I.F. Gosselink , F.J. van Schooten , M.J. Drittij , E.M. Höppener , P. Leonhardt , E. Moschini , T. Serchi , A.C. Gutleb , I.M. Kooter , A.H. Remels
{"title":"利用气液界面模型评估无定形纳米塑料在气道和肺上皮细胞中的毒性。","authors":"I.F. Gosselink , F.J. van Schooten , M.J. Drittij , E.M. Höppener , P. Leonhardt , E. Moschini , T. Serchi , A.C. Gutleb , I.M. Kooter , A.H. Remels","doi":"10.1016/j.chemosphere.2024.143702","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>Inhalation is one of the main exposure routes to nanoplastics. Knowledge of the toxicological impact of nanoplastics on the airway- and lung epithelium is limited and almost exclusively based on submerged <em>in vitro</em> models using spherical polystyrene (PS) particles.</div></div><div><h3>Methods</h3><div>Mono-cultures and advanced (co-)cultures of human bronchial- and alveolar epithelial cells, all air-liquid interface (ALI) cultures, were exposed to nanoplastics and reference nanoparticles. Alveolar models included A549 mono-cultures and A549 cells co-cultured with endothelial cells (Ea.hy926) and macrophage-like cells (differentiated THP-1). Bronchial models included BEAS-2B cells and differentiated primary bronchial epithelial cells (PBEC). Cultures were exposed to PS, copper(II) oxide (CuO) or titanium dioxide (TiO<sub>2</sub>) nanoparticles (50 nm). Additionally, BEAS-2B cells were exposed to well-characterised, amorphous polyvinyl chloride (PVC), polypropylene (PP), or polyamide (PA) nanoplastics. Cytotoxicity and inflammation (IL-8 secretion and IL-8 transcript levels) were assessed after 24 h of exposure.</div></div><div><h3>Results</h3><div>Cell viability remained unaffected by all exposures in all models. Unlike PS and TiO<sub>2</sub>, CuO exposure dose-dependently induced IL-8 protein secretion and mRNA levels. Although the extent of IL-8 secretion differed between models, the relative response to CuO was similar in both mono-cultures and advanced (co-)cultures. None of the environmentally relevant nanoplastics (PVC, PA or PP) impacted inflammation or cell viability in BEAS-2B ALI cultures.</div></div><div><h3>Conclusion</h3><div>Although CuO induced inflammation, PS failed to elicit an inflammatory response in any of our models. For the first time, we show that PVC, PA and PP do not induce cell death or inflammation in a BEAS-2B ALI model.</div></div>","PeriodicalId":276,"journal":{"name":"Chemosphere","volume":"368 ","pages":"Article 143702"},"PeriodicalIF":8.1000,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Assessing toxicity of amorphous nanoplastics in airway- and lung epithelial cells using air-liquid interface models\",\"authors\":\"I.F. Gosselink , F.J. van Schooten , M.J. Drittij , E.M. Höppener , P. Leonhardt , E. Moschini , T. Serchi , A.C. Gutleb , I.M. Kooter , A.H. Remels\",\"doi\":\"10.1016/j.chemosphere.2024.143702\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><div>Inhalation is one of the main exposure routes to nanoplastics. Knowledge of the toxicological impact of nanoplastics on the airway- and lung epithelium is limited and almost exclusively based on submerged <em>in vitro</em> models using spherical polystyrene (PS) particles.</div></div><div><h3>Methods</h3><div>Mono-cultures and advanced (co-)cultures of human bronchial- and alveolar epithelial cells, all air-liquid interface (ALI) cultures, were exposed to nanoplastics and reference nanoparticles. Alveolar models included A549 mono-cultures and A549 cells co-cultured with endothelial cells (Ea.hy926) and macrophage-like cells (differentiated THP-1). Bronchial models included BEAS-2B cells and differentiated primary bronchial epithelial cells (PBEC). Cultures were exposed to PS, copper(II) oxide (CuO) or titanium dioxide (TiO<sub>2</sub>) nanoparticles (50 nm). Additionally, BEAS-2B cells were exposed to well-characterised, amorphous polyvinyl chloride (PVC), polypropylene (PP), or polyamide (PA) nanoplastics. Cytotoxicity and inflammation (IL-8 secretion and IL-8 transcript levels) were assessed after 24 h of exposure.