Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells
- Autores
- 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
- Año de publicación
- 2015
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- 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.
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. - Materia
-
Enfermedad de Chagas
Ratones Noqueados
Miocitos Cardíacos
Interacciones Huésped-Parásitos
Parasitemia - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- Repositorio
- Institución
- Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán"
- OAI Identificador
- oai:sgc.anlis.gob.ar:123456789/1464
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Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac CellsBenatar, Alejandro FranciscoGarcía, Gabriela AndreaBua, JacquelineCerliani, Juan PPostan, MiriamTasso, Laura MónicaScaglione, JorgeStupirski, Juan CToscano, Marta ARabinovich, Gabriel AGómez, Karina AEnfermedad de ChagasRatones NoqueadosMiocitos CardíacosInteracciones Huésped-ParásitosParasitemiaFil: 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.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.2015-10info:ar-repo/semantics/articuloinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttp://sgc.anlis.gob.ar/handle/123456789/1464https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.000414810.1371/journal.pntd.0004148PLoS neglected tropical diseasesenginfo:eu-repo/semantics/openAccessreponame:Sistema de Gestión del Conocimiento ANLIS MALBRÁNinstname:Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán"instacron:ANLIS2025-09-29T14:30:20Zoai:sgc.anlis.gob.ar:123456789/1464Institucionalhttp://sgc.anlis.gob.ar/Organismo científico-tecnológicoNo correspondehttp://sgc.anlis.gob.ar/oai/biblioteca@anlis.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:a2025-09-29 14:30:20.789Sistema de Gestión del Conocimiento ANLIS MALBRÁN - Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán"false |
dc.title.none.fl_str_mv |
Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells |
title |
Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells |
spellingShingle |
Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells Benatar, Alejandro Francisco Enfermedad de Chagas Ratones Noqueados Miocitos Cardíacos Interacciones Huésped-Parásitos Parasitemia |
title_short |
Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells |
title_full |
Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells |
title_fullStr |
Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells |
title_full_unstemmed |
Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells |
title_sort |
Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells |
dc.creator.none.fl_str_mv |
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 |
author |
Benatar, Alejandro Francisco |
author_facet |
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 |
author_role |
author |
author2 |
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 |
author2_role |
author author author author author author author author author author |
dc.subject.none.fl_str_mv |
Enfermedad de Chagas Ratones Noqueados Miocitos Cardíacos Interacciones Huésped-Parásitos Parasitemia |
topic |
Enfermedad de Chagas Ratones Noqueados Miocitos Cardíacos Interacciones Huésped-Parásitos Parasitemia |
dc.description.none.fl_txt_mv |
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. 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. |
publishDate |
2015 |
dc.date.none.fl_str_mv |
2015-10 |
dc.type.none.fl_str_mv |
info:ar-repo/semantics/articulo info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
http://sgc.anlis.gob.ar/handle/123456789/1464 https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0004148 10.1371/journal.pntd.0004148 |
url |
http://sgc.anlis.gob.ar/handle/123456789/1464 https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0004148 |
identifier_str_mv |
10.1371/journal.pntd.0004148 |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
PLoS neglected tropical diseases |
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info:eu-repo/semantics/openAccess |
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openAccess |
dc.format.none.fl_str_mv |
application/pdf |
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reponame:Sistema de Gestión del Conocimiento ANLIS MALBRÁN instname:Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán" instacron:ANLIS |
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Sistema de Gestión del Conocimiento ANLIS MALBRÁN |
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Sistema de Gestión del Conocimiento ANLIS MALBRÁN |
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Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán" |
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ANLIS |
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Sistema de Gestión del Conocimiento ANLIS MALBRÁN - Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán" |
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