Modulación de mecanismos inflamatorios en el Síndrome Urémico Hemolítico
Hemolytic Uremic Syndrome is an endemic microangiopathic disease associated with hemolytic anemia, thrombocytopenia and acute renal failure. The inflammatory response plays a key role in the development of this pathology, but the anti-inflammatory mechanisms have not been widely studied. In this wor...
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| Formato: | Tesis doctoral acceptedVersion |
| Lenguaje: | Español |
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Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica
2022
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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_6711 https://repositoriouba.sisbi.uba.ar/gsdl/collect/posgraafa/index/assoc/HWA_6711.dir/6711.PDF |
| Aporte de: |
| Sumario: | Hemolytic Uremic Syndrome is an endemic microangiopathic disease associated with hemolytic anemia, thrombocytopenia and acute renal failure. The inflammatory response plays a key role in the development of this pathology, but the anti-inflammatory mechanisms have not been widely studied. In this work, we have shown that IL-10 deficiency in mice reduces Stx-triggered renal damage. This phenomenon occurs in the presence of a defective neutrophil activation with alteration of surface markers, retention of these cells in lung and reduced recruitment to the kidney. However, it does not correspond to changes in mechanisms such as respiratory burst or cell death even though circulating pro-inflammatory cytokines (TNF-?, IL-6) and corticosterone are elevated. Additionally, in the renal parenchyma, there are imbalances between increased inflammatory factors and pleiotropic remodeling agents (TGF-? and IL-6) in concordance with proliferation of mesangial cells. These changes occur in the absence of extended tubular affection with conservated renal biomarkers. The outcome produced by these mechanisms which compensate the absence of IL-10 could limit the renal damage caused by the toxin. |
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