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Título

Metabolismo de la L-arginina en la enfermedad de Chagas experimental: papel de la arginasa I y la iNOS en tejido cardiaco

Autor Cuervo, Henar
DirectorGironès, Nuria; Fresno, Manuel
Palabras clave Tripanosomiasis americana
Metabolismo de aminoácidos
Fecha de publicación 2008
EditorUniversidad Autónoma de Madrid
ResumenIn Chagas disease, caused by Trypanosoma cruzi, macrophages and cardiomyocytes are the main targets of infection. On the other hand, macrophages can be activated in different ways by Th1 or Th2 cytokines leading to classic or alternative activation, which results in different functional outcomes. Those different ways are often differentiated by the expression of enzymes involved in L-arginine metabolism. Thus, we studied the expression of such enzymes in heart tissue during in vivo infection of BALB/c and C57BL/6 mice. We found that expression of inducible nitric oxide synthase (iNOS), arginase I and II as well as ornithine decarboxylase, were much higher in BALB/c compared to C57BL/6 mice and related to parasite burden in heart tissue. Th1 and Th2 cytokines were expressed in heart tissue in both infected mouse strains, but the Th1/Th2 balance was predominantly Th1 in C57BL/6 mice and Th2 in BALB/c mice at the peak of parasite infection. By using mice strains genetically deficient in various cytokines or their receptors, we found that IL-13, probably in cooperation with IL-4, IL-10 and prostaglandin E2, induces arginase I expression. Inducible nitric oxide synthase and arginase II were expressed by cardiomyocytes. Interestingly, heart infiltrated CD68+ macrophages were the major cell type expressing arginase I. When purified, CD11b+ heart infiltrating cells expressing both arginase I and iNOS did not present a clear M1/M2 polarization but showed a myeloid suppressor cell phenotype. In addition, these CD11b+ cells modulated T cell proliferation in vitro. Thus, arginase I expression may influence parasite cell survival, and might be also regulating the inflammatory T cell response in heart during infection.
Descripción Tesis doctoral inédita. Universidad Autónoma de Madrid, Facultad de Ciencias, Departamento de Biología Molecular . Fecha de lectura: 25-04-2008
URI http://hdl.handle.net/10261/8341
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