Galectins are animal lectins with high affinity for β-galactosides that drive the immune response through several mechanisms. In particular, the role of galectin-8 (Gal-8) in inflammation remains controversial. To analyze its role in a chronic inflammatory environment, we studied a murine model of Trypanosoma cruzi infection. The parasite induces alterations that lead to the development of chronic cardiomyopathy and/or megaviscera in 30% of infected patients. The strong cardiac inflammation along with fibrosis leads to cardiomyopathy, the most relevant consequence of Chagas disease. By analyzing infected wild-type (iWT) and Gal-8-deficient (iGal-8KO) C57BL/6J mice at the chronic phase (4–5 months post-infection), we observed that the lack of Gal-8 favored a generalized increase in heart, skeletal muscle, and liver inflammation associated with extensive fibrosis, unrelated to tissue parasite loads. Remarkably, increased frequencies of neutrophils and macrophages were observed within cardiac iGal-8KO tissue by flow cytometry. It has been proposed that Gal-8, as well as other galectins, induces the surface expression of the inner molecule phosphatidylserine on activated neutrophils, which serves as an “eat-me” signal for macrophages, favoring viable neutrophil removal and tissue injury protection, a process known as preaparesis. We found that the increased neutrophil rates could be associated with the absence of Gal-8-dependent preaparesis, leading to a diminished neutrophil-clearing capability in macrophages. Thus, our results support that Gal-8 exerts an anti-inflammatory role in chronic T. cruzi infection.

半乳糖凝集素是对 β-半乳糖苷具有高亲和力的动物凝集素，可通过多种机制驱动免疫反应。特别是半乳糖凝集素8（Gal-8）在炎症中的作用仍然存在争议。为了分析其在慢性炎症环境中的作用，我们研究了一种小鼠模型克氏锥虫感染。寄生虫引起的改变导致 30% 的感染患者发展为慢性心肌病和/或巨内脏。强烈的心脏炎症和纤维化导致心肌病，这是恰加斯病最相关的后果。通过在慢性期（感染后 4-5 个月）分析感染的野生型 (iWT) 和 Gal-8 缺陷型 (iGal-8KO) C57BL/6J 小鼠，我们观察到 Gal-8 的缺乏有利于普遍与广泛纤维化相关的心脏、骨骼肌和肝脏炎症增加，与组织寄生虫负荷无关。值得注意的是，通过流式细胞术在心脏 iGal-8KO 组织中观察到中性粒细胞和巨噬细胞的频率增加。有人提出，Gal-8 以及其他半乳凝素，诱导激活的嗜中性粒细胞上的内分子磷脂酰丝氨酸的表面表达，这可作为巨噬细胞的“吃我”信号，有利于去除可行的嗜中性粒细胞和保护组织损伤，这一过程称为预轻瘫。我们发现中性粒细胞率的增加可能与缺乏 Gal-8 依赖性预轻瘫有关，导致巨噬细胞中中性粒细胞清除能力的降低。因此，我们的结果支持 Gal-8 在慢性病中发挥抗炎作用。导致巨噬细胞的中性粒细胞清除能力下降。因此，我们的结果支持 Gal-8 在慢性病中发挥抗炎作用。导致巨噬细胞的中性粒细胞清除能力下降。因此，我们的结果支持 Gal-8 在慢性病中发挥抗炎作用。T. cruzi感染。