2026-06-14T03:42:09Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/182942024-11-28T15:15:58Zcom_20.500.12105_15322com_20.500.12105_2051col_20.500.12105_16927
Repisalud
author
Fernández-Arjona, María Del Mar
author
León-Rodríguez, Ana
author
López-Ávalos, María Dolores
author
Grondona, Jesús M.
authoraffiliation
[Fernández-Arjona,MDM; León-Rodríguez,A; López-Ávalos,MD; Grondona,JM] Laboratorio de Fisiología Animal, Departamento de Biología Celular, Genética y Fisiología, Facultad de Ciencias, Universidad de Málaga, Instituto de Investigación Biomédica de Málaga-IBIMA, Málaga, Spain.
2024-02-19T15:26:38Z
2024-02-19T15:26:38Z
2021-03-23
10.1186/s12987-021-00249-0
2045-8118
Fluids and Barriers of the CNS
http://hdl.handle.net/10668/3941
33757539
http://hdl.handle.net/20.500.12105/18294
The administration of microbial neuraminidase into the brain ventricular cavities of rodents represents a model of acute aseptic neuroinflammation. Ependymal cell death and hydrocephalus are unique features of this model. Here we demonstrate that activated microglia participates in ependymal cell death. Co-cultures of pure microglia with ependymal cells (both obtained from rats) were performed, and neuraminidase or lipopolysaccharide were used to 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 cytokines released by activated microglia, such as IL-1β, was demonstrated by qPCR. Besides, neuraminidase induced the overexpression of both receptors in ventricular wall explants. Finally, ependymal viability was evaluated in the presence of functional blocking antibodies against IL-1β and TNFα. In the co-culture setting, an IL-1β blocking antibody prevented ependymal cell death, while TNFα antibody did not. These results suggest that activated microglia are involved in the ependymal damage that occurs after the administration of neuraminidase in the ventricular cavities, and points to IL-1β as possible mediator of such effect. The relevance of these results lies in the fact that brain infections caused by neuraminidase-bearing pathogens are frequently associated to ependymal death and hydrocephalus.
eng
Microglia
Ependyma
Neuraminidase
Sialic acid
Neuroinfammation
Interleukin-1β
Rats
Microglía
Epéndimo
Neuraminidasa
Ácido N-Acetilneuramínico
Ratas
Microglia activated by microbial neuraminidase contributes to ependymal cell death
research article