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Erschienen in: Rheumatology International 3/2013

01.03.2013 | Original Article

IL-32 aggravates synovial inflammation and bone destruction and increases synovial natural killer cells in experimental arthritis models

verfasst von: Young-Eun Park, Geun-Tae Kim, Seung-Geun Lee, Seong-Hu Park, Seung-Hoon Baek, Sung-Il Kim, Ju-In Kim, Hua-Shu Jin

Erschienen in: Rheumatology International | Ausgabe 3/2013

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Abstract

This study was performed to investigate the effects of IL-32 on joint inflammation, bone destruction, and synovial cytokine expressions, and on synovial natural killer (NK) cell expressions in collagen-induced arthritis (CIA). CIA was induced by type II collagen in DBA1 mice, and phosphate-buffered saline (PBS group) or IL-32 (IL-32 group) were injected into both knee joints at day 28 and 32, then mice were killed at day 35. Severity of synovial inflammation and bone destruction was determined by histological scoring method, and synovial cytokine expressions such as IL-1β, TNF-α, IL-17, IL-18, IFN-γ, IL-21, and IL-23 were measured by real-time RT-PCR and western blot. Synovial NK cell expressions were determined by real-time RT-PCR, western blot and immunohistochemistry, and chemokines and chemokine receptors expressions that are associated with NK cell migration were determined by real-time RT-PCR. Scores of synovial inflammation and bone destruction, synovial expressions of IL-1β, TNF-α, IL-18, and IFN-γ were significantly increased in IL-32 group compared with PBS group. Synovial expressions of NK cell, and chemokines (CCL2 and CXCL9) and chemokine receptors (CCR2 and CCR5) that are associated with NK cell migration were significantly increased in IL-32 group compared with PBS group. IL-32 aggravated joint inflammation and bone destruction and increased synovial expressions of inflammatory cytokine and NK cells in CIA. These results suggest that IL-32 play a role in joint inflammation and bone destruction, and IL-32 might be a new target for treatment of rheumatoid arthritis.
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Metadaten
Titel
IL-32 aggravates synovial inflammation and bone destruction and increases synovial natural killer cells in experimental arthritis models
verfasst von
Young-Eun Park
Geun-Tae Kim
Seung-Geun Lee
Seong-Hu Park
Seung-Hoon Baek
Sung-Il Kim
Ju-In Kim
Hua-Shu Jin
Publikationsdatum
01.03.2013
Verlag
Springer-Verlag
Erschienen in
Rheumatology International / Ausgabe 3/2013
Print ISSN: 0172-8172
Elektronische ISSN: 1437-160X
DOI
https://doi.org/10.1007/s00296-012-2385-5

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