Department of Microbiology and Immunology, University of Illinois at Chicago, Chicago, IL, USA.
Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan, China.
J Nanobiotechnology. 2023 Oct 10;21(1):369. doi: 10.1186/s12951-023-02103-x.
Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb) infection, is still one of the top killers worldwide among infectious diseases. The escape of Mtb from immunological clearance and the low targeting effects of anti-TB drugs remain the substantial challenges for TB control. Iron is particularly required for Mtb growth but also toxic for Mtb in high dosages, which makes iron an ideal toxic decoy for the 'iron-tropic' Mtb. Here, a macrophage-targeted iron oxide nanoparticles (IONPs)-derived IONPs-PAA-PEG-MAN nanodecoy is designed to augment innate immunological and drug killings against intracellular Mtb. IONPs-PAA-PEG-MAN nanodecoy exhibits preferential uptake in macrophages to significantly increase drug uptake with sustained high drug contents in host cells. Moreover, it can serve as a specific nanodecoy for the 'iron-tropic' Mtb to realize the localization of Mtb contained phagosomes surrounding the drug encapsulated nanodecoys and co-localization of Mtb with the drug encapsulated nanodecoys in lysosomes, where the incorporated rifampicin (Rif) can be readily released under acidic lysosomal condition for enhanced Mtb killing. This drug encapsulated nanodecoy can also polarize Mtb infected macrophages into anti-mycobacterial M1 phenotype and enhance M1 macrophage associated pro-inflammatory cytokine (TNF-α) production to trigger innate immunological responses against Mtb. Collectively, Rif@IONPs-PAA-PEG-MAN nanodecoy can synergistically enhance the killing efficiency of intracellular Mtb in in vitro macrophages and ex vivo monocyte-derived macrophages, and also significantly reduce the mycobacterial burdens in the lung of infected mice with alleviated pathology. These results indicate that Rif@IONPs-PAA-PEG-MAN nanodecoy may have a potential for the development of more effective therapeutic strategy against TB by manipulating augmented innate immunity and drug killings.
结核病(TB)是由结核分枝杆菌(Mtb)感染引起的,仍然是全球传染病中导致死亡的主要原因之一。Mtb 逃避免疫清除和抗结核药物靶向作用差仍然是控制 TB 的重大挑战。铁对 Mtb 的生长特别需要,但高剂量对 Mtb 也有毒性,这使得铁成为“嗜铁”Mtb 的理想毒性诱饵。在这里,设计了一种巨噬细胞靶向氧化铁纳米颗粒(IONPs)衍生的 IONPs-PAA-PEG-MAN 纳米诱捕剂,以增强针对细胞内 Mtb 的固有免疫和药物杀伤。IONPs-PAA-PEG-MAN 纳米诱捕剂优先被巨噬细胞摄取,可显著增加药物摄取量,并使宿主细胞内的药物含量持续保持高浓度。此外,它可以作为“嗜铁”Mtb 的特异性纳米诱捕剂,实现含有药物的纳米诱捕剂周围的 Mtb 吞噬体的定位,以及 Mtb 与含有药物的纳米诱捕剂在溶酶体中的共定位,其中结合的利福平(Rif)可以在酸性溶酶体条件下很容易释放出来,以增强 Mtb 杀伤作用。这种载药纳米诱捕剂还可以将感染 Mtb 的巨噬细胞极化到抗分枝杆菌 M1 表型,并增强 M1 巨噬细胞相关的促炎细胞因子(TNF-α)的产生,从而触发针对 Mtb 的固有免疫反应。总的来说,Rif@IONPs-PAA-PEG-MAN 纳米诱捕剂可以协同增强体外巨噬细胞和体外单核细胞衍生巨噬细胞中细胞内 Mtb 的杀伤效率,并显著降低感染小鼠肺部的分枝杆菌负荷,减轻病理。这些结果表明,Rif@IONPs-PAA-PEG-MAN 纳米诱捕剂通过操纵增强的固有免疫和药物杀伤,可能为开发更有效的抗结核治疗策略提供潜力。