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                  <mods:namePart>Fernández-Arjona, María del Mar</mods:namePart>
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                  <mods:namePart>León-Rodríguez, Ana</mods:namePart>
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                  <mods:namePart>López-Ávalos, María  Dolores</mods:namePart>
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                  <mods:namePart>Mateos-Grondona, Jesús</mods:namePart>
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               <mods:identifier type="citation">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</mods:identifier>
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               <mods:identifier type="doi">10.1186/s12987-021-00249-0</mods:identifier>
               <mods: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.</mods:abstract>
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               <mods:accessCondition type="useAndReproduction">Attribution 4.0 Internacional</mods:accessCondition>
               <mods:subject>
                  <mods:topic>Sistema nervioso - Inflamación</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Monosacáridos</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Neuroglia</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Células - Muerte</mods:topic>
               </mods:subject>
               <mods:titleInfo>
                  <mods:title>Microglia activated by microbial neuraminidase contributes to ependymal cell death.</mods:title>
               </mods:titleInfo>
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