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

• Autor(a) principal: da Silva, Aline A.
• Data de Publicação: 2017
• Outros Autores: Teixeira, Thaise L., Teixeira, Samuel C., Machado, Fabricio C. [UNIFESP], dos Santos, Marlus A., Tomiosso, Tatiana C., Tavares, Paula C. B., e Silva Brigido, Rebecca T., Martins, Flavia Alves, de Lira Silva, Nadjania S. [UNIFESP], Rodrigues, Cassiano C., Roque-Barreira, Maria C., Mortara, Renato A. [UNIFESP], Lopes, Daiana S., Rodrigues Avila, Veridiana de Melo, da Silva, Claudio V.
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UNIFESP
• Texto Completo: http://dx.doi.org/10.3389/fcimb.2017.00463; https://repositorio.unifesp.br/handle/11600/58182
• topic: galectin-3; Trypanosoma cruzi; heart; fibrosis; leukocytes

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 beta-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.