dc.creatorGomez, Sonia A.
dc.creatorAbrey-Recalde, M J
dc.creatorPanek, C A
dc.creatorFerrarotti, N F
dc.creatorRepetto, M G
dc.creatorMejías, M P
dc.creatorFernandez, G. C.
dc.creatorVanzulli, S
dc.creatorIsturiz, M.
dc.creatorPalermo, M.
dc.date2020-12-15T14:33:18Z
dc.date2020-12-15T14:33:18Z
dc.date2013-09
dc.date.accessioned2023-08-29T20:07:52Z
dc.date.available2023-08-29T20:07:52Z
dc.identifier1365-2249
dc.identifierhttp://sgc.anlis.gob.ar/handle/123456789/1911
dc.identifier10.1111/cei.12124
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8519882
dc.descriptionFil: Gomez, Sonia A. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Departamento de Bacteriología. Servicio Antimicrobianos; Argentina.
dc.descriptionFil: Abrey-Recalde, M J. Laboratorio de Patogénesis e Inmunología de Procesos Infecciosos, Instituto de Medicina Experimental, (IMEX) (CONICET), Buenos Aires; Argentina.
dc.descriptionFil: Panek, C A. Laboratorio de Patogénesis e Inmunología de Procesos Infecciosos, Instituto de Medicina Experimental, (IMEX) (CONICET), Buenos Aires; Argentina.
dc.descriptionFil: Ferrarotti, N F. Laboratorio de Química General, Departamento de Química Analítica y Fisico‐ química, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires; Argentina.
dc.descriptionFil: Repetto, M G. Laboratorio de Química General, Departamento de Química Analítica y Fisico‐ química, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires; Argentina.
dc.descriptionFil: Mejías, M P. Laboratorio de Patogénesis e Inmunología de Procesos Infecciosos, Instituto de Medicina Experimental, (IMEX) (CONICET), Buenos Aires; Argentina.
dc.descriptionFil: Fernandez, G. C.Laboratorio de Patogénesis e Inmunología de Procesos Infecciosos, Instituto de Medicina Experimental, (IMEX) (CONICET), Buenos Aires; Argentina.
dc.descriptionFil: Vanzulli, S. División Patología, Instituto de Investigaciones Oncológicas, Academia Nacional de Medicina, Buenos Aires, Argentina.
dc.descriptionFil: Isturiz, M.Laboratorio de Patogénesis e Inmunología de Procesos Infecciosos, Instituto de Medicina Experimental, (IMEX) (CONICET), Buenos Aires; Argentina.
dc.descriptionFil: Palermo, M. Laboratorio de Patogénesis e Inmunología de Procesos Infecciosos, Instituto de Medicina Experimental, (IMEX) (CONICET), Buenos Aires; Argentina.
dc.descriptionTypical haemolytic uraemic syndrome (HUS) is caused by Shiga toxin (Stx)-producing Escherichia coli infections and is characterized by thrombotic microangiopathy that leads to haemolytic anaemia, thrombocytopenia and acute renal failure. Renal or neurological sequelae are consequences of irreversible tissue damage during the acute phase. Stx toxicity and the acute inflammatory response raised by the host determine the development of HUS. At present there is no specific therapy to control Stx damage. The pathogenic role of reactive oxygen species (ROS) on endothelial injury has been largely documented. In this study, we investigated the in-vivo effects of Stx on the oxidative balance and its contribution to the development of HUS in mice. In addition, we analysed the effect of anti-oxidant agents as therapeutic tools to counteract Stx toxicity. We demonstrated that Stx induced an oxidative imbalance, evidenced by renal glutathione depletion and increased lipid membrane peroxidation. The increased ROS production by neutrophils may be one of the major sources of oxidative stress during Stx intoxication. All these parameters were ameliorated by anti-oxidants reducing platelet activation, renal damage and increasing survival. To conclude, Stx generates a pro-oxidative state that contributes to kidney failure, and exogenous anti-oxidants could be beneficial to counteract this pathogenic pathway.
dc.formatpdf
dc.languageen
dc.publisherWiley
dc.relationClinical and experimental immunology
dc.rightsopen
dc.sourceClinical and Experimental Immunology 2013;173(3):463-72.
dc.subjectSíndrome Hemolítico-Urémico
dc.subjectToxina Shiga II
dc.subjectEstrés Oxidativo
dc.titleThe oxidative stress induced in vivo by Shiga toxin-2 contributes to the pathogenicity of haemolytic uraemic syndrome
dc.typeArtículo


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