Abstract
Trypanosoma cruzi, the protozoa that causes Chagas disease in humans, is transmitted by insects from the Reduviidae family. The parasite has developed the ability to change the structure of the surface molecules, depending on the host. Among them, the mucins are the most abundant glycoproteins. Structural studies have focused on the epimastigotes and metacyclic trypomastigotes that colonize the insect, and on the mammal trypomastigotes. The carbohydrate in the mucins fulfills crucial functions, the most important of which being the accepting of sialic acid from the host, a process catalyzed by the unique parasite trans-sialidase. The sialylation of the parasite influences the immune response on infection. The O-linked sugars have characteristics that differentiate them from human mucins. One of them is the linkage to the polypeptide chain by the hexosamine, GlcNAc, instead of GalNAc. The main monosaccharide in the mucins oligosaccharides is galactose, and this may be present in three configurations. Whereas β-d-galactopyranose (β-Galp) was found in the insect and the human stages of Trypanosoma cruzi, β-d-galactofuranose (β-Galf) is present only in the mucins of some strains of epimastigotes and α-d-galactopyranose (α-Galp) characterizes the mucins of the bloodstream trypomastigotes. The two last configurations confer high antigenic properties. In this review we discuss the different structures found and we pose the questions that still need investigation on the exchange of the configurations of galactose.
Highlights
Trypanosoma cruzi, the agent of Chagas disease [1], is an intriguing parasite, because of the morphological and biological changes during its life cycle and for the drastic modifications of the sugars at the surface of the parasite
Several biological processes take place in the PV, parasitophorus vacuole (PV) formed by fusion with the host lysosome, an essential step in order to and one of them is due to the action of the T. cruzi trans-sialidase (TcTS), referred later in this review, evade the immune response of the host [12,13]
In relation to the different glycan structures identified in the mucins depending on the strains and stages of T. cruzi, the work of Pineda et al [25] investigated the binding of galectins 1, 3, 4, 7 and 8 with 14 strains of discrete typing units (DTU) I–VI of T
Summary
Trypanosoma cruzi, the agent of Chagas disease [1], is an intriguing parasite, because of the morphological and biological changes during its life cycle and for the drastic modifications of the sugars at the surface of the parasite. Several biological processes take place in the PV, parasitophorus vacuole (PV) formed by fusion with the host lysosome, an essential step in order to and one of them is due to the action of the T. cruzi trans-sialidase (TcTS), referred later in this review, evade the immune response of the host [12,13]. Insect, the trypomastigotes must differentiatewhich into epimastigotes to closelysis the cycle This process starts the stomach; down in the may rich medium of the cells midgut multiply,by anda upon reachingInthe hindgut. The insect, the they transform into the infective metacyclic trypomastigotes, which detach from the cuticle and arein the trypomastigotes must differentiate into epimastigotes to close the cycle. A conclusion, with an addressing of the questions that arise from the current knowledge, is included
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