A549电池
促炎细胞因子
炎症体
炎症
发病机制
化学
细胞凋亡
聚苯乙烯
免疫学
分子生物学
医学
生物
生物化学
聚合物
有机化学
作者
Laganà Antonio,Giuseppa Visalli,Alessio Facciolà,Caterina Saija,Maria Paola Bertuccio,Barbara Baluce,Consuelo Celesti,Daniela Iannazzo,Angela Di Pietro
出处
期刊:Toxicology Research
[Oxford University Press]
日期:2024-08-26
卷期号:13 (5)
标识
DOI:10.1093/toxres/tfae138
摘要
Abstract Sterile inflammation is involved in the lung pathogenesis induced by respirable particles, including micro- and nanoplastics. Their increasing amounts in the ambient and in indoor air pose a risk to human health. In two human cell lines (A549 and THP-1) we assessed the proinflammatory behavior of polystyrene nanoplastics (nPS) and microplastics (mPS) (Ø 0.1 and 1 μm). Reproducing environmental aging, in addition to virgin, the cells were exposed to oxidized nPS/mPS. To study the response of the monocytes to the inflammatory signal transmitted by the A549 through the release of soluble factors (e.g. alarmins and cytokines), THP-1 cells were also exposed to the supernatants of previously nPS/mPS-treated A549. After dynamic-light-scattering (DLS) analysis and protein measurements for the assessment of protein corona in nPS/mPS, real-time PCR and enzyme-linked-immunosorbent (ELISA) assays were performed in exposed cells. The pro-inflammatory effects of v- and ox-nPS/mPS were attested by the imbalance of the Bax/Bcl-2 ratio in A549, which was able to trigger the inflammatory cascade, inhibiting the immunologically silent apoptosis. The involvement of NFkB was confirmed by the overexpression of p65 after exposure to ox-nPS and v- and ox-mPS. The fast and higher levels of IL-1β, only in THP-1 cells, underlined the NLPR3 inflammasome activation.
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