About: Neuronal CCL2 expression drives inflammatory monocyte infiltration into the brain during acute virus infection

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About: Neuronal CCL2 expression drives inflammatory monocyte infiltration into the brain during acute virus infection Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Neuronal CCL2 expression drives inflammatory monocyte infiltration into the brain during acute virus infection
Creator	Mirchia, Kanish Goddery, Emma Howe, Charles Johnson, Renee Lafrance-Corey, Reghann
topic	covid:5e85184d2ba432306c3c21f22113aa590b09fe89#this
Source	Medline; PMC
abstract	BACKGROUND: Viral encephalitis is a dangerous compromise between the need to robustly clear pathogen from the brain and the need to protect neurons from bystander injury. Theiler’s murine encephalomyelitis virus (TMEV) infection of C57Bl/6 mice is a model of viral encephalitis in which the compromise results in hippocampal damage and permanent neurological sequelae. We previously identified brain-infiltrating inflammatory monocytes as the primary driver of this hippocampal pathology, but the mechanisms involved in recruiting these cells to the brain were unclear. METHODS: Chemokine expression levels in the hippocampus were assessed by microarray, ELISA, RT-PCR, and immunofluorescence. Monocyte infiltration during acute TMEV infection was measured by flow cytometry. CCL2 levels were manipulated by immunodepletion and by specific removal from neurons in mice generated by crossing a line expressing the Cre recombinase behind the synapsin promoter to animals with floxed CCL2. RESULTS: Inoculation of the brain with TMEV induced hippocampal production of the proinflammatory chemokine CCL2 that peaked at 6 h postinfection, whereas inoculation with UV-inactivated TMEV did not elicit this response. Immunofluorescence revealed that hippocampal neurons expressed high levels of CCL2 at this timepoint. Genetic deletion of CCR2 and systemic immunodepletion of CCL2 abrogated or blunted the infiltration of inflammatory monocytes into the brain during acute infection. Specific genetic deletion of CCL2 from neurons reduced serum and hippocampal CCL2 levels and inhibited inflammatory monocyte infiltration into the brain. CONCLUSIONS: We conclude that intracranial inoculation with infectious TMEV rapidly induces the expression of CCL2 in neurons, and this cellular source is necessary for CCR2-dependent infiltration of inflammatory monocytes into the brain during the most acute stage of encephalitis. These findings highlight a unique role for neuronal production of chemokines in the initiation of leukocytic infiltration into the infected central nervous system.
has issue date	2017-12-04(xsd:dateTime)
bibo:doi	10.1186/s12974-017-1015-2
bibo:pmid	29202854
has license	cc-by
sha1sum (hex)	5e85184d2ba432306c3c21f22113aa590b09fe89
schema:url	https://doi.org/10.1186/s12974-017-1015-2
resource representing a document's title	Neuronal CCL2 expression drives inflammatory monocyte infiltration into the brain during acute virus infection
has PubMed Central identifier	PMC5715496
has PubMed identifier	29202854
schema:publication	J Neuroinflammation
resource representing a document's body	covid:5e85184d2ba432306c3c21f22113aa590b09fe89#body_text
is http://vocab.deri.ie/void#inDataset of	proxy:http/ns.inria.fr/covid19/5e85184d2ba432306c3c21f22113aa590b09fe89
is schema:about of	named entity 'C57Bl/6' named entity 'hippocampal' named entity 'CCL2' named entity 'brain' named entity 'model' named entity 'inflammatory' covid:arg/5e85184d2ba432306c3c21f22113aa590b09fe89 named entity 'damage' named entity 'Monocyte' named entity 'neurons' named entity 'monocytes' named entity 'promoter' named entity 'TMEV' named entity 'hippocampus' named entity 'floxed' named entity 'infection' named entity 'microarray' named entity 'RT-PCR' named entity 'CCL2' named entity 'flow cytometry' named entity 'infection' named entity 'Cre recombinase' named entity 'CCL2' named entity 'neurological' named entity 'CCL2' named entity 'Ccl2' named entity 'knockout model' named entity 'CCL2' named entity 'monocyte' named entity 'downregulated' named entity 'CCL2' named entity 'biosynthesis' named entity 'Ccl2' named entity 'CCL2' named entity 'serum' named entity 'CD45' named entity 'neurons' named entity 'infection' named entity 'neuron' named entity 'serum' named entity 'ligand' named entity 'electrophysiological' named entity 'CCL2' named entity 'Brain tissue' named entity 'PBS' named entity 'CCL2' named entity 'pyramidal neuron' named entity 'CCL2' named entity 'monocyte' named entity 'CCL2' named entity 'mice' named entity 'hippocampal' named entity 'wildtype' named entity 'CD11b' named entity 'RNA' named entity 'CCR2' named entity 'neurological' named entity 'monocyte' named entity 'sub-clinical' named entity 'neuron' named entity 'mice' named entity 'hpi' named entity 'TMEV' named entity 'lymphocyte' named entity 'monocyte' named entity 'one-way ANOVA' named entity 'homogenate' named entity 'Shapiro-Wilk test' named entity 'PCR' named entity 'National Institutes of Health' named entity 'inflammation' named entity 'infection' named entity 'CCL2' named entity 'knockout mice' named entity 'ligand'

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