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Text
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URL Address
<a href="http://doi.org/10.1016/j.nbd.2017.08.009" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.nbd.2017.08.009</a>
Pages
115–127
Volume
108
Dublin Core
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Title
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Alternative microglial activation is associated with cessation of progressive dopamine neuron loss in mice systemically administered lipopolysaccharide.
Publisher
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Neurobiology of disease
Date
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2017
2017-12
Subject
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Animals; Astrocytes/immunology/pathology; Cell Death/physiology; Corpus Striatum/immunology/pathology; Cytokines/metabolism; Disease Progression; Dopaminergic Neurons/*immunology/pathology; Inbred C57BL; Inflammation/pathology/physiopathology; Lipopolysaccharides/*toxicity; Male; Messenger/metabolism; Mice; Microglia/*immunology/pathology; Nerve Degeneration/*immunology/pathology; Neurodegenerative Diseases/immunology/pathology; Neuroimmunomodulation/physiology; Random Allocation; RNA; Time Factors
Creator
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Beier Eric E; Neal Matthew; Alam Gelerah; Edler Melissa; Wu Long-Jun; Richardson Jason R
Description
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Inflammation arising from central and/or peripheral sources contributes to the pathogenesis of multiple neurodegenerative diseases including Parkinson's disease (PD). Emerging data suggest that differential activation of glia could lead to the pathogenesis and progression of PD. Here, we sought to determine the relationship between lipopolysaccharide (LPS) treatment, loss of dopaminergic neurons and differential activation of glia. Using a model of repeated injections with LPS (1mg/kg, i.p. for 4days), we found that LPS induced a 34% loss of dopamine neurons in the substantia nigra 19days after initiation of treatment, but no further cell loss was observed at 36days. LPS induced a strong pro-inflammatory response with increased mRNA expression of pro-inflammatory markers, including tumor necrosis factor-alpha (4.8-fold), inducible nitric oxide synthase (2.0-fold), interleukin-1 beta (8.9-fold), interleukin-6 (10.7-fold), and robust glial activation were observed at 1day after final dose of LPS. These pro-inflammatory genes were then reduced at 19days after treatment, when there was a rise in the anti-inflammatory genes Ym1 (1.8-fold) and arginase-1 (2.6-fold). Additionally, 36days after the last LPS injection there was a significant increase in interleukin-10 (2.1-fold) expression. The qPCR data results were supported by protein data, including cytokine measurements, western blotting, and immunofluorescence in brain microglia. Taken together, these data demonstrate that progressive neurodegeneration in the substantia nigra following LPS is likely arrested by microglia shifting to an anti-inflammatory phenotype. Thus, strategies to promote resolution of neuroinflammation may be a promising avenue to slow the progressive loss of dopamine neurons in PD.
Identifier
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<a href="http://doi.org/10.1016/j.nbd.2017.08.009" target="_blank" rel="noreferrer noopener">10.1016/j.nbd.2017.08.009</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2017
Alam Gelerah
Animals
Astrocytes/immunology/pathology
Beier Eric E
Cell Death/physiology
Corpus Striatum/immunology/pathology
Cytokines/metabolism
Department of Pharmaceutical Sciences
Disease Progression
Dopaminergic Neurons/*immunology/pathology
Edler Melissa
Inbred C57BL
Inflammation/pathology/physiopathology
Lipopolysaccharides/*toxicity
Male
Messenger/metabolism
Mice
Microglia/*immunology/pathology
Neal Matthew
NEOMED College of Pharmacy
Nerve Degeneration/*immunology/pathology
Neurobiology of disease
Neurodegenerative Diseases/immunology/pathology
Neuroimmunomodulation/physiology
Random Allocation
Richardson Jason R
RNA
Time Factors
Wu Long-Jun