Galectin-3: A Friend but Not a Foe during Trypanosoma cruzi Experimental Infection
Nenhuma Miniatura disponível
Arquivos
Data
2017
Autores
da Silva, Aline A.
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]
Orientadores
Tipo
Artigo
Título da Revista
ISSN da Revista
Título de Volume
Resumo
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.
Descrição
Citação
Frontiers In Cellular And Infection Microbiology. Lausanne, v. 7, p. -, 2017.