Trypanosoma cruzi recognition by macrophages and muscle cells: perspectives after a 15-year study

Abstract

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 absence of a specific immune response), regardless of whether 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 of 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 (alpha-macroglobulins), may also be involved in T. cruzi-host cell interaction.

Increased association of Trypanosoma cruzi with sialoadhesin positive mice macrophages

“…Trypomastigotes is the infective form able to adhere and gain access to the interior of cells. The understanding of how trypomastigotes infects host cells is far from being established (Araujo-Jorge et al 1992;Rosestolato et al 2002); however, evidences point to a phagocytic entrance mechanism in professional phagocytes (Rosestolato et al 2002). This infection plays a crucial role in the maintenance and amplification of this disease.…”

Participation of Host Cell Actin Filaments during Interaction of Trypomastigote Forms of Trypanosoma cruzi with Host Cells.

“…Evidence has accumulated to indicate that the interaction of T. cruzi trypomastigotes with host cells is mediated by specific molecules localized on the surface of both cells Araujo-Jorge et al, 1992;Maria et al, 1982;Nogueira et al, 1976;Procopio et al, 1994). However, there is still some discussion regarding the involvement of host cell actin on the process of parasite internalization.…”

<i>Trypanosoma cruzi</i> Infection Impairs the Endocytosis of Zymosan A by Cardiomyocytes

“…Literature data display evidence for the importance of carbohydrate residues and their counterreceptors during the interaction of T. cruzi with host cells [3,4]. Ultrastructural analysis, employing horseradish peroxidase coupled to colloidal gold particles as the ligand, showed the presence of mannose receptors near the sites of T. cruzi attachment at CM, later on composing the parasitophorous vacuole [15].…”

“…The diversity of molecules implicated in the recognition process seems to be related to different available 'receptors' at the surface of the target cells [reviewed in ref. 3,4].…”