A5034990000- Neuroinflammation and Neurodegeneration Mechanisms
- Tryptophan and brain disorders
- Immune Response and Inflammation
- Stress Responses and Cortisol
- Chemokine receptors and signaling
- Cytokine Signaling Pathways and Interactions
- Neonatal and fetal brain pathology
- Regulation of Appetite and Obesity
- Cerebrospinal fluid and hydrocephalus
- Immune cells in cancer
Universidad de Málaga
2021-2024
Instituto de Investigación Biomédica de Málaga
2021-2024
Andalusian Centre for Nanomedicine and Biotechnology
2024
Abstract Short-term behavioral alterations are associated with infection and aid the recovery from sickness. However, concerns have raised that sustained disturbances after acute neuroinflammation could relate to neurological diseases in long run. We aimed explore medium- long-term rats, using a model based on intracerebroventricular administration of enzyme neuraminidase (NA), which is part some pathogenic bacteria viruses. Neurological assessments were performed 2 10 weeks injection NA,...
Exposure of microglia to an inflammatory environment may lead their priming and exacerbated response future stimuli. Here we aimed explore hypothalamic its consequences on energy balance regulation. A model intracerebroventricular administration neuraminidase (NA, which is present in various pathogens such as influenza virus) was used induce acute neuroinflammation. Evidences primed were observed 3 months after NA injection, namely (1) a heightened located the arcuate nucleus vivo challenge...
Abstract The administration of microbial neuraminidase into the brain ventricular cavities rodents represents a model acute aseptic neuroinflammation. Ependymal cell death and hydrocephalus are unique features this model. Here we demonstrate that activated microglia participates in ependymal death. Co-cultures pure with cells (both obtained from rats) were performed, or lipopolysaccharide used to activate microglia. viability was unaltered absence inflammatory stimulus (neuraminidase...
Abstract In acute neuroinflammation, microglia activate transiently, and return to a resting state later on. However, they may retain immune memory of such event, namely priming. Primed are more sensitive new stimuli develop exacerbated responses, representing risk factor for neurological disorders with an inflammatory component. Strategies control the hyperactivation are, hence, great interest. The receptor colony stimulating 1 (CSF1R), expressed in myeloid cells, is essential viability, so...
Innate immune memory explains the plasticity of responses after repeated stimulation, leading to either enhanced or suppressed responses. This process has been extensively reported in peripheral cells and also, although modestly, brain. Here we explored two relevant aspects brain priming: its persistence over time dependence on TLR receptors. For this purpose, used an experimental paradigm consisting applying inflammatory stimuli three months apart. Wild type, toll-like receptor (TLR) 4 TLR2...