AUTHOR=da Silva Aline A. , Teixeira Thaise L. , Teixeira Samuel C. , Machado Fabrício C. , dos Santos Marlus A. , Tomiosso Tatiana C. , Tavares Paula C. B. , Brígido Rebecca T. e Silva , Martins Flávia Alves , Silva Nadjania S. de Lira , Rodrigues Cassiano C. , Roque-Barreira Maria C. , Mortara Renato A. , Lopes Daiana S. , Ávila Veridiana de Melo Rodrigues , Silva Claudio V. da TITLE=Galectin-3: A Friend but Not a Foe during Trypanosoma cruzi Experimental Infection JOURNAL=Frontiers in Cellular and Infection Microbiology VOLUME=7 YEAR=2017 URL=https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2017.00463 DOI=10.3389/fcimb.2017.00463 ISSN=2235-2988 ABSTRACT=

Trypanosoma cruzi 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 T. cruzi 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 T. cruzi experimental infection. Our results demonstrated that lack of Gal-3 enhanced in vitro replication of intracellular parasites, increased in vivo 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 T. cruzi infection, preventing heart damage and fibrosis.