IIBBA   05544
INSTITUTO DE INVESTIGACIONES BIOQUIMICAS DE BUENOS AIRES
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Meningeal inflammation correlates with neurodegeneration and glial activation in a chronic cortical focal animal model of Multiple Sclerosis
Autor/es:
SILVA, BERENICE; PITOSSI, F; LEAL, MC; FERRARI, CC; FARIAS, MI
Lugar:
Paris
Reunión:
Congreso; ectrims; 2017
Resumen:
Background: The presence of meningeal inflammation was described mainly in progressive forms of multiple sclerosis (MS) mostly associate with cortical pathology in animal models and patients. Meningeal inflammation is associated with increased cortical demyelination, neurodegeneration, glial activation and a more severe disease outcome in MS patients. The aim of this work is to characterize the meningeal inflammation associated with focal cortical demyelination and neurodegeneration in chronic cortical focal animal model. Methods: Chronic cortical lesions were induced by injecting an adenovector expressing either human IL-1b (AdIL-1) or betagalactosidase (AdBgal) as control in the prefrontal cortex of adult rats. Systemic inflammation was induced by peripheral injection of either Ad-IL1b or Adbgal. The analysis were performed 7 and 30 days post peripheral injection (dpi). We performed behavioural, histological, immunohistochemical and electronic microscope. Systemic stimulation was checked by peripheral blood cells counting. Results: Peripherally stimulated IL-1b induced cortical lesions exhibited meningeal inflammation characterized by inflammatory infiltrate mostly composed of macrophages, lymphocytes, neutrophils and follicular dendritic cells: CD4 +, CD8+, CD45+RC+, CD20+ cells were found. Follicular dendritic cells we also observed as CD23+ and CD39+ cells in the follicular like structures in the meninges. The number of follicle-like structures positively correlates with microglia and astroglia activation and neurodegeneration at both time point studied, 7 and 30 dpi. Conclusions: Meningeal inflammation correlates with cortical damage. We demonstrated that cortical injury induces meningeal inflammation, but the relationship and the responsibility of both events on the chronicity of cortical damage remained still controversial.