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

Frontiers in Cellular and Infection Microbiology

Brí¹  Silva, Nadjania S. de Lira¹  cio C.¹  da Silva, Aline A.¹  vila, Veridiana de Melo Rodrigues¹  Lopes, Daiana S.²  Teixeira, Samuel C.⁵  Tomiosso, Tatiana C.⁵  Roque-Barreira, Maria C.⁵  Martins, Flá⁵  Teixeira, Thaise L.⁸  Rodrigues, Cassiano C.⁸  Silva, Claudio V. da⁸  dos Santos, Marlus A.⁸  gido, Rebecca T. e Silva⁸  via Alves⁹  Machado, Fabrí⁹  Tavares, Paula C. B.⁹  Mortara, Renato A.⁹  Á^1,10 

[1] Departamento de Imunologia, Instituto de CiêDepartamento de Microbiologia, Imunologia e Parasitologia, Escola Paulista de Medicina, Universidade Federal de SãFaculdade de Medicina de RibeirãLaboratódicas, Universidade Federal de Uberlâmica e Toxinas Animais, Instituto de Genémica, Universidade Federal de Uberlâncias Bioméndia, Brazil;o Paulo, Brazil;o Preto, Universidade de Sãrio de Bioquítica e Bioquí

关键词: galectin-3;    Trypanosoma cruzi;    Heart;    Fibrosis;    Leukocytes.;   

DOI  :  10.3389/fcimb.2017.00463

学科分类：生物科学（综合）

来源: Frontiers

【 摘 要 】

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 Trypanosoma 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.

【 授权许可】

CC BY