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Sterile inflammation induced by respirable micro and nano polystyrene particles in the pathogenesis of pulmonary diseases

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
A. Laganà,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]
卷期号:13 (5): tfae138-tfae138 被引量:11
标识
DOI:10.1093/toxres/tfae138
摘要

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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