%0 Journal Article
%T Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells
%A Alejandro F. Benatar
%A Gabriel A. Rabinovich
%A Gabriela A. Garc赤a
%A Jacqeline Bua
%A Jorge Scaglione
%A Juan C. Stupirski
%A Juan P. Cerliani
%A Karina A. G車mez
%A Laura M. Tasso
%A Marta A. Toscano
%A Miriam Postan
%J -
%D 2015
%R 10.1371/journal.pntd.0004148
%X 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每1 (Gal每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每1 cardiac cells to Gal每1 reduced the percentage of infection by two different T. cruzi strains, Tulahu谷n (TcVI) and Brazil (TcI). In addition, Gal每1 prevented exposure of phosphatidylserine and early events in the apoptotic program by parasite infection on HL每1 cells. These effects were not mediated by direct interaction with the parasite surface, suggesting that Gal每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每1 to the cell surface. Consistent with these data, Gal每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 Tulahu谷n strain.   Conclusion/Significance Our results indicate that Gal每1 modulates T. cruzi infection of cardiac cells, highlighting the relevance of galectins and their ligands as regulators of host-parasite interactions
%K Parasitic diseases
%K Trypanosoma cruzi
%K Trypomastigotes
%K Lectins
%K Parasitemia
%K Heart
%K Chagas disease
%K Inflammation
%U https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0004148