Review onTrypanosoma cruzi: Host Cell Interaction

Abstract

Trypanosoma cruzi, the causative agent of Chagas' disease, which affects a large number of individuals in Central and South America, is transmitted to vertebrate hosts by blood-sucking insects. This protozoan is an obligate intracellular parasite. The infective forms of the parasite are metacyclic and bloodstream trypomastigote and amastigote. Metacyclic trypomastigotes are released with the feces of the insect while amastigotes and bloodstream trypomastigotes are released from the infected host cells of the vertebrate host after a complex intracellular life cycle. The recognition between parasite and mammalian host cell involves numerous molecules present in both cell types. Here, we present a brief review of the interaction between Trypanosoma cruzi and its host cells, mainly emphasizing the mechanisms and molecules that participate in the T. cruzi invasion process of the mammalian cells.

Differential Expression and Characterization of a Member of the Mucin-Associated Surface Protein Family Secreted by Trypanosoma cruzi

“…The TSs transfer sialic acid from the host cell membrane to the parasite's glycoproteins and bind the parasite to the host cell during the invasion process (27,45). gp82 is another glycoprotein known to be involved in the invasion process; it forms an integral part of the surface of the parasite, where it plays a role in freeing calcium from the intracellular deposits and the disassembly of F-actin (4,15,21,25,47).…”

New carbohydrazide derivatives of 1H-pyrazolo[3,4-b]pyridine and trypanocidal activity

“…This feature may have contributed to activity from 4b against amastigote form. Thus, it is possible that a lipophilic character allows better penetration of the compound 4b through the plasma membrane of the parasite (de Souza et al 2010).…”

“…In this phase, the parasitaemia is greatly reduced and the patients become asymptomatic but about one third of infected people will enter the symptomatic chronic stage of the disease associated with the manifestation of organ damage. High mortality rates have been recorded for the chronic phase due to Chagas' heart disease (de Souza et al 2010, Hidron et al 2010, Coura and Borges-Pereira 2012.…”

La respuesta inmunitaria adaptativa en la infección crónica por Trypanosoma cruzi

“…Una vez dentro de la célula, se desarrollan los amastigotes, los cuales se multiplican por división binaria (Brener, 1973;Campo, et al, 2016). En el sitio de inoculación, los tripomastigotes usualmente invaden células fagocíticas, como los macró-fagos, y células no fagocíticas, como los fibroblastos (de Souza, et al, 2010;Rosestolato, et al, 2002). Aunque se han identificado algunos ligandos que el parásito utiliza para unirse a las células huéspedes, son múltiples las moléculas que participan en esta interacción (Magdesian, et al, 2001).…”

“…Después de la unión a la membrana celular, se presenta la formación de la vacuola parasitofora, donde operan diferentes mecanismos de endocitosis (Barrias, et al, 2013). Una vez dentro de la célula, empieza la formación de los amastigotes, los cuales pasan de la vacuola al citoplasma y entran en contacto directo con los organelos de las células huéspedes (Ley, et al, 1990;de Souza, et al, 2010). Ya que una de la formas del parásito es extracelular, los anticuerpos contra antígenos de superficie son uno de los mecanismos de defensa del huésped para lisar los tripomastigotes o evitar la invasión de las células (Krettli & Brener, 1976).…”