Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells.
| Autor: | Alejandro F Benatar, Gabriela A García, Jacqeline Bua, Juan P Cerliani, Miriam Postan, Laura M Tasso, Jorge Scaglione, Juan C Stupirski, Marta A Toscano, Gabriel A Rabinovich, Karina A Gómez |
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| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: | |
| Zdroj: | PLoS Neglected Tropical Diseases, Vol 9, Iss 10, p e0004148 (2015) |
| Druh dokumentu: | article |
| ISSN: | 1935-2727 1935-2735 |
| DOI: | 10.1371/journal.pntd.0004148 |
| Popis: | BACKGROUND:Chronic Chagas cardiomyopathy caused by Trypanosoma cruzi is the result of a pathologic process starting during the acute phase of parasite infection. Among different factors, the specific recognition of glycan structures by glycan-binding proteins from the parasite or from the mammalian host cells may play a critical role in the evolution of the infection. METHODOLOGY AND PRINCIPAL FINDINGS:Here we investigated the contribution of galectin-1 (Gal-1), an endogenous glycan-binding protein abundantly expressed in human and mouse heart, to the pathophysiology of T. cruzi infection, particularly in the context of cardiac pathology. We found that exposure of HL-1 cardiac cells to Gal-1 reduced the percentage of infection by two different T. cruzi strains, Tulahuén (TcVI) and Brazil (TcI). In addition, Gal-1 prevented exposure of phosphatidylserine and early events in the apoptotic program by parasite infection on HL-1 cells. These effects were not mediated by direct interaction with the parasite surface, suggesting that Gal-1 may act through binding to host cells. Moreover, we also observed that T. cruzi infection altered the glycophenotype of cardiac cells, reducing binding of exogenous Gal-1 to the cell surface. Consistent with these data, Gal-1 deficient (Lgals1-/-) mice showed increased parasitemia, reduced signs of inflammation in heart and skeletal muscle tissues, and lower survival rates as compared to wild-type (WT) mice in response to intraperitoneal infection with T. cruzi Tulahuén strain. CONCLUSION/SIGNIFICANCE:Our results indicate that Gal-1 modulates T. cruzi infection of cardiac cells, highlighting the relevance of galectins and their ligands as regulators of host-parasite interactions. |
| Databáze: | Directory of Open Access Journals |
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