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吸入型杂化仿生纳米平台用于急性肺损伤治疗中序贯药物释放和重塑肺免疫稳态

An Inhalable Hybrid Biomimetic Nanoplatform for Sequential Drug Release and Remodeling Lung Immune Homeostasis in Acute Lung Injury Treatment.

机构信息

State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macau 999078, China.

Department of Pharmacology and Pharmacy, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong 999077, China.

出版信息

ACS Nano. 2023 Jun 27;17(12):11626-11644. doi: 10.1021/acsnano.3c02075. Epub 2023 Jun 7.

Abstract

Interactions of lung macrophages and recruited neutrophils with the lung microenvironment continuously aggravate the dysregulation of lung inflammation in the pathogenesis of acute lung injury (ALI) or acute respiratory distress syndrome (ARDS). Either modulating macrophages or destroying neutrophil counts cannot guarantee a satisfactory outcome in ARDS treatment. Aimed at inhibiting the coordinated action of neutrophils and macrophages and modulating the hyper-inflammatory condition, an inhalable biomimetic sequential drug-releasing nanoplatform was developed for the combinatorial treatment of ALI. The nanoplatform (termed D-SEL) was made by conjugating DNase I, as outer cleavable arms, to a serum exosomal and liposomal hybrid nanocarrier (termed SEL) via a matrix metalloproteinase 9 (MMP-9)-cleavable peptide and then encapsulating methylprednisolone sodium succinate (MPS). In lipopolysaccharide (LPS) induced ALI in mice, the MPS/D-SEL moved through muco-obstructive airways and was retained in the alveoli for over 24 h postinhalation. DNase I was then released from the nanocarrier first after responding to MMP-9, resulting in inner SEL core exposure, which precisely delivered MPS into macrophages for promoting M2 macrophage polarization. Local and sustained DNase I release degraded dysregulated neutrophil extracellular traps (NETs) and suppressed neutrophil activation and the mucus plugging microenvironment, which in turn amplified M2 macrophage polarization efficiency. Such dual-stage drug release behavior facilitated down-regulation of pro-inflammatory cytokines in the lung but anti-inflammatory cytokine production through remodeling lung immune homeostasis, ultimately promoting lung tissue repair. This work presents a versatile hybrid biomimetic nanoplatform for the local pulmonary delivery of dual-drug therapeutics and displays potential in the treatment of acute inflammation.

摘要

肺巨噬细胞和募集的中性粒细胞与肺部微环境的相互作用不断加剧急性肺损伤 (ALI) 或急性呼吸窘迫综合征 (ARDS) 发病机制中肺炎症的失调。调节巨噬细胞或破坏中性粒细胞计数都不能保证 ARDS 治疗的满意结果。为了抑制中性粒细胞和巨噬细胞的协同作用,并调节过度炎症状态,开发了一种可吸入的仿生序贯药物释放纳米平台,用于 ALI 的联合治疗。该纳米平台(称为 D-SEL)是通过基质金属蛋白酶 9(MMP-9)可切割肽将 DNA 酶 I(作为外可切割臂)与血清外泌体和脂质体混合纳米载体(称为 SEL)连接,然后包封甲泼尼龙琥珀酸钠(MPS)而制成的。在脂多糖(LPS)诱导的小鼠 ALI 中,MPS/D-SEL 通过黏液阻塞性气道移动,并在吸入后 24 小时以上保留在肺泡中。然后,DNase I 首先从纳米载体中释放出来,响应 MMP-9,导致内 SEL 核心暴露,将 MPS 精确递送至巨噬细胞以促进 M2 巨噬细胞极化。局部和持续的 DNA 酶 I 释放降解失调的中性粒细胞胞外陷阱(NETs)并抑制中性粒细胞激活和黏液塞微环境,从而放大 M2 巨噬细胞极化效率。这种双阶段药物释放行为通过重塑肺部免疫稳态来促进肺部促炎细胞因子的下调和抗炎细胞因子的产生,最终促进肺部组织修复。这项工作提出了一种多功能混合仿生纳米平台,用于局部肺部递送达两种药物的治疗,并显示出在治疗急性炎症方面的潜力。

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