Efecto de la toxina Shiga tipo 2 en ratas en períodos de gestación : implicancias en la placentación y el desarrollo fetal

In Argentina, with Escherichia coli producing Shiga toxin (STEC) associated infections produce the highest incidence of hemolytic uremic syndrome (HUS) in the world. Epidemiological evidence shows that a high number of adults are carriers of STEC. About 15% of spontaneous abortions are caused by inf...

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Detalles Bibliográficos
Autor principal: Sacerdoti, Flavia
Otros Autores: Franchi, Ana María
Formato: Tesis doctoral acceptedVersion
Lenguaje:Español
Publicado: Facultad de Farmacia y Bioquímica 2016
Materias:
Toxina Shiga
Preñez
Aborto
Rata
Fisiología
Desarrollo fetal
Escherichia coli
Síndrome uremico hemolítico
Ciencia de la vida
Acceso en línea:http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgraafa&cl=CL1&d=HWA_1397
http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgraafa/index/assoc/HWA_1397.dir/1397.PDF
Aporte de:
Repositorio Digital de la Universidad de Buenos Aires (UBA) de Universidad de Buenos Aires
Descripción
Sumario:In Argentina, with Escherichia coli producing Shiga toxin (STEC) associated infections produce the highest incidence of hemolytic uremic syndrome (HUS) in the world. Epidemiological evidence shows that a high number of adults are carriers of STEC. About 15% of spontaneous abortions are caused by infections. The hypothesis of this work is that STEC infections can cause complications in early pregnancy mediated by Shiga toxin type 2 (Stx2). Stx2 effects were evaluated in rats injected in early pregnancy. The sublethal dose of 0.5 Stx2 ng / g caused damage in placental tissues, hypoxia, local inflammation, intrauterine growth restriction and finally abortion. Immunization of rats with BLS-Stx2B induced high serum titers of anti-Stx2B with neutralizing capacity of Stx2. Immunized mothers injected with Stx2 had a normal delivery at term and the offspring breastfed by immunized mothers, challenged at weaning with a lethal dose of Stx2 survived in 100%. These results indicate that Stx2 produces abortion in the developed model. Local inflammation and decidual hypoxia play an important role in pregnancy loss. Neutralizing antibodies against Stx2 in the maternal sera are an effective tool to prevent Stx2 mediated pregnancy loss and protect the offspring.

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