RT Journal Article
T1 Microglia activated by microbial neuraminidase contributes to ependymal cell death.
A1 Fernández-Arjona, María del Mar
A1 León-Rodríguez, Ana
A1 López-Ávalos, María  Dolores
A1 Mateos-Grondona, Jesús
K1 Sistema nervioso - Inflamación
K1 Monosacáridos
K1 Neuroglia
K1 Células - Muerte
AB The administration of microbial neuraminidase into the brain ventricular cavities of rodents represents a model ofacute aseptic neuroinflammation. Ependymal cell death and hydrocephalus are unique features of this model. Herewe demonstrate that activated microglia participates in ependymal cell death. Co-cultures of pure microglia withependymal cells (both obtained from rats) were performed, and neuraminidase or lipopolysaccharide were usedto activate microglia. Ependymal cell viability was unaltered in the absence of microglia or inflammatory stimulus(neuraminidase or lipopolysaccharide). The constitutive expression by ependymal cells of receptors for cytokinesreleased by activated microglia, such as IL-1β, was demonstrated by qPCR. Besides, neuraminidase induced the overexpressionof both receptors in ventricular wall explants. Finally, ependymal viability was evaluated in the presence offunctional blocking antibodies against IL-1β and TNFα. In the co-culture setting, an IL-1β blocking antibody preventedependymal cell death, while TNFα antibody did not. These results suggest that activated microglia are involved in theependymal damage that occurs after the administration of neuraminidase in the ventricular cavities, and points toIL-1β as possible mediator of such effect. The relevance of these results lies in the fact that brain infections caused byneuraminidase-bearing pathogens are frequently associated to ependymal death and hydrocephalus.
PB Springer Nature
YR 2021
FD 2021-03-23
LK https://hdl.handle.net/10630/35273
UL https://hdl.handle.net/10630/35273
LA eng
NO 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
NO This work was carried out with funding from: Ministerio de Economía yCompetitividad (SAF2010-19087), Consejería de Innovación Ciencia y Empleo,Junta de Andalucía (P11-CVI-07637), and Ministerio de Economía, Industriay Competitividad (MINECO, SAF2017-83645). Publication in open access wassupported by Universidad de Malaga.
DS RIUMA. Repositorio Institucional de la Universidad de Málaga
RD 20 ene 2026