The Effect of Inhaled Air Particulate Matter SRM 1648a on the Development of Mild Collagen-Induced Arthritis in DBA/J Mice.


Journal

Archivum immunologiae et therapiae experimentalis
ISSN: 1661-4917
Titre abrégé: Arch Immunol Ther Exp (Warsz)
Pays: Switzerland
ID NLM: 0114365

Informations de publication

Date de publication:
28 Jul 2022
Historique:
received: 26 04 2022
accepted: 05 07 2022
entrez: 28 7 2022
pubmed: 29 7 2022
medline: 2 8 2022
Statut: epublish

Résumé

Air pollution is considered to be one of a risk factor for rheumatoid arthritis (RA). Collagen-induced arthritis (CIA) is commonly used as a mouse model of human RA. However, the impact of specific particulate matter (PM) components on the incidence and severity of RA has still not been established. The aim of this study was to develop an experimental model of CIA suitable to test arthritogenicity of inhaled PM. A mild form of CIA was induced in DBA1/J mice inhaled with various components of SRM 1648a PM. The incidence and severity of arthritis was assessed, and the selected serum markers of autoimmunity and inflammation were determined. Clinical arthritis was observed from the booster CII immunisation onward. Anti-cyclic citrullinated peptide antibodies, a diagnostic marker of RA, were detected in serum of these mice. All inhaled pollutants, crude PM, PM with reduced organic content, ferric, and silica nanoparticles markedly increased CIA incidence and severity. The fastest progression of CIA development was caused by crude PM and was linked to enhanced serum levels of anti-CII IgG, the prominent arthritogenic autoantibodies. On the other hand, inhaled nanoparticles enhanced serum levels of TNFα, a major proinflammatory arthritogenic cytokine. We recommend this experimental model of mild CIA to test the mechanisms of arthritis exacerbation by inhaled air pollutants. Further studies are necessary to determine whether PM-aggravated arthritis is caused by inflammatory mediators translocated from inflamed lung into systemic circulation or whether PM translocated into the bloodstream directly exacerbate joint inflammation.

Identifiants

pubmed: 35900599
doi: 10.1007/s00005-022-00654-9
pii: 10.1007/s00005-022-00654-9
pmc: PMC9334371
doi:

Substances chimiques

Particulate Matter 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

17

Subventions

Organisme : Narodowe Centrum Nauki
ID : 2015/16/WST5/00005

Informations de copyright

© 2022. The Author(s).

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Auteurs

Bernadeta Nowak (B)

Chair of Immunology, Faculty of Medicine, Jagiellonian University Medical College, Krakow, Poland.

Grzegorz Majka (G)

Chair of Immunology, Faculty of Medicine, Jagiellonian University Medical College, Krakow, Poland. grzegorz.majka@uj.edu.pl.

Małgorzata Śróttek (M)

Chair of Immunology, Faculty of Medicine, Jagiellonian University Medical College, Krakow, Poland.

Anna Skałkowska (A)

Chair of Immunology, Faculty of Medicine, Jagiellonian University Medical College, Krakow, Poland.

Janusz Marcinkiewicz (J)

Chair of Immunology, Faculty of Medicine, Jagiellonian University Medical College, Krakow, Poland.

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Classifications MeSH