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

  • da Silva A
  • Teixeira T
  • Teixeira S
  • et al.
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Abstract

© 2017 da Silva, Teixeira, Teixeira, Machado, dos Santos, Tomiosso, Tavares, Brígido, Martins, Silva, Rodrigues, Roque-Barreira, Mortara, Lopes, ávila and Silva. 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.

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APA

da Silva, A. A., Teixeira, T. L., Teixeira, S. C., Machado, F. C., dos Santos, M. A., Tomiosso, T. C., … Silva, C. V. da. (2017). Galectin-3: A Friend but Not a Foe during Trypanosoma cruzi Experimental Infection. Frontiers in Cellular and Infection Microbiology, 7. https://doi.org/10.3389/fcimb.2017.00463

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