可吸入微型和纳米聚苯乙烯颗粒在肺部疾病发病机制中诱发的无菌炎症。

IF 2.2 4区 医学 Q3 TOXICOLOGY Toxicology Research Pub Date : 2024-09-02 eCollection Date: 2024-10-01 DOI:10.1093/toxres/tfae138
Laganà Antonio, Giuseppa Visalli, Alessio Facciolà, Caterina Saija, Maria Paola Bertuccio, Barbara Baluce, Consuelo Celesti, Daniela Iannazzo, Angela Di Pietro
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引用次数: 0

摘要

无菌性炎症与包括微塑料和纳米塑料在内的可吸入颗粒物诱发的肺部发病机制有关。它们在环境和室内空气中的含量不断增加,对人类健康构成了威胁。在两种人类细胞系(A549 和 THP-1)中,我们评估了聚苯乙烯纳米塑料(nPS)和微塑料(mPS)(直径 0.1 和 1 μm)的促炎行为。除原始环境外,细胞还暴露于氧化的 nPS/mPS 中,以再现环境老化。为了研究单核细胞对 A549 通过释放可溶性因子(如报警素和细胞因子)传递的炎症信号的反应,THP-1 细胞也暴露于先前经 nPS/mPS 处理的 A549 的上清液中。在进行动态光散射(DLS)分析和蛋白质测量以评估 nPS/mPS 中的蛋白质电晕后,对暴露的细胞进行了实时 PCR 和酶联免疫吸附(ELISA)测定。A549 细胞中 Bax/Bcl-2 比率的失衡证明了 v- 和 ox-nPS/mPS 的促炎作用,它能够触发炎症级联,抑制免疫学上的静默凋亡。暴露于 ox-nPS 和 v- 及 ox-mPS 后,p65 的过表达证实了 NFkB 的参与。仅在 THP-1 细胞中,IL-1β 的快速和较高水平突出了 NLPR3 炎性体的激活。
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Sterile inflammation induced by respirable micro and nano polystyrene particles in the pathogenesis of pulmonary diseases.

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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来源期刊
Toxicology Research
Toxicology Research TOXICOLOGY-
CiteScore
3.60
自引率
0.00%
发文量
82
期刊介绍: A multi-disciplinary journal covering the best research in both fundamental and applied aspects of toxicology
期刊最新文献
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