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

Autores
Benatar, Alejandro Francisco; Garcia, Gabriela Andrea; Bua, Jacqueline Elena; Cerliani, Juan Pablo; Postan, Miriam; Tasso, Laura Mónica; Scaglione, Jorge; Stupirski, Juan Carlos; Toscano, Marta Alicia; Rabinovich, Gabriel Adrián; Gomez, Karina Andrea
Año de publicación
2015
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
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.
Fil: Benatar, Alejandro Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular; Argentina
Fil: Garcia, Gabriela Andrea. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud. Instituto Nacional de Parasitología; Argentina
Fil: Bua, Jacqueline Elena. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio E Instituto de Salud. Instituto Nacional de Parasitología; Argentina
Fil: Cerliani, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); Argentina
Fil: Postan, Miriam. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud. Instituto Nacional de Parasitología; Argentina
Fil: Tasso, Laura Mónica. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular; Argentina
Fil: Scaglione, Jorge. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños "Pedro Elizalde" (ex Casa Cuna); Argentina
Fil: Stupirski, Juan Carlos. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); Argentina
Fil: Toscano, Marta Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); Argentina
Fil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Gomez, Karina Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular; Argentina
Materia
Galectin-1
Trypanosoma Cruzi
Cardiac
Chronic Chagasic Cardiomyopathy
Hl-1
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/3956
Acceder
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network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac CellsBenatar, Alejandro FranciscoGarcia, Gabriela AndreaBua, Jacqueline ElenaCerliani, Juan PabloPostan, MiriamTasso, Laura MónicaScaglione, JorgeStupirski, Juan CarlosToscano, Marta AliciaRabinovich, Gabriel AdriánGomez, Karina AndreaGalectin-1Trypanosoma CruziCardiacChronic Chagasic CardiomyopathyHl-1https://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3https://purl.org/becyt/ford/3.2https://purl.org/becyt/ford/3Chronic 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.Fil: Benatar, Alejandro Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular; ArgentinaFil: Garcia, Gabriela Andrea. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud. Instituto Nacional de Parasitología; ArgentinaFil: Bua, Jacqueline Elena. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio E Instituto de Salud. Instituto Nacional de Parasitología; ArgentinaFil: Cerliani, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); ArgentinaFil: Postan, Miriam. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud. Instituto Nacional de Parasitología; ArgentinaFil: Tasso, Laura Mónica. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular; ArgentinaFil: Scaglione, Jorge. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños "Pedro Elizalde" (ex Casa Cuna); ArgentinaFil: Stupirski, Juan Carlos. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); ArgentinaFil: Toscano, Marta Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); ArgentinaFil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; ArgentinaFil: Gomez, Karina Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular; ArgentinaPublic Library of Science2015-10-09info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/3956Benatar, Alejandro Francisco; Garcia, Gabriela Andrea; Bua, Jacqueline Elena; Cerliani, Juan Pablo; Postan, Miriam; et al.; Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells; Public Library of Science; Neglected Tropical Diseases; 9; 10; 9-10-2015; 4148-41481935-2735enginfo:eu-repo/semantics/altIdentifier/url/http://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0004148info:eu-repo/semantics/altIdentifier/doi/DOI:10.1371/journal.pntd.0004148info:eu-repo/semantics/altIdentifier/url/http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4599936/info:eu-repo/semantics/altIdentifier/issn/1935-2735info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T15:26:30Zoai:ri.conicet.gov.ar:11336/3956instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-15 15:26:31.001CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
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
Galectin-1
Trypanosoma Cruzi
Cardiac
Chronic Chagasic Cardiomyopathy
Hl-1
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
Garcia, Gabriela Andrea
Bua, Jacqueline Elena
Cerliani, Juan Pablo
Postan, Miriam
Tasso, Laura Mónica
Scaglione, Jorge
Stupirski, Juan Carlos
Toscano, Marta Alicia
Rabinovich, Gabriel Adrián
Gomez, Karina Andrea
author Benatar, Alejandro Francisco
author_facet Benatar, Alejandro Francisco
Garcia, Gabriela Andrea
Bua, Jacqueline Elena
Cerliani, Juan Pablo
Postan, Miriam
Tasso, Laura Mónica
Scaglione, Jorge
Stupirski, Juan Carlos
Toscano, Marta Alicia
Rabinovich, Gabriel Adrián
Gomez, Karina Andrea
author_role author
author2 Garcia, Gabriela Andrea
Bua, Jacqueline Elena
Cerliani, Juan Pablo
Postan, Miriam
Tasso, Laura Mónica
Scaglione, Jorge
Stupirski, Juan Carlos
Toscano, Marta Alicia
Rabinovich, Gabriel Adrián
Gomez, Karina Andrea
author2_role author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Galectin-1
Trypanosoma Cruzi
Cardiac
Chronic Chagasic Cardiomyopathy
Hl-1
topic Galectin-1
Trypanosoma Cruzi
Cardiac
Chronic Chagasic Cardiomyopathy
Hl-1
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
https://purl.org/becyt/ford/3.2
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv 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.
Fil: Benatar, Alejandro Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular; Argentina
Fil: Garcia, Gabriela Andrea. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud. Instituto Nacional de Parasitología; Argentina
Fil: Bua, Jacqueline Elena. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio E Instituto de Salud. Instituto Nacional de Parasitología; Argentina
Fil: Cerliani, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); Argentina
Fil: Postan, Miriam. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud. Instituto Nacional de Parasitología; Argentina
Fil: Tasso, Laura Mónica. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular; Argentina
Fil: Scaglione, Jorge. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños "Pedro Elizalde" (ex Casa Cuna); Argentina
Fil: Stupirski, Juan Carlos. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); Argentina
Fil: Toscano, Marta Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); Argentina
Fil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Gomez, Karina Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular; Argentina
description 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.
publishDate 2015
dc.date.none.fl_str_mv 2015-10-09
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/3956
Benatar, Alejandro Francisco; Garcia, Gabriela Andrea; Bua, Jacqueline Elena; Cerliani, Juan Pablo; Postan, Miriam; et al.; Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells; Public Library of Science; Neglected Tropical Diseases; 9; 10; 9-10-2015; 4148-4148
1935-2735
url http://hdl.handle.net/11336/3956
identifier_str_mv Benatar, Alejandro Francisco; Garcia, Gabriela Andrea; Bua, Jacqueline Elena; Cerliani, Juan Pablo; Postan, Miriam; et al.; Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells; Public Library of Science; Neglected Tropical Diseases; 9; 10; 9-10-2015; 4148-4148
1935-2735
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0004148
info:eu-repo/semantics/altIdentifier/doi/DOI:10.1371/journal.pntd.0004148
info:eu-repo/semantics/altIdentifier/url/http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4599936/
info:eu-repo/semantics/altIdentifier/issn/1935-2735
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
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dc.publisher.none.fl_str_mv Public Library of Science
publisher.none.fl_str_mv Public Library of Science
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repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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