%A da Silva,Aline A. %A Teixeira,Thaise L. %A Teixeira,Samuel C. %A Machado,Fabrício C. %A dos Santos,Marlus A. %A Tomiosso,Tatiana C. %A Tavares,Paula C. B. %A Brígido,Rebecca T. e Silva %A Martins,Flávia Alves %A Silva,Nadjania S. de Lira %A Rodrigues,Cassiano C. %A Roque-Barreira,Maria C. %A Mortara,Renato A. %A Lopes,Daiana S. %A Ávila,Veridiana de Melo Rodrigues %A Silva,Claudio V. da %D 2017 %J Frontiers in Cellular and Infection Microbiology %C %F %G English %K galectin-3,Trypanosoma cruzi,Heart,Fibrosis,Leukocytes. %Q %R 10.3389/fcimb.2017.00463 %W %L %M %P %7 %8 2017-November-03 %9 Original Research %+ Aline A. da Silva,Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia,Brazil,alinealvesufu@hotmail.com %+ Claudio V. da Silva,Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia,Brazil,silva_cv@yahoo.com.br %# %! Galectin-3 controls Trypanosoma cruzi infection and limits heart damage %* %< %T Galectin-3: A Friend but Not a Foe during Trypanosoma cruzi Experimental Infection %U https://www.frontiersin.org/articles/10.3389/fcimb.2017.00463 %V 7 %0 JOURNAL ARTICLE %@ 2235-2988 %X 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.