Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells

dc.creatorBenatar, Alejandro Francisco
dc.creatorGarcía, Gabriela Andrea
dc.creatorBua, Jacqueline
dc.creatorCerliani, Juan P
dc.creatorPostan, Miriam
dc.creatorTasso, Laura Mónica
dc.creatorScaglione, Jorge
dc.creatorStupirski, Juan C
dc.creatorToscano, Marta A
dc.creatorRabinovich, Gabriel A
dc.creatorGómez, Karina A
dc.date2019-12-09T18:00:02Z
dc.date2019-12-09T18:00:02Z
dc.date2015-10
dc.date.accessioned2023-08-29T20:06:29Z
dc.date.available2023-08-29T20:06:29Z
dc.identifierhttp://sgc.anlis.gob.ar/handle/123456789/1464
dc.identifierhttps://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0004148
dc.identifier10.1371/journal.pntd.0004148
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8519176
dc.descriptionFil: Benatar, Alejandro Francisco. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular (INGEBI). Laboratorio de Biología Molecular de la Enfermedad de Chagas (LabMECh); Argentina.
dc.descriptionFil: García, Gabriela Andrea. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología Dr. Mario Fatala Chaben; Argentina.
dc.descriptionFil: Bua, Jacqueline. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología Dr. Mario Fatala Chaben; Argentina.
dc.descriptionFil: Cerliani, Juan P. Instituto de Biología y Medicina Experimental (IBYME). Laboratorio de Inmunopatología; Argentina.
dc.descriptionFil: Postam, Miriam. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología Dr. Mario Fatala Chaben; Argentina.
dc.descriptionFil: Tasso, Laura Mónica. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular (INGEBI). Laboratorio de Biología Molecular de la Enfermedad de Chagas (LabMECh); Argentina.
dc.descriptionFil: Scaglione, Jorge. Hospital Pedro de Elizalde. Servicio de Cardiología. Sección Electrofisiología; Buenos Aires, Argentina.
dc.descriptionFil: Stupirski, Juan C. Instituto de Biología y Medicina Experimental (IBYME). Laboratorio de Inmunopatología; Argentina.
dc.descriptionFil: Toscano, Marta A. Instituto de Biología y Medicina Experimental (IBYME). Laboratorio de Inmunopatología; Argentina.
dc.descriptionFil: Rabinovich, Gabriel A. Instituto de Biología y Medicina Experimental (IBYME). Laboratorio de Inmunopatología; Argentina.
dc.descriptionFil: Gómez, Karina A. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular (INGEBI). Laboratorio de Biología Molecular de la Enfermedad de Chagas (LabMECh); Argentina.
dc.descriptionBackground: 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.
dc.formatPdf
dc.languageen
dc.relationPLoS neglected tropical diseases
dc.rightsopen
dc.subjectEnfermedad de Chagas
dc.subjectRatones Noqueados
dc.subjectMiocitos Cardíacos
dc.subjectInteracciones Huésped-Parásitos
dc.subjectParasitemia
dc.titleGalectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells
dc.typeArtículo


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