Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5737759 | Neuroscience | 2017 | 14 Pages |
Abstract
A translational murine model of encephalopathy was employed to demonstrate that systemic administration of a sublethal dose of Stx2 damaged the striatal microvasculature and astrocytes, increase the blood brain barrier permeability and caused neuronal degeneration. All these events were aggravated by lipopolysaccharide (LPS). The injury observed in the striatum coincided with locomotor behavioral alterations. The anti-inflammatory Dexamethasone resulted to prevent the observed neurologic and clinical signs, proving to be an effective drug. Therefore, the present work demonstrates that: (i) systemic sub-lethal Stx2 damages the striatal neurovascular unit as it succeeds to pass through the blood brain barrier. (ii) This damage is aggravated by the contribution of LPS which is also produced and secreted by EHEC, and (iii) the observed neurological alterations may be prevented by an anti-inflammatory treatment.
Keywords
LPSMicrovasculatureGFAPSTECEHECstx2PBSIODEnterohemorrhagic Escherichia coliEncephalopathyinflammationintegral optical densityHUSNeuronal damageCNSBlood–brain barrierShiga toxin 2Hemolytic uremic syndromecentral nervous systemVascular endothelial growth factorVascular Endothelial Growth Factor (VEGF)lipopolysaccharidephosphate-buffered solutionGlial fibrillary acidic protein
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Authors
Alipio Pinto, Adriana Cangelosi, Patricia A. Geoghegan, Jorge Goldstein,