About: Induced CNS expression of CXCL1 augments neurologic disease in a murine model of multiple sclerosis via enhanced neutrophil recruitment

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About: Induced CNS expression of CXCL1 augments neurologic disease in a murine model of multiple sclerosis via enhanced neutrophil recruitment 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	Induced CNS expression of CXCL1 augments neurologic disease in a murine model of multiple sclerosis via enhanced neutrophil recruitment
Creator	Worne, Colleen Marro, Brett Skinner, Dominic Doty, Daniel Fujinami, Robert Grist, Jonathan Lane, Thomas Syage, Amber
topic	covid:d06c36f9ef81b72f1bdad04a8fd4579d0016c2e9#this
Source	PMC
abstract	Increasing evidence points to an important role for neutrophils in participating in the pathogenesis of the human demyelinating disease MS and the animal model EAE. Therefore, a better understanding of the signals controlling migration of neutrophils as well as evaluating the role of these cells in demyelination is important to define cellular components that contribute to disease in MS patients. In this study, we examined the functional role of the chemokine CXCL1 in contributing to neuroinflammation and demyelination in EAE. Using transgenic mice in which expression of CXCL1 is under the control of a tetracycline‐inducible promoter active within glial fibrillary acidic protein‐positive cells, we have shown that sustained CXCL1 expression within the CNS increased the severity of clinical and histologic disease that was independent of an increase in the frequency of encephalitogenic Th1 and Th17 cells. Rather, disease was associated with enhanced recruitment of CD11b(+)Ly6G(+) neutrophils into the spinal cord. Targeting neutrophils resulted in a reduction in demyelination arguing for a role for these cells in myelin damage. Collectively, these findings emphasize that CXCL1‐mediated attraction of neutrophils into the CNS augments demyelination suggesting that this signaling pathway may offer new targets for therapeutic intervention.
has issue date	2018-05-16(xsd:dateTime)
bibo:doi	10.1002/eji.201747442
bibo:pmid	29697856
has license	cc-by
sha1sum (hex)	d06c36f9ef81b72f1bdad04a8fd4579d0016c2e9
schema:url	https://doi.org/10.1002/eji.201747442
resource representing a document's title	Induced CNS expression of CXCL1 augments neurologic disease in a murine model of multiple sclerosis via enhanced neutrophil recruitment
has PubMed Central identifier	PMC6033633
has PubMed identifier	29697856
schema:publication	Eur J Immunol
resource representing a document's body	covid:d06c36f9ef81b72f1bdad04a8fd4579d0016c2e9#body_text
is http://vocab.deri.ie/void#inDataset of	proxy:http/ns.inria.fr/covid19/d06c36f9ef81b72f1bdad04a8fd4579d0016c2e9
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