Fernandez Alarcon Jennifer, Perez Schmidt Patricia, Panini Nicolo, Caruso Francesca, Violatto Martina B, Sukubo Naths Grazia, Martinez-Serra Alberto, Ekalle-Soppo Charlotte Blanche, Morelli Annalisa, Moscatiello Giulia Yuri, Grasselli Chiara, Corbelli Alessandro, Fiordaliso Fabio, Kelk Joe, Petrosilli Laura, d'Orazio Giuseppe, Mateu Ferrando Ruth, Verdaguer Ferrer Ariadna, Fornaguera Cristina, Lay Luigi, Fumagalli Stefano, Recchia Sandro, Monopoli Marco P, Polito Laura, Bigini Paolo, Sitia Giovanni
Department of Molecular Biochemistry and Pharmacology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, Milano, 20156, Italy.
Grup d'Enginyeria de Materials (GEMAT), Institut Químic de Sarrià (IQS), Universitat Ramon Llull (URL), Via Augusta 390, Barcelona, 08017, Spain.
Adv Sci (Weinh). 2025 Apr;12(16):e2407458. doi: 10.1002/advs.202407458. Epub 2025 Feb 14.
Macrophages are crucial drivers of innate immunity. Reprogramming macrophages to a restorative phenotype in cancer or autoimmune diseases can stop their cancer-promoting activity or trigger anti-inflammatory immunity. Glycans have emerged as key components for immunity as they are involved in many pathophysiological disorders. Previous studies have demonstrated that supraphysiological amounts of mannose (Man) or sialic acid (Sia) can inhibit tumor growth and stimulate differentiation of regulatory T cells. Man is known to affect glucose metabolism in glycolysis by competing for the same intracellular transporters and affecting macrophage polarization, whereas Sia alters macrophage differentiation via signaling through Siglec-1. Herein, this work describes a macrophage targeting platform using gold nanoparticles (GNPs) functionalized with Man and Sia monosaccharides which exhibit high liver tropism. A single dose of glyco-GNPs can convert macrophages to a restorative phenotype in two completely different immune environments. Man promotes tumor-associated macrophages toward an antitumorigenic activity in a MC38 liver colorectal cancer model by secretion of TNF-α, IL -1β, and IL -6 in the tumor microenvironment. However, in a proinflammatory environment, as observed in a mouse model of autoimmune disease, primary biliary cholangitis, Man impairs the production of TNF-α, IL-1β, Arg1, and IL-6 cytokines. The results probe the dual role of Man in macrophage repolarization in response to the immune system. This study is a proof-of-concept that demonstrates that nanomedicine using specific glycans designed to target other immune cells such as myeloid cells, are a promising strategy not only against cancer but also against other pathologies such as autoimmune diseases.
巨噬细胞是固有免疫的关键驱动因素。在癌症或自身免疫性疾病中将巨噬细胞重编程为具有修复功能的表型,可以阻止其促进癌症的活性或触发抗炎免疫。聚糖已成为免疫的关键组成部分,因为它们参与了许多病理生理紊乱。先前的研究表明,超生理量的甘露糖(Man)或唾液酸(Sia)可以抑制肿瘤生长并刺激调节性T细胞的分化。已知Man通过竞争相同的细胞内转运蛋白影响糖酵解中的葡萄糖代谢并影响巨噬细胞极化,而Sia通过Siglec-1信号传导改变巨噬细胞分化。在此,这项工作描述了一种巨噬细胞靶向平台,该平台使用用Man和Sia单糖功能化的金纳米颗粒(GNP),其表现出高肝脏嗜性。单剂量的糖基化GNP可以在两种完全不同的免疫环境中将巨噬细胞转化为具有修复功能的表型。在MC38肝结直肠癌模型中,Man通过在肿瘤微环境中分泌TNF-α、IL-1β和IL-6促进肿瘤相关巨噬细胞向抗肿瘤活性发展。然而,在自身免疫性疾病原发性胆汁性胆管炎的小鼠模型中观察到的促炎环境中,Man会损害TNF-α、IL-1β、精氨酸酶1和IL-6细胞因子的产生。这些结果探究了Man在响应免疫系统时巨噬细胞重极化中的双重作用。这项研究是一个概念验证,表明使用设计用于靶向其他免疫细胞(如髓样细胞)的特定聚糖的纳米药物不仅是对抗癌症的有前景的策略,也是对抗自身免疫性疾病等其他病症的有前景的策略。