Surface PEGylation suppresses pulmonary effects of CuO in allergen-induced lung inflammation.


Journal

Particle and fibre toxicology
ISSN: 1743-8977
Titre abrégé: Part Fibre Toxicol
Pays: England
ID NLM: 101236354

Informations de publication

Date de publication:
05 07 2019
Historique:
received: 20 07 2018
accepted: 04 06 2019
entrez: 7 7 2019
pubmed: 7 7 2019
medline: 25 2 2020
Statut: epublish

Résumé

Copper oxide (CuO) nanomaterials are used in a wide range of industrial and commercial applications. These materials can be hazardous, especially if they are inhaled. As a result, the pulmonary effects of CuO nanomaterials have been studied in healthy subjects but limited knowledge exists today about their effects on lungs with allergic airway inflammation (AAI). The objective of this study was to investigate how pristine CuO modulates allergic lung inflammation and whether surface modifications can influence its reactivity. CuO and its carboxylated (CuO COOH), methylaminated (CuO NH Our data demonstrates that although CuO materials did not considerably influence hallmarks of allergic airway inflammation, the materials exacerbated the existing lung inflammation by eliciting dramatic pulmonary neutrophilia. Transcriptomic analysis showed that CuO, CuO COOH and CuO NH CuO as well as its functionalized forms worsen allergic airway inflammation by causing neutrophilia in the lungs, however, our results also show that surface PEGylation can be a promising approach for inhibiting the effects of pristine CuO. Our study provides information for health and safety assessment of modified CuO materials, and it can be useful in the development of nanomedical applications.

Sections du résumé

BACKGROUND
Copper oxide (CuO) nanomaterials are used in a wide range of industrial and commercial applications. These materials can be hazardous, especially if they are inhaled. As a result, the pulmonary effects of CuO nanomaterials have been studied in healthy subjects but limited knowledge exists today about their effects on lungs with allergic airway inflammation (AAI). The objective of this study was to investigate how pristine CuO modulates allergic lung inflammation and whether surface modifications can influence its reactivity. CuO and its carboxylated (CuO COOH), methylaminated (CuO NH
RESULTS
Our data demonstrates that although CuO materials did not considerably influence hallmarks of allergic airway inflammation, the materials exacerbated the existing lung inflammation by eliciting dramatic pulmonary neutrophilia. Transcriptomic analysis showed that CuO, CuO COOH and CuO NH
CONCLUSIONS
CuO as well as its functionalized forms worsen allergic airway inflammation by causing neutrophilia in the lungs, however, our results also show that surface PEGylation can be a promising approach for inhibiting the effects of pristine CuO. Our study provides information for health and safety assessment of modified CuO materials, and it can be useful in the development of nanomedical applications.

Identifiants

pubmed: 31277695
doi: 10.1186/s12989-019-0309-1
pii: 10.1186/s12989-019-0309-1
pmc: PMC6612204
doi:

Substances chimiques

Polyethylene Glycols 3WJQ0SDW1A
Copper 789U1901C5
Ovalbumin 9006-59-1
cupric oxide V1XJQ704R4

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

28

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Auteurs

Marit Ilves (M)

Human Microbiome Research Program, Faculty of Medicine, University of Helsinki, 00290, Helsinki, Finland.

Pia Anneli Sofia Kinaret (PAS)

Institute of Biotechnology, University of Helsinki, 00790, Helsinki, Finland.
Faculty of Medicine and Life Sciences, University of Tampere, 33100, Tampere, Finland.

Joseph Ndika (J)

Human Microbiome Research Program, Faculty of Medicine, University of Helsinki, 00290, Helsinki, Finland.

Piia Karisola (P)

Human Microbiome Research Program, Faculty of Medicine, University of Helsinki, 00290, Helsinki, Finland.

Veer Marwah (V)

Institute of Biotechnology, University of Helsinki, 00790, Helsinki, Finland.
Faculty of Medicine and Life Sciences, University of Tampere, 33100, Tampere, Finland.

Vittorio Fortino (V)

Institute of Biotechnology, University of Helsinki, 00790, Helsinki, Finland.
Biomedicine Institute, University of Eastern Finland, 70211, Kuopio, Finland.

Yuri Fedutik (Y)

PlasmaChem GmbH, 12489, Berlin, Germany.

Manuel Correia (M)

National Food Institute, Technical University of Denmark, 2800, Lyngby, Denmark.

Nicky Ehrlich (N)

Department of Chemical and Biochemical Engineering, Technical University of Denmark, 2800, Lyngby, Denmark.

Katrin Loeschner (K)

National Food Institute, Technical University of Denmark, 2800, Lyngby, Denmark.

Alexandros Besinis (A)

School of Biological and Marine Sciences, Faculty of Science and Engineering, University of Plymouth, Drake Circus, Plymouth, PL4 8AA, UK.
Plymouth University Peninsula Schools of Medicine and Dentistry, University of Plymouth, John Bull Building, Tamar Science Park, Plymouth, PL6 8BU, UK.

Joanne Vassallo (J)

School of Biological and Marine Sciences, Faculty of Science and Engineering, University of Plymouth, Drake Circus, Plymouth, PL4 8AA, UK.

Richard D Handy (RD)

School of Biological and Marine Sciences, Faculty of Science and Engineering, University of Plymouth, Drake Circus, Plymouth, PL4 8AA, UK.

Henrik Wolff (H)

Finnish Institute of Occupational Health, 00250, Helsinki, Finland.
Department of Pathology, University of Helsinki, 00014, Helsinki, Finland.

Kai Savolainen (K)

Finnish Institute of Occupational Health, 00250, Helsinki, Finland.

Dario Greco (D)

Institute of Biotechnology, University of Helsinki, 00790, Helsinki, Finland.
Faculty of Medicine and Life Sciences, University of Tampere, 33100, Tampere, Finland.

Harri Alenius (H)

Human Microbiome Research Program, Faculty of Medicine, University of Helsinki, 00290, Helsinki, Finland. harri.alenius@helsinki.fi.
Institute of Environmental Medicine, Karolinska Institutet, 171 77, Stockholm, Sweden. harri.alenius@helsinki.fi.

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Classifications MeSH