Acción de la toxina Shiga en órganos blanco. Estrategias de prevención del Síndrome Urémico Hemolítico.

IBARRA CRISTINA

Mendoza

Congreso; XXX Reunión Anual de la Sociedad de Biología de Cuyo.; 2012

Gastrointestinal infection with STEC/EHEC strains causes diarrhea and hemorrhagic colitis, and in addition, Hemolytic Uremic Syndrome (HUS) defined by a triad of hemolytic anemia, thrombocytopenia, and acute renal failure. HUS develops in 10%-15% of small children several days after bloody diarrhea and is the most common cause of acute renal failure in infants in Argentina. It is transmitted to humans primarily through consumption of contaminated foods, such as raw or undercooked ground meat products or direct contact with cattle. Because STEC are non-invasive, it is generally accepted that Shiga toxin (Stx) must be absorbed from the intestine to cause HUS by different mechanisms that contribute to the intestinal pathology. Renal damage has been strongly associated with Stx, which binds to the globotriaosylceramide (Gb3) receptor on the plasma membrane of epithelial andendothelial cells causing cellular death. We have shown that kidney lesions similar to those described in humans may be obtained in rats treated with Stx2 and that the kidney was protected by previous treatment with inhibitors of Gb3 synthesis. Furthermore, we have shown that Stx2 interrupted pregnancy in rats and we speculate that STEC infections during pregnancy could be detrimental to human fetuses.