| Full text | |
| Author(s): |
Bambino-Medeiros, R.
[1]
;
Oliveira, Jr., F. O. R.
[1]
;
Calvet, C. M.
[1]
;
Vicente, D.
[1]
;
Toma, L.
[2]
;
Krieger, M. A.
[3]
;
Meirelles, M. N.
[1]
;
Pereira, M. C. S.
[1]
Total Authors: 8
|
| Affiliation: | [1] Fiocruz MS, Lab Ultraestrutura Celular, Inst Oswaldo Cruz, BR-21045900 Rio De Janeiro - Brazil
[2] Univ Fed Sao Paulo, Dept Bioquim, UNIFESP, SP, BR-04044020 Sao Paulo - Brazil
[3] Inst Biol Mol Parana FIOCRUZ, Inst Carlos Chagas, BR-81350010 Curitiba, Parana - Brazil
Total Affiliations: 3
|
| Document type: | Journal article |
| Source: | Parasitology; v. 138, n. 5, p. 593-601, APR 2011. |
| Web of Science Citations: | 19 |
| Abstract | |
Cell surface glycosaminoglycans (GAGs) play an important role in the attachment and invasion process of a variety of intracellular pathogens. We have previously demonstrated that heparan sulfate proteoglycans (HSPG) mediate the invasion of trypomastigote forms of Trypanosoma cruzi in cardiomyocytes. Herein, we analysed whether GAGs are also implicated in amastigote invasion. Competition assays with soluble GAGs revealed that treatment of T. cruzi amastigotes with heparin and heparan sulfate leads to a reduction in the infection ratio, achieving 82% and 65% inhibition of invasion, respectively. Other sulfated GAGs, such as chondroitin sulfate, dermatan sulfate and keratan sulfate, had no effect on the invasion process. In addition, a significant decrease in infection occurred after interaction of amastigotes with GAG-deficient Chinese Hamster Ovary (CHO) cells, decreasing from 20% and 28% in wild-type CHO cells to 5% and 9% in the mutant cells after 2 h and 4 h of infection, respectively. These findings suggest that amastigote invasion also involves host cell surface heparan sulfate proteoglycans. The knowledge of the mechanism triggered by heparan sulfate-binding T. cruzi proteins may provide new potential candidates for Chagas disease therapy. (AU) | |