Encefalopatía asociada a casos de infección con Escherichia coli enterohemorrágica (EHEC) : interacción de la Toxina Shiga 2 con endoxina de EHEC. Rol de agentes neuroprotectores

Shiga toxin 2 (Stx2) produced by enterohemorrhagic Escherichia coli (EHEC) causes diarrhea, hemorrhagic colitis, hemolytic uremic syndrome (HUS) and acute encephalopathies. The HUS mortality rate increases dramatically when the central nervous system (CNS) is involved. EHEC secretes Stx 2 and LPS. T...

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Autor principal: Vasconcelos Esteves Pinto, Alípio
Otros Autores: Vaccaro, María I.
Formato: Tesis doctoral acceptedVersion
Lenguaje:Español
Publicado: Facultad de Farmacia y Bioquímica 2016
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Acceso en línea:http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgraafa&cl=CL1&d=HWA_3141
http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgraafa/index/assoc/HWA_3141.dir/3141.PDF
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Sumario:Shiga toxin 2 (Stx2) produced by enterohemorrhagic Escherichia coli (EHEC) causes diarrhea, hemorrhagic colitis, hemolytic uremic syndrome (HUS) and acute encephalopathies. The HUS mortality rate increases dramatically when the central nervous system (CNS) is involved. EHEC secretes Stx 2 and LPS. Therefore, the objective of this work was to determine the sublethal effects of Stx2 in the CNS and the proinflammatory contribution of LPS in the encephalopathy. Mice and rats were used for immunofluorescent, electronic microscopy, physiological and behavioral studies. In addition, Dexamethasone and Etanercept were used to assess the degree of inflammatory involvement caused by the toxins. The Stx2 produced damage to the blood-brain barrier. Furthermore, in the parenchyma produced astrocytic reaction, neurodegeneration, demyelination and microglial activation. LPS increases the deleterious effects of Stx2. These events led to motor deficits while treatment with anti-inflammatory, Dexamethasone and Etanercept, significantly reversed the pathological condition. In light of the results, it is suggested that the damage caused by LPS and Stx2 is accompanied by an inflammatory process. In conclusion, anti-inflammatory agents may be beneficial to minimize the alterations observed by toxins in the neurovascular unit, to reduce the cell damage, and thus ameliorate imbalances engines frequently diagnosed in patients.