About: Inflammatory monocytes damage the hippocampus during acute picornavirus infection of the brain

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About: Inflammatory monocytes damage the hippocampus during acute picornavirus infection of the brain 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	Inflammatory monocytes damage the hippocampus during acute picornavirus infection of the brain
Creator	Howe, Charles Lafrance, Stephanie Lafrance-Corey, Reghann, G Sundsbak, Rhianna
Source	Medline; PMC
abstract	BACKGROUND: Neuropathology caused by acute viral infection of the brain is associated with the development of persistent neurological deficits. Identification of the immune effectors responsible for injuring the brain during acute infection is necessary for the development of therapeutic strategies that reduce neuropathology but maintain immune control of the virus. METHODS: The identity of brain-infiltrating leukocytes was determined using microscopy and flow cytometry at several acute time points following intracranial infection of mice with the Theiler's murine encephalomyelitis virus. Behavioral consequences of immune cell depletion were assessed by Morris water maze. RESULTS: Inflammatory monocytes, defined as CD45(hi)CD11b(++)F4/80(+)Gr1(+)1A8(-), and neutrophils, defined as CD45(hi)CD11b(+++)F4/80(-)Gr1(+)1A8(+), were found in the brain at 12 h after infection. Flow cytometry of brain-infiltrating leukocytes collected from LysM: GFP reporter mice confirmed the identification of neutrophils and inflammatory monocytes in the brain. Microscopy of sections from infected LysM:GFP mice showed that infiltrating cells were concentrated in the hippocampal formation. Immunostaining confirmed that neutrophils and inflammatory monocytes were localized to the hippocampal formation at 12 h after infection. Immunodepletion of inflammatory monocytes and neutrophils but not of neutrophils only resulted in preservation of hippocampal neurons. Immunodepletion of inflammatory monocytes also preserved cognitive function as assessed by the Morris water maze. CONCLUSIONS: Neutrophils and inflammatory monocytes rapidly and robustly responded to Theiler's virus infection by infiltrating the brain. Inflammatory monocytes preceded neutrophils, but both cell types were present in the hippocampal formation at a timepoint that is consistent with a role in triggering hippocampal pathology. Depletion of inflammatory monocytes and neutrophils with the Gr1 antibody resulted in hippocampal neuroprotection and preservation of cognitive function. Specific depletion of neutrophils with the 1A8 antibody failed to preserve neurons, suggesting that inflammatory monocytes are the key effectors of brain injury during acute picornavirus infection of the brain. These effector cells may be important therapeutic targets for immunomodulatory or immunosuppressive therapies aimed at reducing or preventing central nervous system pathology associated with acute viral infection.
has issue date	2012-03-09(xsd:dateTime)
bibo:doi	10.1186/1742-2094-9-50
bibo:pmid	22405261
has license	cc-by
sha1sum (hex)	6694490cc1353addf66465e4d06419ff0b0af753
schema:url	https://doi.org/10.1186/1742-2094-9-50
resource representing a document's title	Inflammatory monocytes damage the hippocampus during acute picornavirus infection of the brain
has PubMed Central identifier	PMC3368782
has PubMed identifier	22405261
schema:publication	J Neuroinflammation
resource representing a document's body	covid:6694490cc1353addf66465e4d06419ff0b0af753#body_text
is schema:about of	named entity 'BACKGROUND' named entity 'ACUTE INFECTION' named entity 'NEUROPATHOLOGY' named entity '27S' named entity 'IMMUNE CONTROL' named entity 'IMMUNE CELL' named entity 'NECESSARY' named entity 'MURINE ENCEPHALOMYELITIS VIRUS' named entity 'BRAIN' named entity 'NEUROLOGICAL' named entity 'PERSISTENT' named entity 'USING' named entity 'IDENTIFICATION' named entity 'BEHAVIORAL' named entity 'MICROSCOPY' named entity 'therapeutic' named entity 'consequences' named entity 'virus' named entity 'mice' named entity 'strategies' named entity 'Methods' named entity 'THE BRAIN' named entity 'INFILTRATING' named entity 'THERAPEUTIC' named entity 'MAINTAIN' named entity 'DEFICITS' named entity 'REDUCE' named entity 'DEVELOPMENT' named entity 'ACUTE' named entity 'RESPONSIBLE' named entity 'INJURING' named entity 'VIRAL INFECTION' named entity 'MICE' named entity 'METHODS' named entity 'HIPPOCAMPUS' named entity 'INFLAMMATORY' named entity 'ACUTE' named entity 'PICORNAVIRUS INFECTION' named entity 'MONOCYTES' named entity 'THE BRAIN' named entity 'CONSEQUENCES' named entity 'BUT' named entity 'ASSESSED' named entity 'DEPLETION' named entity 'POINTS' named entity 'MORRIS WATER MAZE' named entity 'DAMAGE' named entity 'INTRACRANIAL INFECTION' named entity 'VIRUS' named entity 'ASSOCIATED WITH' named entity 'IDENTITY' named entity 'FOLLOWING' named entity 'FLOW CYTOMETRY' named entity 'IMMUNE' named entity 'LEUKOCYTES' named entity 'STRATEGIES' named entity 'DETERMINED' named entity 'CAUSED BY' named entity 'TIME' covid:arg/6694490cc1353addf66465e4d06419ff0b0af753 named entity 'persistent' named entity 'leukocytes' named entity 'acute' named entity 'flow cytometry' named entity 'caused' named entity 'microscopy' named entity 'mice' named entity 'flow cytometry' named entity 'virus' named entity 'viral infection of the brain' named entity 'picornavirus' named entity 'GFP' named entity 'hpi' named entity 'RPMI' named entity 'BILs' named entity 'monocytes' named entity 'perfusion'

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