Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Uberlândia, Brazil.
Departamento de Microbiologia, Imunologia e Parasitologia, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, Brazil.
Front Cell Infect Microbiol. 2017 Nov 3;7:463. doi: 10.3389/fcimb.2017.00463. eCollection 2017.
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 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 experimental infection. Our results demonstrated that lack of Gal-3 enhanced replication of intracellular parasites, increased 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 infection, preventing heart damage and fibrosis.
与宿主细胞相互作用，包括心肌细胞，并诱导细胞因子、趋化因子、金属蛋白酶和聚糖结合蛋白的产生。在聚糖结合蛋白中有一种是半乳糖凝集素-3（Galectin-3，Gal-3），它在感染后上调。Gal-3 是凝集素家族的一员，对含有β-半乳糖的分子具有亲和力；它可以存在于细胞核和细胞质中，可以与膜结合或分泌。这种凝集素参与多种免疫调节和寄生虫感染过程。在这里，我们探讨了 Gal-3 缺乏在急性和慢性实验感染期间的后果。我们的结果表明，缺乏 Gal-3 会增强细胞内寄生虫的复制，增加全身寄生虫血症，并减少白细胞募集。此外，我们还观察到感染 Gal-3 基因敲除小鼠的脾脏和心脏中促炎细胞因子的分泌减少。Gal-3 的缺乏还导致肥大细胞募集增加和心脏组织纤维化。总之，半乳糖凝集素-3 的表达在控制感染、预防心脏损伤和纤维化方面起着关键作用。
