Metabolomics reveals that PS-NPs promote lung injury by regulating prostaglandin B1 through the cGAS-STING pathway

Lihui Xuan; Yin Wang; Can Qu; Yuhui Yan; Wensen Yi; Jingjing Yang; Magdalena Skonieczna; Cuimei Chen; Justyna Miszczyk; Dmitry S Ivanov; Hesham M H Zakaly; Vladimir Markovic; Ruixue Huang

doi:10.1016/j.chemosphere.2023.140108

Metabolomics reveals that PS-NPs promote lung injury by regulating prostaglandin B1 through the cGAS-STING pathway

Chemosphere. 2023 Nov:342:140108. doi: 10.1016/j.chemosphere.2023.140108. Epub 2023 Sep 13.

Authors

Affiliations

¹ Department of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, Hunan Province, 410078, China.
² Department of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, Hunan Province, 410078, China. Electronic address: 2959165855@qq.com.
³ Department of Systems Biology and Engineering, Silesian University of Technology, Institute of Automatic Control, Akademicka 16, Gliwice, 44-100, Poland; Biotechnology Centre, Silesian University of Technology, Krzywoustego 8, Gliwice, 44-100, Poland. Electronic address: magdalena.skonieczna@polsl.pl.
⁴ School of Public Health, Xiang Nan University, Chenzhou, 423000, Hunan, China. Electronic address: cmc_xnxy66@163.com.
⁵ Department of Medical Physics, Cyclotron Centre Bronowice Institute of Nuclear Physics Polish Academy of Sciences, PL-31342, Krakow, Poland. Electronic address: Justyna.Miszczyk@ifj.edu.pl.
⁶ Quantum Electronics Division, Lebedev Physical Institute, 119991, Moscow, Russia. Electronic address: ivanov@uni-kassel.ed.
⁷ Institute of Physics and Technology, Ural Federal University, Yekaterinburg, 620002, Russia; Physics Department, Faculty of Science, Al-Azhar University, 71524, Assuit, Egypt. Electronic address: h.m.zakaly@gmail.com.
⁸ Faculty of Sciences, University of Kragujevac, 34000, Kragujevac, Serbia. Electronic address: vmarkovic@kg.ac.rs.
⁹ Department of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, Hunan Province, 410078, China. Electronic address: huangruixue@csu.edu.cn.

PMID: 37714480
DOI: 10.1016/j.chemosphere.2023.140108

Abstract

Nanoplastics have been widely studied as environmental pollutants, which can accumulate in the human body through the food chain or direct contact. Research has shown that nanoplastics can affect the immune system and mitochondrial function, but the underlying mechanisms are unclear. Lungs and macrophages have important immune and metabolic functions. This study explored the effects of 100 nm PS-NPs on innate immunity, mitochondrial function, and cellular metabolism-related pathways in lung (BEAS-2B) cells and macrophages (RAW264.7). The results had shown that PS-NPs exposure caused a decrease in mitochondrial membrane potential, intracellular ROS accumulation, and Ca²⁺ overload, and activated the cGAS-STING signaling pathway related to innate immunity. These changes had been observed at concentrations of PS-NPs as low as 60 μg/mL, which might have been comparable to environmental levels. Non-target metabolomics and Western Blotting results confirmed that PS-NPs regulated prostaglandin B1 and other metabolites to cause cell damage through the cGAS-STING pathway. Supplementation of prostaglandin B1 alleviated the immune activation and metabolic disturbance caused by PS-NPs exposure. This study identified PS-NPs-induced innate immune activation, mitochondrial dysfunction, and metabolic toxicity pathways, providing new insights into the potential for adverse outcomes of NPs in human life.

Keywords: Cytotoxicity; Innate immunity; Metabolic toxicity; Mitochondrial damage; Nanoplastics.