</div></div><div><h3>Results</h3><div>Cell viability remained unaffected by all exposures in all models. Unlike PS and TiO<sub>2</sub>, CuO exposure dose-dependently induced IL-8 protein secretion and mRNA levels. Although the extent of IL-8 secretion differed between models, the relative response to CuO was similar in both mono-cultures and advanced (co-)cultures. None of the environmentally relevant nanoplastics (PVC, PA or PP) impacted inflammation or cell viability in BEAS-2B ALI cultures.</div></div><div><h3>Conclusion</h3><div>Although CuO induced inflammation, PS failed to elicit an inflammatory response in any of our models. For the first time, we show that PVC, PA and PP do not induce cell death or inflammation in a BEAS-2B ALI model.</div></div>\",\"PeriodicalId\":276,\"journal\":{\"name\":\"Chemosphere\",\"volume\":\"368 \",\"pages\":\"Article 143702\"},\"PeriodicalIF\":8.1000,\"publicationDate\":\"2024-11-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Chemosphere\",\"FirstCategoryId\":\"93\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S004565352402602X\",\"RegionNum\":2,\"RegionCategory\":\"环境科学与生态学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"ENVIRONMENTAL SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Chemosphere","FirstCategoryId":"93","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S004565352402602X","RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ENVIRONMENTAL SCIENCES","Score":null,"Total":0}
Assessing toxicity of amorphous nanoplastics in airway- and lung epithelial cells using air-liquid interface models
Background
Inhalation is one of the main exposure routes to nanoplastics. Knowledge of the toxicological impact of nanoplastics on the airway- and lung epithelium is limited and almost exclusively based on submerged in vitro models using spherical polystyrene (PS) particles.
Methods
Mono-cultures and advanced (co-)cultures of human bronchial- and alveolar epithelial cells, all air-liquid interface (ALI) cultures, were exposed to nanoplastics and reference nanoparticles. Alveolar models included A549 mono-cultures and A549 cells co-cultured with endothelial cells (Ea.hy926) and macrophage-like cells (differentiated THP-1). Bronchial models included BEAS-2B cells and differentiated primary bronchial epithelial cells (PBEC). Cultures were exposed to PS, copper(II) oxide (CuO) or titanium dioxide (TiO2) nanoparticles (50 nm). Additionally, BEAS-2B cells were exposed to well-characterised, amorphous polyvinyl chloride (PVC), polypropylene (PP), or polyamide (PA) nanoplastics. Cytotoxicity and inflammation (IL-8 secretion and IL-8 transcript levels) were assessed after 24 h of exposure.
Results
Cell viability remained unaffected by all exposures in all models. Unlike PS and TiO2, CuO exposure dose-dependently induced IL-8 protein secretion and mRNA levels. Although the extent of IL-8 secretion differed between models, the relative response to CuO was similar in both mono-cultures and advanced (co-)cultures. None of the environmentally relevant nanoplastics (PVC, PA or PP) impacted inflammation or cell viability in BEAS-2B ALI cultures.
Conclusion
Although CuO induced inflammation, PS failed to elicit an inflammatory response in any of our models. For the first time, we show that PVC, PA and PP do not induce cell death or inflammation in a BEAS-2B ALI model.
期刊介绍:
Chemosphere, being an international multidisciplinary journal, is dedicated to publishing original communications and review articles on chemicals in the environment. The scope covers a wide range of topics, including the identification, quantification, behavior, fate, toxicology, treatment, and remediation of chemicals in the bio-, hydro-, litho-, and atmosphere, ensuring the broad dissemination of research in this field.