ArticleNeurobiology of disease2017
Alternative microglial activation is associated with cessation of progressive dopamine neuron loss in mice systemically administered lipopolysaccharide.
Article in Neurobiology of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 72 citations in OpenAlex.
- IL-33 Regulates the Phenotypic Transformation of Reactive Astrocytes via PENK-ERK/MAPK Pathway in Parkinson's Disease.Neuroscience bulletin · 2026Article
- Prostaglandin signaling drives peripheral inflammation-induced reduction of hypothalamic oxytocin-positive neurons.Cellular and molecular life sciences : CMLS · 2026Article
- O-GlcNAcylation regulates microglial neuroinflammation in Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Galectin-3 as a Key Driver of Neuroinflammation and α-Synuclein Aggregation in Parkinson's Disease: Unlocking New Paths for Biomarkers and Therapies.Cell biochemistry and biophysics · 2026Review
- Microparticles Mediate Lipopolysaccharide-induced Inflammation and Chronic Pain in Mouse Model.Neuromolecular medicine · 2024Article
- Systemic inflammation accelerates neurodegeneration in a rat model of Parkinson's disease overexpressing human alpha synuclein.NPJ Parkinson's disease · 2024Article
- Nuclear GAPDH in cortical microglia mediates cellular stress-induced cognitive inflexibility.Molecular psychiatry · 2024Article
- Helicobacter pylori infection and Parkinson's Disease: etiology, pathogenesis and levodopa bioavailability.Immunity & ageing : I & A · 2024Review
- Fecal microbiota transplantation and short-chain fatty acids protected against cognitive dysfunction in a rat model of chronic cerebral hypoperfusion.CNS neuroscience & therapeutics · 2023Article
- Mitochondrial dynamics in macrophages: divide to conquer or unite to survive?Biochemical Society transactions · 2023Article
- Voltage-Gated Proton Channel Hv1 Regulates Neuroinflammation and Dopaminergic Neurodegeneration in Parkinson's Disease Models.Antioxidants (Basel, Switzerland) · 2023Article
- Characterization of Lipopolysaccharide Effects on LRRK2 Signaling in RAW Macrophages.International journal of molecular sciences · 2023Article
- Regulation of microglia function by neural stem cells.Frontiers in cellular neuroscience · 2023Review
- Lipopolysaccharide mouse models for Parkinson's disease research: a critical appraisal.Neural regeneration research · 2022Review
- Enhanced M-CSF/CSF1R Signaling Closely Associates with PrPMolecular neurobiology · 2022Article
- High mobility group box 1 (HMGB1) inhibition attenuates lipopolysaccharide-induced cognitive dysfunction and sickness-like behavior in mice.Immunologic research · 2022Article
- Nilotinib modulates LPS-induced cognitive impairment and neuroinflammatory responses by regulating P38/STAT3 signaling.Journal of neuroinflammation · 2022Article
- Neuroinflammation in neurodegenerationFrontiers in immunology · 2022Review
- Phosphorylated α-synuclein aggregated in Schwann cells exacerbates peripheral neuroinflammation and nerve dysfunction in Parkinson's disease through TLR2/NF-κB pathway.Cell death discovery · 2021Article
- Inflammatory neuronal loss in the substantia nigra induced by systemic lipopolysaccharide is prevented by knockout of the P2YJournal of neuroinflammation · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
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-α (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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.