RESUMEN
The C57Bl/6 mouse is the preferred host for the maintenance of gene deletion mutants and holds a unique place in investigations of cytokine/chemokine networks in neuroinflammation. It is also susceptible to experimental autoimmune encephalomyelitis (EAE), a multiple sclerosis (MS)-like disease commonly used to assess potential MS therapies. Investigations of glial reactivity in EAE have revealed hitherto undescribed astroglial responses in this model, characterized by progressively diminishing glial fibrillary acidic protein and aquaporin-4 immunostaining, from early disease. These observations show that astrocyte responses vary with the EAE paradigm and are an important pathological criterion for disease mapping and therapy evaluation.
Asunto(s)
Encefalomielitis Autoinmune Experimental/patología , Gliosis/patología , Animales , Acuaporina 4/biosíntesis , Astrocitos/metabolismo , Astrocitos/patología , Western Blotting , Encefalomielitis Autoinmune Experimental/metabolismo , Técnica del Anticuerpo Fluorescente , Proteína Ácida Fibrilar de la Glía/biosíntesis , Gliosis/metabolismo , Inmunohistoquímica , Ratones , Ratones Endogámicos C57BL , Ratones Endogámicos NOD , Médula Espinal/metabolismo , Médula Espinal/patologíaRESUMEN
An unexpectedly prominent aspect of murine experimental autoimmune encephalomyelitis is pre-onset astrocyte reactivity. Further examination of this phenomenon in the spinal cord demonstrates that grey matter, as well as white matter astrocytes, change their morphology and cell density from the earliest disease manifestation. Comparison of the two compartments reveals that, whereas white matter changes are rostro-caudally consistent, grey matter reactivity is spatially restricted and of varying amplitude between spinal cord levels. These data strongly suggest that in neuroinflammation early, cross-compartmental recruitment of astrocytes occurs, but with different expression patterns.