<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-05-29T21:15:23Z</responseDate><request verb="GetRecord" identifier="oai:riuma.uma.es:10630/35273" metadataPrefix="qdc">https://riuma.uma.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:riuma.uma.es:10630/35273</identifier><datestamp>2026-02-03T11:29:00Z</datestamp><setSpec>com_10630_2254</setSpec><setSpec>col_10630_37953</setSpec></header><metadata><qdc:qualifieddc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:qdc="http://dspace.org/qualifieddc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://purl.org/dc/elements/1.1/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dc.xsd http://purl.org/dc/terms/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dcterms.xsd http://dspace.org/qualifieddc/ http://www.ukoln.ac.uk/metadata/dcmi/xmlschema/qualifieddc.xsd">
   <dc:title>Microglia activated by microbial neuraminidase contributes to ependymal cell death.</dc:title>
   <dc:creator>Fernández-Arjona, María del Mar</dc:creator>
   <dc:creator>León-Rodríguez, Ana</dc:creator>
   <dc:creator>López-Ávalos, María  Dolores</dc:creator>
   <dc:creator>Mateos-Grondona, Jesús</dc:creator>
   <dc:subject>Sistema nervioso - Inflamación</dc:subject>
   <dc:subject>Monosacáridos</dc:subject>
   <dc:subject>Neuroglia</dc:subject>
   <dc:subject>Células - Muerte</dc:subject>
   <dcterms:abstract>The administration of microbial neuraminidase into the brain ventricular cavities of rodents represents a model of&#xd;
acute aseptic neuroinflammation. Ependymal cell death and hydrocephalus are unique features of this model. Here&#xd;
we demonstrate that activated microglia participates in ependymal cell death. Co-cultures of pure microglia with&#xd;
ependymal cells (both obtained from rats) were performed, and neuraminidase or lipopolysaccharide were used&#xd;
to activate microglia. Ependymal cell viability was unaltered in the absence of microglia or inflammatory stimulus&#xd;
(neuraminidase or lipopolysaccharide). The constitutive expression by ependymal cells of receptors for cytokines&#xd;
released by activated microglia, such as IL-1β, was demonstrated by qPCR. Besides, neuraminidase induced the overexpression&#xd;
of both receptors in ventricular wall explants. Finally, ependymal viability was evaluated in the presence of&#xd;
functional blocking antibodies against IL-1β and TNFα. In the co-culture setting, an IL-1β blocking antibody prevented&#xd;
ependymal cell death, while TNFα antibody did not. These results suggest that activated microglia are involved in the&#xd;
ependymal damage that occurs after the administration of neuraminidase in the ventricular cavities, and points to&#xd;
IL-1β as possible mediator of such effect. The relevance of these results lies in the fact that brain infections caused by&#xd;
neuraminidase-bearing pathogens are frequently associated to ependymal death and hydrocephalus.</dcterms:abstract>
   <dcterms:dateAccepted>2024-11-25T09:51:10Z</dcterms:dateAccepted>
   <dcterms:available>2024-11-25T09:51:10Z</dcterms:available>
   <dcterms:created>2024-11-25T09:51:10Z</dcterms:created>
   <dcterms:issued>2021-03-23</dcterms:issued>
   <dc:type>journal article</dc:type>
   <dc:identifier>Fernández-Arjona, M.d., León-Rodríguez, A., López-Ávalos, M.D. et al. Microglia activated by microbial neuraminidase contributes to ependymal cell death. Fluids Barriers CNS 18, 15 (2021). https://doi.org/10.1186/s12987-021-00249-0</dc:identifier>
   <dc:identifier>https://hdl.handle.net/10630/35273</dc:identifier>
   <dc:identifier>10.1186/s12987-021-00249-0</dc:identifier>
   <dc:language>eng</dc:language>
   <dc:rights>http://creativecommons.org/licenses/by/4.0/</dc:rights>
   <dc:rights>open access</dc:rights>
   <dc:rights>Attribution 4.0 Internacional</dc:rights>
   <dc:publisher>Springer Nature</dc:publisher>
</qdc:qualifieddc>
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