Exposure to polystyrene nanoplastics induces abnormal activation of innate immunity via the cGAS-STING pathway
Endogenous immune defenses provide an intrinsic barrier against external entity invasion. Microplastics in the environment, especially those at the nanoscale (nanoplastics or NPs), may pose latent health risks through direct exposure. While links between nanoplastics and inflammatory processes have...
| প্রধান লেখক: | , , , , , , , , , , |
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| বিন্যাস: | প্রবন্ধ |
| ভাষা: | English |
| প্রকাশিত: |
Elsevier
2024-04-01
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| মালা: | Ecotoxicology and Environmental Safety |
| বিষয়গুলি: | |
| অনলাইন ব্যবহার করুন: | http://www.sciencedirect.com/science/article/pii/S0147651324003312 |
| _version_ | 1827289800740175872 |
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| author | Lihui Xuan Yin Wang Can Qu Wensen Yi Jingjing Yang Huiji Pan Jing Zhang Cuimei Chen Chenjun Bai Ping-Kun Zhou Ruixue Huang |
| author_facet | Lihui Xuan Yin Wang Can Qu Wensen Yi Jingjing Yang Huiji Pan Jing Zhang Cuimei Chen Chenjun Bai Ping-Kun Zhou Ruixue Huang |
| author_sort | Lihui Xuan |
| collection | DOAJ |
| description | Endogenous immune defenses provide an intrinsic barrier against external entity invasion. Microplastics in the environment, especially those at the nanoscale (nanoplastics or NPs), may pose latent health risks through direct exposure. While links between nanoplastics and inflammatory processes have been established, detailed insights into how they may perturb the innate immune mechanisms remain uncharted. Employing murine and macrophage (RAW264.7) cellular models subjected to polystyrene nanoplastics (PS-NPs), our investigative approach encompassed an array of techniques: Cell Counting Kit-8 assays, flow cytometric analysis, acridine orange/ethidium bromide (AO/EB) fluorescence staining, cell transfection, cell cycle scrutiny, genetic manipulation, messenger RNA expression profiling via quantitative real-time PCR, and protein expression evaluation through western blotting. The results showed that PS-NPs caused RAW264.7 cell apoptosis, leading to cell cycle arrest, and activated the cGAS-STING pathway. This resulted in NF-κB signaling activation and increased pro-inflammatory mediator expression. Importantly, PS-NPs-induced activation of NF-κB and its downstream inflammatory cascade were markedly diminished after the silencing of the STING gene. Our findings highlight the critical role of the cGAS-STING pathway in the immunotoxic effects induced by PS-NPs. We outline a new mechanism whereby nanoplastics may trigger dysregulated innate immune and inflammatory responses via the cGAS/STING pathway. |
| first_indexed | 2024-04-24T11:56:13Z |
| format | Article |
| id | doaj.art-20a9f50a4ea1468b86ce84e4c897734a |
| institution | Directory Open Access Journal |
| issn | 0147-6513 |
| language | English |
| last_indexed | 2024-04-24T11:56:13Z |
| publishDate | 2024-04-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj.art-20a9f50a4ea1468b86ce84e4c897734a2024-04-09T04:12:33ZengElsevierEcotoxicology and Environmental Safety0147-65132024-04-01275116255Exposure to polystyrene nanoplastics induces abnormal activation of innate immunity via the cGAS-STING pathwayLihui Xuan0Yin Wang1Can Qu2Wensen Yi3Jingjing Yang4Huiji Pan5Jing Zhang6Cuimei Chen7Chenjun Bai8Ping-Kun Zhou9Ruixue Huang10Department of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, Hunan Province 410078, ChinaDepartment of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, Hunan Province 410078, ChinaDepartment of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, Hunan Province 410078, ChinaDepartment of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, Hunan Province 410078, ChinaDepartment of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, Hunan Province 410078, ChinaDepartment of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, Hunan Province 410078, ChinaClinical Medical Oncology, Xiangya Medical College, Central South University, ChinaSchool of Public Health, Xiang Nan University, Chenzhou, Hunan 423000, ChinaDepartment of Radiation Biology, Beijing Key Laboratory for Radiobiology, Beijing Institute of Radiation Medicine, Beijing 100850, China; Corresponding authors.Department of Radiation Biology, Beijing Key Laboratory for Radiobiology, Beijing Institute of Radiation Medicine, Beijing 100850, China; Corresponding authors.Department of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, Hunan Province 410078, China; Corresponding authors.Endogenous immune defenses provide an intrinsic barrier against external entity invasion. Microplastics in the environment, especially those at the nanoscale (nanoplastics or NPs), may pose latent health risks through direct exposure. While links between nanoplastics and inflammatory processes have been established, detailed insights into how they may perturb the innate immune mechanisms remain uncharted. Employing murine and macrophage (RAW264.7) cellular models subjected to polystyrene nanoplastics (PS-NPs), our investigative approach encompassed an array of techniques: Cell Counting Kit-8 assays, flow cytometric analysis, acridine orange/ethidium bromide (AO/EB) fluorescence staining, cell transfection, cell cycle scrutiny, genetic manipulation, messenger RNA expression profiling via quantitative real-time PCR, and protein expression evaluation through western blotting. The results showed that PS-NPs caused RAW264.7 cell apoptosis, leading to cell cycle arrest, and activated the cGAS-STING pathway. This resulted in NF-κB signaling activation and increased pro-inflammatory mediator expression. Importantly, PS-NPs-induced activation of NF-κB and its downstream inflammatory cascade were markedly diminished after the silencing of the STING gene. Our findings highlight the critical role of the cGAS-STING pathway in the immunotoxic effects induced by PS-NPs. We outline a new mechanism whereby nanoplastics may trigger dysregulated innate immune and inflammatory responses via the cGAS/STING pathway.http://www.sciencedirect.com/science/article/pii/S0147651324003312NanoplasticInnate immunityCGAS-STING pathwayInflammatory factor |
| spellingShingle | Lihui Xuan Yin Wang Can Qu Wensen Yi Jingjing Yang Huiji Pan Jing Zhang Cuimei Chen Chenjun Bai Ping-Kun Zhou Ruixue Huang Exposure to polystyrene nanoplastics induces abnormal activation of innate immunity via the cGAS-STING pathway Ecotoxicology and Environmental Safety Nanoplastic Innate immunity CGAS-STING pathway Inflammatory factor |
| title | Exposure to polystyrene nanoplastics induces abnormal activation of innate immunity via the cGAS-STING pathway |
| title_full | Exposure to polystyrene nanoplastics induces abnormal activation of innate immunity via the cGAS-STING pathway |
| title_fullStr | Exposure to polystyrene nanoplastics induces abnormal activation of innate immunity via the cGAS-STING pathway |
| title_full_unstemmed | Exposure to polystyrene nanoplastics induces abnormal activation of innate immunity via the cGAS-STING pathway |
| title_short | Exposure to polystyrene nanoplastics induces abnormal activation of innate immunity via the cGAS-STING pathway |
| title_sort | exposure to polystyrene nanoplastics induces abnormal activation of innate immunity via the cgas sting pathway |
| topic | Nanoplastic Innate immunity CGAS-STING pathway Inflammatory factor |
| url | http://www.sciencedirect.com/science/article/pii/S0147651324003312 |
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