Please use this identifier to cite or link to this item: http://sgc.anlis.gob.ar/handle/123456789/1464
Title: Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells
Authors: Benatar, Alejandro Francisco 
García, Gabriela Andrea 
Bua, Jacqueline 
Cerliani, Juan P 
Postan, Miriam 
Tasso, Laura Mónica 
Scaglione, Jorge 
Stupirski, Juan C 
Toscano, Marta A 
Rabinovich, Gabriel A 
Gómez, Karina A 
Keywords: Enfermedad de Chagas;Ratones Noqueados;Miocitos Cardíacos;Interacciones Huésped-Parásitos;Parasitemia
Issue Date: Oct-2015
Journal: PLoS neglected tropical diseases 
Abstract: 
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.
Description: 
Fil: Benatar, Alejandro Francisco. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular (INGEBI). Laboratorio de Biología Molecular de la Enfermedad de Chagas (LabMECh); Argentina.

Fil: García, Gabriela Andrea. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología Dr. Mario Fatala Chaben; Argentina.

Fil: Bua, Jacqueline. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología Dr. Mario Fatala Chaben; Argentina.

Fil: Cerliani, Juan P. Instituto de Biología y Medicina Experimental (IBYME). Laboratorio de Inmunopatología; Argentina.

Fil: Postam, Miriam. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología Dr. Mario Fatala Chaben; Argentina.

Fil: Tasso, Laura Mónica. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular (INGEBI). Laboratorio de Biología Molecular de la Enfermedad de Chagas (LabMECh); Argentina.

Fil: Scaglione, Jorge. Hospital Pedro de Elizalde. Servicio de Cardiología. Sección Electrofisiología; Buenos Aires, Argentina.

Fil: Stupirski, Juan C. Instituto de Biología y Medicina Experimental (IBYME). Laboratorio de Inmunopatología; Argentina.

Fil: Toscano, Marta A. Instituto de Biología y Medicina Experimental (IBYME). Laboratorio de Inmunopatología; Argentina.

Fil: Rabinovich, Gabriel A. Instituto de Biología y Medicina Experimental (IBYME). Laboratorio de Inmunopatología; Argentina.

Fil: Gómez, Karina A. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular (INGEBI). Laboratorio de Biología Molecular de la Enfermedad de Chagas (LabMECh); Argentina.
URI: http://sgc.anlis.gob.ar/handle/123456789/1464
https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0004148
DOI: 10.1371/journal.pntd.0004148
Rights: Open Access
Creative Commons Attribution 4.0 International License
Appears in Collections:Publicaciones INP

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