Polypropylene nanoplastic exposure leads to lung inflammation through p38-mediated NF-κB pathway due to mitochondrial damage.

IF 7.2 1区 医学 Q1 TOXICOLOGY Particle and Fibre Toxicology Pub Date : 2023-01-10 DOI:10.1186/s12989-022-00512-8
Jong-Hwan Woo, Hyeon Jin Seo, Jun-Young Lee, Iljung Lee, Kisoo Jeon, Bumseok Kim, Kyuhong Lee
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引用次数: 13

Abstract

Background: Polypropylene (PP) is used in various products such as disposable containers, spoons, and automobile parts. The disposable masks used for COVID-19 prevention mainly comprise PP, and the disposal of such masks is concerning because of the potential environmental pollution. Recent reports have suggested that weathered PP microparticles can be inhaled, however, the inhalation toxicology of PP microparticles is poorly understood.

Results: Inflammatory cell numbers, reactive oxygen species (ROS) production, and the levels of inflammatory cytokines and chemokines in PP-instilled mice (2.5 or 5 mg/kg) increased significantly compared to with those in the control. Histopathological analysis of the lung tissue of PP-stimulated mice revealed lung injuries, including the infiltration of inflammatory cells into the perivascular/parenchymal space, alveolar epithelial hyperplasia, and foamy macrophage aggregates. The in vitro study indicated that PP stimulation causes mitochondrial dysfunction including mitochondrial depolarization and decreased adenosine triphosphate (ATP) levels. PP stimulation led to cytotoxicity, ROS production, increase of inflammatory cytokines, and cell deaths in A549 cells. The results showed that PP stimulation increased the p-p38 and p-NF-κB protein levels both in vivo and in vitro, while p-ERK and p-JNK remained unchanged. Interestingly, the cytotoxicity that was induced by PP exposure was regulated by p38 and ROS inhibition in A549 cells.

Conclusions: These results suggest that PP stimulation may contribute to inflammation pathogenesis via the p38 phosphorylation-mediated NF-κB pathway as a result of mitochondrial damage.

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聚丙烯纳米塑料暴露通过p38介导的NF-κB途径导致线粒体损伤导致肺部炎症。
背景:聚丙烯(PP)用于各种产品,如一次性容器、勺子和汽车零部件。用于新型冠状病毒防护的一次性口罩主要由PP材料组成,其处理可能会对环境造成污染,值得关注。最近的报道表明,风化的PP微粒可以被吸入,然而,PP微粒的吸入毒性尚不清楚。结果:与对照组相比,注射pp(2.5或5 mg/kg)小鼠的炎症细胞数量、活性氧(ROS)产生以及炎症细胞因子和趋化因子水平显著增加。pp刺激小鼠肺组织的组织病理学分析显示肺损伤,包括炎症细胞浸润到血管周围/实质间隙,肺泡上皮增生,泡沫状巨噬细胞聚集。体外研究表明,PP刺激引起线粒体功能障碍,包括线粒体去极化和三磷酸腺苷(ATP)水平下降。PP刺激导致A549细胞的细胞毒性、ROS产生、炎症细胞因子增加和细胞死亡。结果表明,PP刺激提高了体内和体外p-p38和p-NF-κB蛋白水平,而p-ERK和p-JNK保持不变。有趣的是,在A549细胞中,PP暴露诱导的细胞毒性受到p38和ROS抑制的调节。结论:这些结果表明,PP刺激可能通过p38磷酸化介导的NF-κB途径导致线粒体损伤,从而促进炎症发病。
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来源期刊
CiteScore
15.90
自引率
4.00%
发文量
69
审稿时长
6 months
期刊介绍: Particle and Fibre Toxicology is an online journal that is open access and peer-reviewed. It covers a range of disciplines such as material science, biomaterials, and nanomedicine, focusing on the toxicological effects of particles and fibres. The journal serves as a platform for scientific debate and communication among toxicologists and scientists from different fields who work with particle and fibre materials. The main objective of the journal is to deepen our understanding of the physico-chemical properties of particles, their potential for human exposure, and the resulting biological effects. It also addresses regulatory issues related to particle exposure in workplaces and the general environment. Moreover, the journal recognizes that there are various situations where particles can pose a toxicological threat, such as the use of old materials in new applications or the introduction of new materials altogether. By encompassing all these disciplines, Particle and Fibre Toxicology provides a comprehensive source for research in this field.
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