFAP (for astroglia), ED1 and OX-42 (for microglia) antibodies. From birth to the 4th day of postnatal life most GFAP-positive cells in the paraclaustral reservoir are similar to transitional astroglia. From the end of the first postnatal week they have the morphology of mature astrocytes, although during the next week, their density was a slightly higher than in neighboring structures. On the 21st day, the morphology and density of astroglial cells in the ventral part of the external capsule did not differ from the surrounding regions. ED1/OX-42- positive microglial cells present in the paraclaustral reservoir during the first postnatal week represented ameboid microglia; their density was clearly higher than in the neighboring structures. During the second week they began to transform into ramified microglia and from the 21st day on, only OX-42 positive resting microglial cells were observed in the ventral part of the external capsule. We suggest that the paraclaustral reservoir is a place of accumulation of astroglia and microglia during brain development and may possibly serve as source of glial cells for neighboring structures. Alternatively, these glial populations may perform local developmental functions.
EN
The effects of photothrombotic stroke in primary somatosensory cortex on astroglial and microglial activation in various regions of lesioned brain were examined at different time points, using immunohistochemistry and lectin binding. The increase in GFAP expression was observed exclusively in the ipsilateral hemisphere, both in the perilesional area and cortical regions distant from the infarct. This remote increase was detectable up to sixty days after the infarct. Transient GFAP elevation was also found in the hippocampus one day after photothrombosis, whereas it was more prolonged in amygdala, as demonstrated at four days after lesion. In contrast to a widespread astrocytic activation, the microglial response was shortlasting and local, confined to lesion and perilesional area. Widespread and prolonged activation of astrocytes after stroke may provide factors promoting slowly developing recovery processes in the whole brain, while microglial response seems to be involved in local repair and removal of cellular debris.
EN
Introduction: Macrophages/microglial cells are considered as immune cells in the central nervous system. Interleukin (IL)-16 is a proinflammatory cytokine produced by activated monocytic cells. Materials and Methods: Expression of IL-16 was analyzed by immunohistochemistry in human astrocytic brain tumors and the rat C6 glioblastoma tumor model. IL-16 was detected in both human astrocytic brain tumors and rat C6 glioma. Results: Compared with human control brains, a significant increase in the percentages of parenchymal IL-16+ macrophages/microglia was observed already in grade II astrocytomas, indicating that IL-16+ immunostaining could be a descriptor of a macrophage/microglia subset in astrocytic brain tumors. A further increase was observed at the transition from grade II to III astrocytomas. This increase in IL-16 immunoreactivity correlated with WHO grades of human astrocytic brain tumors. Conclusions: Therefore, IL-16 might be a so far unknown factor in the regulation of the local inflammatory milieu of human and experimental astrocytomas.
EN
Spatial and temporal relations between transcriptional factor NFkB activation and glia reaction in gerbil hippocampus after transient cerebral ischemia has been studied. Activation of protein binding to NFkB consensus oligonucleotide was determined by electrophoretic mobility gel shift assay (EMSA) in homogenates from dorsal (DP- an equivalent of CA1 sector) and abdominal (AbP- containing CA2-4 and gyrus dentatus) parts of hippocampus. A significant activation of NFkB binding was observed exclusively in DP as early as 3 h after ischemia and at this time that response preceded any other morphological signs of postischemic tissue injury. This early enhancement of NFkB binding was followed by microglia activation visualized in CA1 pyramidal region at 24 h of recovery by histochemical staining with lectin from Ricinus communis (RCA-120). Simultaneously, only a moderate increase of immunostaining against glial fibrillary acidic protein (GFAP) was observed homogeneously in all parts of hippocampus. This uniform pattern of astrogliosis was preserved until postischemic day 3-4, when apoptotic DNA fragmentation in CA1 pyramidal neurons had been clearly documented by TUNEL staining. At this period however, continuous elevation of NFkB binding in DP corresponded with similar response manifested also in AbP of the hippocampus. These results evidence a preferential NFkB involvement in an early microglia activation in the apoptogenic CA1 sector, although its role in a later astrocytic response to ischemia could not be neglected too.
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