ArticlePLoS neglected tropical diseases2015
Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells.
Article in PLoS neglected tropical diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Healing mechanisms of Galectin-1 in the ischemic heart.Cell biochemistry and biophysics · 2026Review
- Regulated expression of galectins 1 and 3 IS associated with dysregulated T cell responses in pulmonary and pleural tuberculosis.Medical microbiology and immunology · 2025Article
- Novel 3D human trophoblast culture to exploreFrontiers in cellular and infection microbiology · 2024Article
- Haptoglobin is dispensable for haemoglobin uptake byFrontiers in immunology · 2024Article
- Differential cardiomyocyte transcriptomic remodeling during in vitro Trypanosoma cruzi infection using laboratory strains provides implications on pathogenic host responses.Tropical medicine and health · 2023Article
- Galectins in Protozoan Parasitic Diseases: Potential Applications in Diagnostics and Therapeutics.Cells · 2023Review
- Inflammation and mitochondria in the pathogenesis of chronic Chagas disease cardiomyopathy.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Host Cell Rap1b mediates cAMP-dependent invasion by Trypanosoma cruzi.PLoS neglected tropical diseases · 2023Article
- The interplay of galectins-1, -3, and -9 in the immune-inflammatory response underlying cardiovascular and metabolic disease.Cardiovascular diabetology · 2022Review
- Molecular and Clinical Aspects of Chronic Manifestations in Chagas Disease: A State-of-the-Art Review.Pathogens (Basel, Switzerland) · 2021Review
- Chagas Cardiomyopathy: From Romaña Sign to Heart Failure and Sudden Cardiac Death.Pathogens (Basel, Switzerland) · 2021Review
- Host-parasite dynamics in Chagas disease from systemic to hyper-local scales.Parasite immunology · 2021Review
- Galectin-Receptor Interactions Regulates Cardiac Pathology Caused byFrontiers in immunology · 2021Article
- Biomarkers and Their Possible Functions in the Intestinal Microenvironment of Chagasic Megacolon: An Overview of the (Neuro)inflammatory Process.Journal of immunology research · 2021Review
- Article
- Galectins in Chagas Disease: A Missing Link BetweenFrontiers in microbiology · 2021Review
- The Glycan Structure ofMolecules (Basel, Switzerland) · 2020Review
- The oligomeric assembly of galectin-11 is critical for anti-parasitic activity in sheep (Ovis aries).Communications biology · 2020Article
- Utilization of Galectins by Pathogens for Infection.Frontiers in immunology · 2020Review
- Anti-inflammatory Role of Galectin-8 DuringFrontiers in cellular and infection microbiology · 2020Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic 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
findingsHere 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.
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