The alarmins S100A8 and S100A9 mediate acute pain in experimental synovitis.


Journal

Arthritis research & therapy
ISSN: 1478-6362
Titre abrégé: Arthritis Res Ther
Pays: England
ID NLM: 101154438

Informations de publication

Date de publication:
27 08 2020
Historique:
received: 23 03 2020
accepted: 17 08 2020
entrez: 29 8 2020
pubmed: 29 8 2020
medline: 22 6 2021
Statut: epublish

Résumé

Synovitis-associated pain is mediated by inflammatory factors that may include S100A8/9, which is able to stimulate nociceptive neurons via Toll-like receptor 4. In this study, we investigated the role of S100A9 in pain response during acute synovitis. Acute synovitis was induced by streptococcal cell wall (SCW) injection in the knee joint of C57Bl/6 (WT) and S100A9 Intra-articular SCW injection resulted in increased synovial expression and serum levels of S100A8/A9 at day 1. These increased levels, however, did not contribute to the development of inflammation, since this was equal in S100A9 S100A8/9, released from the synovium upon inflammation, is an important mediator of pain response in the knee during the acute phase of inflammation.

Sections du résumé

BACKGROUND
Synovitis-associated pain is mediated by inflammatory factors that may include S100A8/9, which is able to stimulate nociceptive neurons via Toll-like receptor 4. In this study, we investigated the role of S100A9 in pain response during acute synovitis.
METHODS
Acute synovitis was induced by streptococcal cell wall (SCW) injection in the knee joint of C57Bl/6 (WT) and S100A9
RESULTS
Intra-articular SCW injection resulted in increased synovial expression and serum levels of S100A8/A9 at day 1. These increased levels, however, did not contribute to the development of inflammation, since this was equal in S100A9
CONCLUSIONS
S100A8/9, released from the synovium upon inflammation, is an important mediator of pain response in the knee during the acute phase of inflammation.

Identifiants

pubmed: 32854769
doi: 10.1186/s13075-020-02295-9
pii: 10.1186/s13075-020-02295-9
pmc: PMC7457270
doi:

Substances chimiques

Alarmins 0
Calgranulin A 0
Calgranulin B 0
S100A9 protein, mouse 0
S100a8 protein, mouse 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

199

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Auteurs

Arjen B Blom (AB)

Experimental Rheumatology, Radboud university medical center, Geert Grooteplein 28, 6525 GA, Nijmegen, The Netherlands. arjen.blom@radboudumc.nl.

Martijn H van den Bosch (MH)

Experimental Rheumatology, Radboud university medical center, Geert Grooteplein 28, 6525 GA, Nijmegen, The Netherlands.

Esmeralda N Blaney Davidson (EN)

Experimental Rheumatology, Radboud university medical center, Geert Grooteplein 28, 6525 GA, Nijmegen, The Netherlands.

Johannes Roth (J)

Institute of Immunology, University of Münster, Münster, Germany.

Thomas Vogl (T)

Institute of Immunology, University of Münster, Münster, Germany.

Fons A van de Loo (FA)

Experimental Rheumatology, Radboud university medical center, Geert Grooteplein 28, 6525 GA, Nijmegen, The Netherlands.

Marije Koenders (M)

Experimental Rheumatology, Radboud university medical center, Geert Grooteplein 28, 6525 GA, Nijmegen, The Netherlands.

Peter M van der Kraan (PM)

Experimental Rheumatology, Radboud university medical center, Geert Grooteplein 28, 6525 GA, Nijmegen, The Netherlands.

Edwin J Geven (EJ)

Experimental Rheumatology, Radboud university medical center, Geert Grooteplein 28, 6525 GA, Nijmegen, The Netherlands.

Peter L van Lent (PL)

Experimental Rheumatology, Radboud university medical center, Geert Grooteplein 28, 6525 GA, Nijmegen, The Netherlands.

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