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

TitleInfluence of neurons on lipopolysaccharide-stimulated production of nitric oxide and tumor necrosis factor-α by cultured glia
Authors
Issue Date2000
PublisherElsevier 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?
AbstractCerebral 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 Identifierhttp://hdl.handle.net/10722/149589
ISSN
2015 Impact Factor: 2.561
2015 SCImago Journal Rankings: 1.351
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChang, RCCen_US
dc.contributor.authorHudson, Pen_US
dc.contributor.authorWilson, Ben_US
dc.contributor.authorHaddon, Len_US
dc.contributor.authorHong, JSen_US
dc.date.accessioned2012-06-26T05:55:39Z-
dc.date.available2012-06-26T05:55:39Z-
dc.date.issued2000en_US
dc.identifier.citationBrain Research, 2000, v. 853 n. 2, p. 236-244en_US
dc.identifier.issn0006-8993en_US
dc.identifier.urihttp://hdl.handle.net/10722/149589-
dc.description.abstractCerebral 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.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainresen_US
dc.relation.ispartofBrain Researchen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnimals, Newbornen_US
dc.subject.meshCell Communication - Drug Effectsen_US
dc.subject.meshCell Size - Drug Effectsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCoculture Techniquesen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshDown-Regulationen_US
dc.subject.meshInflammation - Chemically Induced - Metabolismen_US
dc.subject.meshL-Lactate Dehydrogenase - Secretionen_US
dc.subject.meshLipopolysaccharides - Pharmacologyen_US
dc.subject.meshMiceen_US
dc.subject.meshNeural Cell Adhesion Molecules - Metabolism - Pharmacologyen_US
dc.subject.meshNeuroglia - Cytology - Drug Effects - Enzymologyen_US
dc.subject.meshNeurons - Cytology - Metabolismen_US
dc.subject.meshNitric Oxide - Biosynthesisen_US
dc.subject.meshNitric Oxide Synthase - Metabolismen_US
dc.subject.meshNitric Oxide Synthase Type Iien_US
dc.subject.meshPc12 Cellsen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred F344en_US
dc.subject.meshTumor Necrosis Factor-Alpha - Biosynthesisen_US
dc.titleInfluence of neurons on lipopolysaccharide-stimulated production of nitric oxide and tumor necrosis factor-α by cultured gliaen_US
dc.typeArticleen_US
dc.identifier.emailChang, RCC:rccchang@hkucc.hku.hken_US
dc.identifier.authorityChang, RCC=rp00470en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0006-8993(99)02255-6en_US
dc.identifier.pmid10640621-
dc.identifier.scopuseid_2-s2.0-0033987949en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033987949&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume853en_US
dc.identifier.issue2en_US
dc.identifier.spage236en_US
dc.identifier.epage244en_US
dc.identifier.isiWOS:000085194700008-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridChang, RCC=7403713410en_US
dc.identifier.scopusauthoridHudson, P=35566903000en_US
dc.identifier.scopusauthoridWilson, B=35243580200en_US
dc.identifier.scopusauthoridHaddon, L=6602252253en_US
dc.identifier.scopusauthoridHong, JS=34770185100en_US

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