Research Laboratory of Lung Diseases, Section of Cell Biology, IRCCS Policlinico San Matteo Foundation, 27100 Pavia, Italy.
Institut Galien Paris-Saclay, CNRS, Université Paris-Saclay, Châtenay-Malabry, 92296 Paris, France.
Int J Mol Sci. 2021 Jul 20;22(14):7743. doi: 10.3390/ijms22147743.
Chronic lung allograft dysfunction (CLAD) and interstitial lung disease associated with collagen tissue diseases (CTD-ILD) are two end-stage lung disorders in which different chronic triggers induce activation of myo-/fibroblasts (LFs). Everolimus, an mTOR inhibitor, can be adopted as a potential strategy for CLAD and CTD-ILD, however it exerts important side effects. This study aims to exploit nanomedicine to reduce everolimus side effects encapsulating it inside liposomes targeted against LFs, expressing a high rate of CD44. PEGylated liposomes were modified with high molecular weight hyaluronic acid and loaded with everolimus (PEG-LIP(ev)-HA400kDa). Liposomes were tested by in vitro experiments using LFs derived from broncholveolar lavage (BAL) of patients affected by CLAD and CTD-ILD, and on alveolar macrophages (AM) and lymphocytes isolated, respectively, from BAL and peripheral blood. PEG-LIP-HA400kDa demonstrated to be specific for LFs, but not for CD44-negative cells, and after loading everolimus, PEG-LIP(ev)-HA400kDa were able to arrest cell cycle arrest and to decrease phospho-mTOR level. PEG-LIP(ev)-HA400kDa showed anti-inflammatory effect on immune cells. This study opens the possibility to use everolimus in lung fibrotic diseases, demonstrating that our lipids-based vehicles can vehicle everolimus inside cells exerting the same drug molecular effect, not only in LFs, but also in immune cells.
慢性肺移植物功能障碍 (CLAD) 和与胶原组织疾病相关的间质性肺疾病 (CTD-ILD) 是两种终末期肺部疾病,其中不同的慢性触发因素诱导肌成纤维细胞 (LFs) 的激活。雷帕霉素,一种 mTOR 抑制剂,可作为 CLAD 和 CTD-ILD 的潜在策略,但它会产生重要的副作用。本研究旨在利用纳米医学通过将其包裹在针对表达高比率 CD44 的 LF 的脂质体中来减少雷帕霉素的副作用。聚乙二醇化脂质体用高分子量透明质酸进行修饰,并负载雷帕霉素 (PEG-LIP(ev)-HA400kDa)。使用源自 CLAD 和 CTD-ILD 患者支气管肺泡灌洗液 (BAL) 的 LF、分别从 BAL 和外周血中分离的肺泡巨噬细胞 (AM) 和淋巴细胞进行了体外实验来测试脂质体。PEG-LIP-HA400kDa 被证明对 LF 具有特异性,但对 CD44 阴性细胞没有特异性,并且在负载雷帕霉素后,PEG-LIP(ev)-HA400kDa 能够阻止细胞周期停滞并降低磷酸化 mTOR 水平。PEG-LIP(ev)-HA400kDa 对免疫细胞具有抗炎作用。本研究为在肺纤维化疾病中使用雷帕霉素开辟了可能性,证明我们基于脂质的载体可以将雷帕霉素输送到细胞内,发挥相同的药物分子作用,不仅在 LFs 中,而且在免疫细胞中。