dc.creator | da Silva, Aline A. | |
dc.creator | Teixeira, Thaise L. | |
dc.creator | Teixeira, Samuel C. | |
dc.creator | Machado, Fabricio C. [UNIFESP] | |
dc.creator | dos Santos, Marlus A. | |
dc.creator | Tomiosso, Tatiana C. | |
dc.creator | Tavares, Paula C. B. | |
dc.creator | e Silva Brigido, Rebecca T. | |
dc.creator | Martins, Flavia Alves | |
dc.creator | de Lira Silva, Nadjania S. [UNIFESP] | |
dc.creator | Rodrigues, Cassiano C. | |
dc.creator | Roque-Barreira, Maria C. | |
dc.creator | Mortara, Renato A. [UNIFESP] | |
dc.creator | Lopes, Daiana S. | |
dc.creator | Rodrigues Avila, Veridiana de Melo | |
dc.creator | da Silva, Claudio V. | |
dc.date.accessioned | 2020-09-01T13:21:18Z | |
dc.date.accessioned | 2022-10-07T20:47:07Z | |
dc.date.available | 2020-09-01T13:21:18Z | |
dc.date.available | 2022-10-07T20:47:07Z | |
dc.date.created | 2020-09-01T13:21:18Z | |
dc.date.issued | 2017 | |
dc.identifier | Frontiers In Cellular And Infection Microbiology. Lausanne, v. 7, p. -, 2017. | |
dc.identifier | 2235-2988 | |
dc.identifier | https://repositorio.unifesp.br/handle/11600/58182 | |
dc.identifier | WOS000414310700001.pdf | |
dc.identifier | 10.3389/fcimb.2017.00463 | |
dc.identifier | WOS:000414310700001 | |
dc.identifier.uri | http://repositorioslatinoamericanos.uchile.cl/handle/2250/4022821 | |
dc.description.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 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. | |
dc.language | eng | |
dc.publisher | Frontiers Media Sa | |
dc.relation | Frontiers In Cellular And Infection Microbiology | |
dc.rights | Acesso aberto | |
dc.subject | galectin-3 | |
dc.subject | Trypanosoma cruzi | |
dc.subject | heart | |
dc.subject | fibrosis | |
dc.subject | leukocytes | |
dc.title | Galectin-3: A Friend but Not a Foe during Trypanosoma cruzi Experimental Infection | |
dc.type | Artigo | |