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PLoS Negl Trop Dis. 2015 Oct 9;9(10):e0004148. doi: 10.1371/journal.pntd.0004148. eCollection 2015.

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

Author information

1
Laboratorio de Biología Molecular de la Enfermedad de Chagas (LabMECh), Instituto de Investigaciones en Ingeniería Genética y Biología Molecular (INGEBI-CONICET), Buenos Aires, Argentina.
2
Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben", Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán", Buenos Aires, Argentina.
3
Laboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME-CONICET), Buenos Aires, Argentina.
4
Hospital Pedro de Elizalde, Servicio de Cardiología, Sección Electrofisiología, Buenos Aires, Argentina.
5
Laboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME-CONICET), Buenos Aires, Argentina; Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina.

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.

PMID:
26451839
PMCID:
PMC4599936
DOI:
10.1371/journal.pntd.0004148
[Indexed for MEDLINE]
Free PMC Article

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