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TRYPANOSOMA CRUZI RECOGNITION BY MACROPHAGES AND MUSCLE CELLS: PERSPECTIVES AFTER A 15-YEAR STUDY
Macrófagos
Ultraestrutura
Miócitos Cardíacos
Lectinas
Endocitose
Proteases
Macrophage
Heart muscle cell
Lectins
Ligand-receptor interaction
Ultrastructure
Endocytosis
Proteinases
Alpha-2-macroglobulin
Afiliación
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Ultraestrutura e Biologia Celular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Ultraestrutura e Biologia Celular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Ultraestrutura e Biologia Celular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Ultraestrutura e Biologia Celular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Ultraestrutura e Biologia Celular. Rio de Janeiro, RJ, Brasil.
Resumen en ingles
Macrophages and muscle cells are the main targets for invasion of Trypanosoma cruzi. Ultrastructural studies of this phenomenon in vitro showed that invasion occurs by endocytosis, with attachment and internalization being mediated by different components capable of recognizing epi-or trypomastigotes (TRY). A parasitophorus vacuole was formed in both cell types, thereafter fusing with lysosomes. Then, the mechanism of T. cruzi invasion of host cells (HC) is essentially similar (during a primary infection in the abscence of a specific immune response), regardless of wether the target cell is a professional or a non-professional phagocytic cell. Using sugars, lectins, glycosidases, proteinases and proteinase inhibitors, we observed that the relative balance between exposed sialic acid and galactose/N-acetyl galactosamine (GAL) residues on the TRY surface, determines the parasite's capacity to invade HC, and that lectin-mediated phagocytosis with GAL specificity is important for internalization of T. cruzi into macrophages. On the other hand, GAL on the surface to heart muscle cells participate on TRY adhesion. TRY need to process proteolytically both the HC and their own surface, to expose the necessary ligands and receptors that allow binding to, and internalization in the host cell. The diverse range of molecular mechanisms which the parasite could use to invade the host cell may correspond to differences in the available "receptors"on the surface of each specific cell type. Acute phase components, with lectin or proteinase inhibitory activities (a-macroglobulins), may also be involved in T. cruzi-host cell interaction.
Palabras clave en portugues
Trypanosoma cruziMacrófagos
Ultraestrutura
Miócitos Cardíacos
Lectinas
Endocitose
Proteases
Palabras clave en ingles
Trypanosoma cruziMacrophage
Heart muscle cell
Lectins
Ligand-receptor interaction
Ultrastructure
Endocytosis
Proteinases
Alpha-2-macroglobulin
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