Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells
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...
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_19352727_v9_n10_p_Benatar http://hdl.handle.net/20.500.12110/paper_19352727_v9_n10_p_Benatar |
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paper:paper_19352727_v9_n10_p_Benatar2023-06-08T16:31:53Z Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells García, Gabriela Andrea Búa, Jacqueline Elena Toscano, Marta Alicia agglutinin galectin 1 lipocortin 5 phytohemagglutinin galectin 1 adult aged animal cell Article cell invasion assay Chagas disease clinical article clinical assessment controlled study Doppler echocardiography electrocardiography enzyme linked immunosorbent assay flow cytometry gene deletion genetic transfection glycosylation heart transplantation histopathology host parasite interaction human image analysis immunoblotting mouse nonhuman protein expression reverse transcription polymerase chain reaction RNA extraction survival thorax radiography Trypanosoma cruzi trypomastigote animal Brazil cardiac muscle cell cell culture Chagas disease disease model female host parasite interaction immunology knockout mouse male metabolism middle aged parasitemia parasitology pathology physiology survival analysis Adult Aged Animals Brazil Cells, Cultured Chagas Disease Disease Models, Animal Female Galectin 1 Host-Parasite Interactions Humans Male Mice Mice, Knockout Middle Aged Myocytes, Cardiac Parasitemia Survival Analysis Trypanosoma cruzi 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 Benatar et al. Fil:García, G.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Bua, J. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Toscano, M.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2015 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_19352727_v9_n10_p_Benatar http://hdl.handle.net/20.500.12110/paper_19352727_v9_n10_p_Benatar |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
agglutinin galectin 1 lipocortin 5 phytohemagglutinin galectin 1 adult aged animal cell Article cell invasion assay Chagas disease clinical article clinical assessment controlled study Doppler echocardiography electrocardiography enzyme linked immunosorbent assay flow cytometry gene deletion genetic transfection glycosylation heart transplantation histopathology host parasite interaction human image analysis immunoblotting mouse nonhuman protein expression reverse transcription polymerase chain reaction RNA extraction survival thorax radiography Trypanosoma cruzi trypomastigote animal Brazil cardiac muscle cell cell culture Chagas disease disease model female host parasite interaction immunology knockout mouse male metabolism middle aged parasitemia parasitology pathology physiology survival analysis Adult Aged Animals Brazil Cells, Cultured Chagas Disease Disease Models, Animal Female Galectin 1 Host-Parasite Interactions Humans Male Mice Mice, Knockout Middle Aged Myocytes, Cardiac Parasitemia Survival Analysis Trypanosoma cruzi |
| spellingShingle |
agglutinin galectin 1 lipocortin 5 phytohemagglutinin galectin 1 adult aged animal cell Article cell invasion assay Chagas disease clinical article clinical assessment controlled study Doppler echocardiography electrocardiography enzyme linked immunosorbent assay flow cytometry gene deletion genetic transfection glycosylation heart transplantation histopathology host parasite interaction human image analysis immunoblotting mouse nonhuman protein expression reverse transcription polymerase chain reaction RNA extraction survival thorax radiography Trypanosoma cruzi trypomastigote animal Brazil cardiac muscle cell cell culture Chagas disease disease model female host parasite interaction immunology knockout mouse male metabolism middle aged parasitemia parasitology pathology physiology survival analysis Adult Aged Animals Brazil Cells, Cultured Chagas Disease Disease Models, Animal Female Galectin 1 Host-Parasite Interactions Humans Male Mice Mice, Knockout Middle Aged Myocytes, Cardiac Parasitemia Survival Analysis Trypanosoma cruzi García, Gabriela Andrea Búa, Jacqueline Elena Toscano, Marta Alicia Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells |
| topic_facet |
agglutinin galectin 1 lipocortin 5 phytohemagglutinin galectin 1 adult aged animal cell Article cell invasion assay Chagas disease clinical article clinical assessment controlled study Doppler echocardiography electrocardiography enzyme linked immunosorbent assay flow cytometry gene deletion genetic transfection glycosylation heart transplantation histopathology host parasite interaction human image analysis immunoblotting mouse nonhuman protein expression reverse transcription polymerase chain reaction RNA extraction survival thorax radiography Trypanosoma cruzi trypomastigote animal Brazil cardiac muscle cell cell culture Chagas disease disease model female host parasite interaction immunology knockout mouse male metabolism middle aged parasitemia parasitology pathology physiology survival analysis Adult Aged Animals Brazil Cells, Cultured Chagas Disease Disease Models, Animal Female Galectin 1 Host-Parasite Interactions Humans Male Mice Mice, Knockout Middle Aged Myocytes, Cardiac Parasitemia Survival Analysis Trypanosoma cruzi |
| description |
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 Benatar et al. |
| author |
García, Gabriela Andrea Búa, Jacqueline Elena Toscano, Marta Alicia |
| author_facet |
García, Gabriela Andrea Búa, Jacqueline Elena Toscano, Marta Alicia |
| author_sort |
García, Gabriela Andrea |
| title |
Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells |
| 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 |
| publishDate |
2015 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_19352727_v9_n10_p_Benatar http://hdl.handle.net/20.500.12110/paper_19352727_v9_n10_p_Benatar |
| work_keys_str_mv |
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| _version_ |
1768543008274251776 |