Galectin-3: A Friend but Not a Foe during Trypanosoma cruzi Experimental Infection

Abstract

<i>Trypanosoma cruzi</i> interacts with host cells, including cardiomyocytes, and induces the production of cytokines, chemokines, metalloproteinases, and glycan-binding proteins. Among the glycan-binding proteins is Galectin-3 (Gal-3), which is upregulated after <i>T. cruzi</i> infection. Gal-3 is a member of the lectin family with affinity for β-galactose containing molecules; it can be found in both the nucleus and the cytoplasm and can be either membrane-associated or secreted. This lectin is involved in several immunoregulatory and parasite infection process. Here, we explored the consequences of Gal-3 deficiency during acute and chronic <i>T. cruzi</i> experimental infection. Our results demonstrated that lack of Gal-3 enhanced <i>in vitro</i> replication of intracellular parasites, increased <i>in vivo</i> systemic parasitaemia, and reduced leukocyte recruitment. Moreover, we observed decreased secretion of pro-inflammatory cytokines in spleen and heart of infected Gal-3 knockout mice. Lack of Gal-3 also led to elevated mast cell recruitment and fibrosis of heart tissue. In conclusion, galectin-3 expression plays a pivotal role in controlling <i>T. cruzi</i> infection, preventing heart damage and fibrosis.