Taxonomic group: protista / Euglenozoa
(Phylum: Euglenozoa)
Host organism: (mammal)
Organ / tissue: cell surface,
Life stage: epimastigote,
trypomastigoteAssociated disease: Chagas disease [ICD11:
1F53 
, ICD11:
XN56V ];
infection due to Trypanosoma cruzi [ICD11:
XN56V ]
The structure was elucidated in this paperNCBI PubMed ID: 24879929Publication DOI: 10.1016/j.actatropica.2014.05.014Journal NLM ID: 0370374Publisher: Elsevier
Correspondence: vduschak
conicet.gov.ar
Institutions: Area de Bioquimica de Proteinas y Glicobiologia de Parasitos, Departamento de Investigacion, Instituto Nacional de Parasitologia, 'Dr Mario Fatala Chaben', ANLIS-Malbran, Ministerio de Salud de la Nacion, Buenos Aires, Argentina, CIHIDECAR, Departamento de Quimica Organica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina
Sulfation, a post-translational modification which plays a key role in various biological processes, is inhibited by competition with chlorate. In Trypanosoma cruzi, the agent of Chagas' disease, sulfated structures have been described as part of glycolipids and we have reported sulfated high-mannose type oligosaccharides in the C-T domain of the cruzipain (Cz) glycoprotein. However, sulfation pathways have not been described yet in this parasite. Herein, we studied the effect of chlorate treatment on T. cruzi with the aim to gain some knowledge about sulfation metabolism and the role of sulfated molecules in this parasite. In chlorate-treated epimastigotes, immunoblotting with anti-sulfates enriched Cz IgGs (AS-enriched IgGs) showed Cz undersulfation. Accordingly, a Cz mobility shift toward higher isoelectric points was observed in 2D-PAGE probed with anti-Cz antibodies. Ultrastructural membrane abnormalities and a significant decrease of dark lipid reservosomes were shown by electron microscopy and a significant decrease in sulfatide levels was confirmed by TLC/UV-MALDI-TOF-MS analysis. Altogether, these results suggest T. cruzi sulfation occurs via PAPS. Sulfated epitopes in trypomastigote and amastigote forms were evidenced using AS-enriched IgGs by immunoblotting. Their presence on trypomastigotes surface was demonstrated by flow cytometry and IF with Cz/dCz specific antibodies. Interestingly, the percentage of infected cardiac HL-1 cells decreased 40% when using chlorate-treated trypomastigotes, suggesting sulfates are involved in the invasion process. The same effect was observed when cells were pre-incubated with dCz, dC-T or an anti-high mannose receptor (HMR) antibody, suggesting Cz sulfates and HMR are also involved in the infection process by T. cruzi.
glycoconjugates, sulfation, Trypanosoma cruzi, Sulfoglycosphingolipids, Cruzipain, Invasion process
Structure type: oligomer ; 1002.5 [M+NaSO3+Na]+
Location inside paper: Fig. S5B
Compound class: glycosphingolipid
Contained glycoepitopes: IEDB_115136,IEDB_137339,IEDB_140630,IEDB_141181,IEDB_142488,IEDB_146664,IEDB_423153,IEDB_983931,SB_192,SB_5
Methods: SDS-PAGE, TLC, ELISA, anion-exchange chromatography, Western blotting, statistical analysis, desulfation, immunization, fluorescence microscopy, UV-MALDI-TOF MS, flow cytometry analysis, parasite treatment with chlorate, infection assays of HL-1 cells
NCBI Taxonomy refs (TaxIDs): 5693
Show glycosyltransferases
There is only one chemically distinct structure:
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