Department of Materials Science and Engineering, College of Engineering, Drexel University, Philadelphia, PA, USA.
Biomater Sci. 2017 Sep 26;5(10):2131-2143. doi: 10.1039/c7bm00294g.
Chronic inflammatory disorders such as rheumatoid arthritis are characterized by excessive pro-inflammatory or "M1" activation of macrophages, the primary cells of the innate immune system. Current treatments include delivery of glucocorticoids (e.g. dexamethasone - Dex), which reduce pro-inflammatory M1 behaviour in macrophages. However, these treatments have many off-target effects on cells other than macrophages, resulting in broad immunosuppression. To limit such side effects, drug-incorporated nano- and microparticles may be used to selectively target macrophages via phagocytosis, because of their roles as highly effective phagocytes in the body. In this study, surface-modified nanodiamond (ND) was explored as a platform for the delivery of dexamethasone to macrophages because of ND's rich surface chemistry, which contributes to ND's high potential as a versatile drug delivery platform. After finding that octadecylamine-functionalized nanodiamond (ND-ODA) enhanced adsorption of Dex compared to carboxylated ND, the effects of Dex, ND-ODA, and Dex-adsorbed ND-ODA on primary human macrophage gene expression were characterized. Surprisingly, even in the absence of Dex, ND-ODA had strong anti-inflammatory effects, as determined by multiplex gene expression via NanoString and by protein secretion analysis via ELISA. ND-ODA also inhibited expression of M2a markers yet increased the expression of M2c markers and phagocytic receptors. Interestingly, the adsorption of Dex to ND-ODA further increased some anti-inflammatory effects, but abrogated the effect on phagocytic receptors, compared to its individual components. Overall, the ability of ND-ODA to promote anti-inflammatory and pro-phagocytic behaviour in macrophages, even in the absence of loaded drugs, suggests its potential for use as an anti-inflammatory therapeutic to directly target macrophages through phagocytosis.
慢性炎症性疾病,如类风湿关节炎,其特征在于巨噬细胞过度的促炎或“M1”激活,巨噬细胞是先天免疫系统的主要细胞。目前的治疗方法包括糖皮质激素(如地塞米松-Dex)的递送,它可以降低巨噬细胞中促炎的 M1 行为。然而,这些治疗方法对除巨噬细胞以外的细胞有许多脱靶效应,导致广泛的免疫抑制。为了限制这种副作用,可以使用载药的纳米和微颗粒通过吞噬作用来选择性地靶向巨噬细胞,因为它们在体内作为高效的吞噬细胞发挥作用。在这项研究中,由于纳米金刚石(ND)丰富的表面化学性质,它是一种具有高潜力的多功能药物递送平台,因此被探索作为递送地塞米松到巨噬细胞的平台。在发现十八胺功能化纳米金刚石(ND-ODA)比羧基化 ND 更能增强地塞米松的吸附后,研究了地塞米松、ND-ODA 和吸附在地塞米松的 ND-ODA 上的地塞米松对原代人巨噬细胞基因表达的影响。令人惊讶的是,即使没有地塞米松,ND-ODA 也具有很强的抗炎作用,这是通过 NanoString 进行的多重基因表达和通过 ELISA 进行的蛋白质分泌分析来确定的。ND-ODA 还抑制了 M2a 标志物的表达,但增加了 M2c 标志物和吞噬受体的表达。有趣的是,与单独的成分相比,地塞米松吸附到 ND-ODA 上进一步增加了一些抗炎作用,但取消了对吞噬受体的作用。总的来说,ND-ODA 能够促进巨噬细胞中的抗炎和促吞噬作用,即使在没有负载药物的情况下,这表明它有可能作为一种抗炎治疗剂,通过吞噬作用直接靶向巨噬细胞。