Cited by 68Neuroinflammation and Neurodegeneration MechanismsPain Mechanisms and TreatmentsNeuroscience and Neuropharmacology Research

Influence of neurons on lipopolysaccharide-stimulated production of nitric oxide and tumor necrosis factor-α by cultured glia

Chang, Raymond C.C., Hudson, Pearlie, Wilson, Belinda, Haddon, Lisa, Hong, Jau-Shyong·2000·Brain Research

Abstract

Cerebral inflammation often originates in a region where neuronal death occurs and thereafter slowly spreads outward. This study aimed to elucidate the roles of neurons in modulating the production of inflammatory factors stimulated by the bacterial endotoxin lipopolysaccharide (LPS). Culturing neurons with mixed glia reduced nitrite and tumor necrosis factor-alpha (TNF-alpha) production compared to cultures with only mixed glia, and shifted the dose-response curve to the right. The decreased nitrite and TNF-alpha production were not due to the cytotoxicity of LPS. Immunocytochemical analysis of glia-neuron co-cultures revealed the morphological changes in the activated microglia. Culturing PC12 cells with rat mixed-glia also reduced nitrite production. The influence of neurons on glial inflammation was partly due to the cell-cell contacts between neurons and glia via neural cell adhesion molecules (NCAM) because NCAM significantly reduced LPS-stimulated nitrite production. These results demonstrate that neurons reduce the production of inflammatory factors by glia. Since cerebral inflammation is important in many neurological disorders, this study might provide insight about the role of glia-neuron interactions in inflammatory responses in the brain.

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Registry

Crossref · 10.1016/s0006-8993(99)02255-6

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27 of 27 references verified0 citation errors · 0 not checkable

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  • Immunomodulators including CX3CL1, CD200, CD22, CD47, CD95, and neural cell adhesion molecule sustain the rest state of microglia under normal conditions.

    “Immunomodulators, including the CX3CL1, CD200, CD22, CD47, CD95, and neural cell adhesion molecule, sustain the rest state of microglia under normal conditions (Chang et al., 2000; Sheridan and Murphy, 2013).”

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Authors
Chang, R. C. C., Hudson, P., Wilson, B., Haddon, L., & Hong, J.-S.
Affiliations
National Institutes of Health (US)
Corresponding author
Hong, Jau-Shyong
Venue
Brain Research
Publisher
Elsevier BV
Published
2000-01
Volume
853
Issue
2
Pages
236-244
ISSN
0006-8993 (ISSN-L)
OpenAlex
W2050094645
Cited by
68
References
27
Citations by year
2025: 2 · 2024: 4 · 2023: 3 · 2022: 2 · 2021: 2 · 2020: 1 · 2018: 2 · 2017: 4 · 2016: 2 · 2015: 4 · 2013: 6 · 2012: 2
FWCI
2.77
Type
journal article
Language
en
Open access
closed
Locations
  • Brain Research (publishedVersion)
  • PubMed (publishedVersion)
  • The HKU Scholars Hub (University of Hong Kong) (submittedVersion)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
neuron-glia interactions, lipopolysaccharide, nitric oxide, TNF-α, microglial activation, neuroinflammation, CD56, PC12 cells, neuroprotection
MeSH terms
Animals, Animals, Newborn, Cell Communication, Cells, Cultured, Dose-Response Relationship, Drug, Inflammation, L-Lactate Dehydrogenase, Lipopolysaccharides, Neuroglia, Neurons, Nitric Oxide, Rats, Inbred F344, Tumor Necrosis Factor-alpha, Down-Regulation, PC12 Cells, Coculture Techniques, Nitric Oxide Synthase, Neural Cell Adhesion Molecules, Cell Size, Mice, Rats, Nitric Oxide Synthase Type II

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