Enantiomer-Dependent Uptake of Chiral Nanoparticles in Macrophages Modulates the Inflammatory Response through the NF-κB Pathway

NF-κB 对映体 炎症反应 化学 炎症 NFKB1型 纳米颗粒 细胞生物学 信号转导 药理学 生物 立体化学 纳米技术 生物化学 材料科学 免疫学 基因 转录因子
作者
Jinghua Hao,Yijin Tian,Jie Tang,Nali Zhu,Zhigang Li,Lingxiangyu Li,Yawei Wang,Guibin Jiang
出处
期刊:Environmental Science & Technology [American Chemical Society]
卷期号:59 (13): 6428-6439 被引量:7
标识
DOI:10.1021/acs.est.4c12577
摘要

Infectious inflammation caused by pathogens or environmental pollutants remains a major global health issue. Therefore the development of novel strategies to efficaciously control infectious inflammation is urgently required. Nuclear factor-κB (NF-κB) as the central activator of pro-inflammatory genes plays a pivotal role in infectious inflammation. Here, nanoscale chirality was designed to modulate the inflammatory response through enantiomer-dependent blockade of the NF-κB signaling pathway. Chiral gold nanoparticles (AuNPs) with good cytocompatibility were prepared through a one-pot seedless method under wild conditions, showing efficacious alleviation of lipopolysaccharide (LPS)-induced inflammation in vitro and in vivo only by AuNPs with levorotatory chirality (L-AuNPs) rather than the dextrorotatory enantiomer (D-AuNPs). Mechanism investigation elucidated that lysosomal acidification of macrophages was inhibited through a high cellular uptake of L-AuNPs due to their weak interaction energy with cell membranes. Accordingly, the NF-κB rather than mitogen-activated protein kinase pathway was blocked by L-AuNPs through the selective inhibition of p65 phosphorylation, wherein the nuclear translocation of p65 was simultaneously depressed, so the secretion of pro-inflammatory mediators was reduced significantly. This study suggests that imparting chirality to nanoparticles can provide a novel protocol to efficaciously modulate health risks arising from infectious inflammation by improving the uptake of nanoparticles with anti-inflammatory activity.
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