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- Publisher Website: 10.1016/S0006-8993(99)02255-6
- Scopus: eid_2-s2.0-0033987949
- PMID: 10640621
- WOS: WOS:000085194700008
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Article: Influence of neurons on lipopolysaccharide-stimulated production of nitric oxide and tumor necrosis factor-α by cultured glia
Title | Influence of neurons on lipopolysaccharide-stimulated production of nitric oxide and tumor necrosis factor-α by cultured glia |
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Authors | |
Keywords | Astrocyte Cerebral inflammation Lipopolysaccharide Microglia Neural cell adhesion molecule Neuron-glia interaction |
Issue Date | 2000 |
Publisher | Elsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainres |
Citation | Brain Research, 2000, v. 853 n. 2, p. 236-244 How to Cite? |
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-α (TNF-α) production compared to cultures with only mixed glia, and shifted the dose-response curve to the right. The decreased nitrite and TNF-α 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. Copyright (C) 2000 Elsevier Science B.V. |
Persistent Identifier | http://hdl.handle.net/10722/149589 |
ISSN | 2021 Impact Factor: 3.610 2020 SCImago Journal Rankings: 1.037 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Chang, RCC | en_US |
dc.contributor.author | Hudson, P | en_US |
dc.contributor.author | Wilson, B | en_US |
dc.contributor.author | Haddon, L | en_US |
dc.contributor.author | Hong, JS | en_US |
dc.date.accessioned | 2012-06-26T05:55:39Z | - |
dc.date.available | 2012-06-26T05:55:39Z | - |
dc.date.issued | 2000 | en_US |
dc.identifier.citation | Brain Research, 2000, v. 853 n. 2, p. 236-244 | en_US |
dc.identifier.issn | 0006-8993 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/149589 | - |
dc.description.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-α (TNF-α) production compared to cultures with only mixed glia, and shifted the dose-response curve to the right. The decreased nitrite and TNF-α 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. Copyright (C) 2000 Elsevier Science B.V. | en_US |
dc.language | eng | en_US |
dc.publisher | Elsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainres | en_US |
dc.relation.ispartof | Brain Research | en_US |
dc.subject | Astrocyte | - |
dc.subject | Cerebral inflammation | - |
dc.subject | Lipopolysaccharide | - |
dc.subject | Microglia | - |
dc.subject | Neural cell adhesion molecule | - |
dc.subject | Neuron-glia interaction | - |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Animals, Newborn | en_US |
dc.subject.mesh | Cell Communication - Drug Effects | en_US |
dc.subject.mesh | Cell Size - Drug Effects | en_US |
dc.subject.mesh | Cells, Cultured | en_US |
dc.subject.mesh | Coculture Techniques | en_US |
dc.subject.mesh | Dose-Response Relationship, Drug | en_US |
dc.subject.mesh | Down-Regulation | en_US |
dc.subject.mesh | Inflammation - Chemically Induced - Metabolism | en_US |
dc.subject.mesh | L-Lactate Dehydrogenase - Secretion | en_US |
dc.subject.mesh | Lipopolysaccharides - Pharmacology | en_US |
dc.subject.mesh | Mice | en_US |
dc.subject.mesh | Neural Cell Adhesion Molecules - Metabolism - Pharmacology | en_US |
dc.subject.mesh | Neuroglia - Cytology - Drug Effects - Enzymology | en_US |
dc.subject.mesh | Neurons - Cytology - Metabolism | en_US |
dc.subject.mesh | Nitric Oxide - Biosynthesis | en_US |
dc.subject.mesh | Nitric Oxide Synthase - Metabolism | en_US |
dc.subject.mesh | Nitric Oxide Synthase Type Ii | en_US |
dc.subject.mesh | Pc12 Cells | en_US |
dc.subject.mesh | Rats | en_US |
dc.subject.mesh | Rats, Inbred F344 | en_US |
dc.subject.mesh | Tumor Necrosis Factor-Alpha - Biosynthesis | en_US |
dc.title | Influence of neurons on lipopolysaccharide-stimulated production of nitric oxide and tumor necrosis factor-α by cultured glia | en_US |
dc.type | Article | en_US |
dc.identifier.email | Chang, RCC:rccchang@hkucc.hku.hk | en_US |
dc.identifier.authority | Chang, RCC=rp00470 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1016/S0006-8993(99)02255-6 | en_US |
dc.identifier.pmid | 10640621 | - |
dc.identifier.scopus | eid_2-s2.0-0033987949 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0033987949&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 853 | en_US |
dc.identifier.issue | 2 | en_US |
dc.identifier.spage | 236 | en_US |
dc.identifier.epage | 244 | en_US |
dc.identifier.isi | WOS:000085194700008 | - |
dc.publisher.place | Netherlands | en_US |
dc.identifier.scopusauthorid | Chang, RCC=7403713410 | en_US |
dc.identifier.scopusauthorid | Hudson, P=35566903000 | en_US |
dc.identifier.scopusauthorid | Wilson, B=35243580200 | en_US |
dc.identifier.scopusauthorid | Haddon, L=6602252253 | en_US |
dc.identifier.scopusauthorid | Hong, JS=34770185100 | en_US |
dc.identifier.issnl | 0006-8993 | - |