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

Author:

Antonio Laganà12,Visalli Giuseppa1,Facciolà Alessio1,Saija Caterina1,Bertuccio Maria Paola1,Baluce Barbara3,Celesti Consuelo45,Iannazzo Daniela45,Di Pietro Angela1ORCID

Affiliation:

1. Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina , Via Consolare Valeria, 98125 Messina, Italy

2. Istituto Clinico Polispecialistico C.O.T. Cure Ortopediche Traumatologiche s.p.a. , Viale Italia, 98124 Messina, Italy

3. Department of Transfusion Medicine and Hematology and Lombardy Regional Rare Blood Bank, IRCCS Ca’ Granda Ospedale Maggiore Policlinico , Via Francesco Sforza, 35, 20122 Milan, Italy

4. Department of Electronic Engineering , Industrial Chemistry and Engineering, , Via Stagno d'Alcontres, 98125 Messina, Italy

5. University of Messina , Industrial Chemistry and Engineering, , Via Stagno d'Alcontres, 98125 Messina, Italy

Abstract

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.

Funder

University of Messina

Publisher

Oxford University Press (OUP)

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