About: Inflammation and primary demyelination induced by the intraspinal injection of lipopolysaccharide

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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	Inflammation and primary demyelination induced by the intraspinal injection of lipopolysaccharide
Creator	Smith, Kenneth Asquith, Stephen Felts, Paul Fernando, Himali Gregson, Norman Mizzi, Oliver Woolston, Anne-Marie
Source	PMC
abstract	Inflammation is a prominent feature of several disorders characterized by primary demyelination, but it is not clear whether a relationship exists between inflammation and myelin damage. We have found that substantial demyelination results from the focal inflammatory lesion caused by the injection of lipopolysaccharide (LPS; 200 ng) directly into the rat dorsal funiculus. Within 24 h, such injections caused a focal inflammatory response consisting of a substantial number of polymorphonuclear cells and ED1-positive and inducible nitric oxide synthase (iNOS)-positive macrophages/microglia. The number of inflammatory cells was substantially reduced by day 7. OX-52-positive T-cells were less frequently observed but were present in the meninges at 8 h, reached a maximum in the dorsal funiculus at 7 days, and were rare at 14 days. The inflammation was followed by the appearance of a large lesion of primary demyelination that encompassed up to ∼75% of the cross-sectional area of the dorsal funiculus. Treatment with dexamethasone significantly reduced the number of cells expressing iNOS, but did not prevent the demyelination. By 28 days the lesions were largely remyelinated, usually by Schwann cells. These changes were not observed in control, saline-injected animals. We conclude that the intraspinal injection of LPS results in inflammation and subsequently in prominent demyelination. The mechanisms underlying the demyelination are not clear, but it is notable that it typically begins with disruption of the adaxonal myelin. Indeed, there is an early loss of myelin-associated glycoprotein within the lesion, despite the persistence of proteolipid protein. This combination is a feature of the pattern III lesion recently described in multiple sclerosis (Lucchinetti et al., 2000), and we therefore suggest that LPS-induced demyelination may serve as the first experimental model available for the study of this type of multiple sclerosis lesion.
has issue date	2005-05-04(xsd:dateTime)
bibo:doi	10.1093/brain/awh516
bibo:pmid	15872019
has license	no-cc
sha1sum (hex)	97a9e3baea51f98bf86d442616d998d328997b6b
schema:url	https://doi.org/10.1093/brain/awh516
resource representing a document's title	Inflammation and primary demyelination induced by the intraspinal injection of lipopolysaccharide
has PubMed Central identifier	PMC7109778
has PubMed identifier	15872019
schema:publication	Brain
resource representing a document's body	covid:97a9e3baea51f98bf86d442616d998d328997b6b#body_text
is schema:about of	named entity 'focal' named entity 'inflammatory cells' named entity 'LPS' named entity 'demyelination' named entity 'PRIMARY DEMYELINATION' named entity 'DAY 7' named entity 'III' named entity 'CLEAR' named entity '2000' named entity 'DIRECTLY' named entity 'INTRASPINAL' named entity 'DAMAGE' named entity 'DORSAL FUNICULUS' named entity 'FEATURE' named entity 'DISORDERS' named entity 'CROSS-SECTIONAL AREA' named entity 'INJECTIONS' named entity 'MECHANISMS' named entity 'INDUCIBLE NITRIC OXIDE SYNTHASE' named entity 'PRESENT' named entity 'RESULTS' named entity 'NOT OBSERVED' named entity 'UNDERLYING' named entity 'PROTEOLIPID' named entity 'CONCLUDE' named entity 'MAXIMUM' covid:arg/97a9e3baea51f98bf86d442616d998d328997b6b named entity 'ANIMALS' named entity 'DEMYELINATION' named entity 'INFLAMMATION' named entity 'INJECTION' named entity 'INDUCED' named entity 'PREVENT' named entity 'COMBINATION' named entity 'NUMBER OF' named entity 'LESION' named entity 'LIPOPOLYSACCHARIDE' named entity 'INTRASPINAL' named entity 'INFLAMMATORY RESPONSE' named entity 'TYPE' named entity 'TREATMENT' named entity 'THESE' named entity 'OBSERVED' named entity 'ED1' named entity 'AVAILABLE' named entity 'LPS' named entity 'INFLAMMATORY CELLS' named entity 'USUALLY' named entity 'MYELIN' named entity '200' named entity 'FOLLOWED BY' named entity 'LIPOPOLYSACCHARIDE' named entity 'HAVE' named entity 'MACROPHAGES' named entity 'PRIMARY DEMYELINATION' named entity 'POLYMORPHONUCLEAR CELLS' named entity 'FUNICULUS ' named entity 'LARGE' named entity 'INFLAMMATORY LESION' named entity 'CHANGES' named entity 'SUGGEST' named entity 'SCHWANN CELLS' named entity 'APPEARANCE' named entity 'FOCAL' named entity 'INDUCED' named entity 'FREQUENTLY' named entity 'RELATIONSHIP' named entity 'REDUCED' named entity 'LOSS OF MYELIN' named entity 'FOUND' named entity 'DISRUPTION' named entity 'MULTIPLE SCLEROSIS LESION' named entity 'INOS' named entity 'POSITIVE' named entity 'MENINGES'

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