Sterile inflammation induced by respirable micro and nano polystyrene particles in the pathogenesis of pulmonary diseases.
Alveolar cells
Cytokines
Microplastics
Monocytic cells
Nanoplastics
Sterile inflammation
Journal
Toxicology research
ISSN: 2045-452X
Titre abrégé: Toxicol Res (Camb)
Pays: England
ID NLM: 101587950
Informations de publication
Date de publication:
Oct 2024
Oct 2024
Historique:
received:
07
05
2024
revised:
24
07
2024
accepted:
26
08
2024
pmc-release:
02
09
2025
medline:
5
9
2024
pubmed:
5
9
2024
entrez:
5
9
2024
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 39233846
doi: 10.1093/toxres/tfae138
pii: tfae138
pmc: PMC11368663
doi:
Types de publication
Journal Article
Langues
eng
Pagination
tfae138Informations de copyright
© The Author(s) 2024. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.