ArticleArthritis research & therapy2012
A 4-trifluoromethyl analogue of celecoxib inhibits arthritis by suppressing innate immune cell activation.
Article in Arthritis research & therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Mucosal-Associated Invariant T Cells in Autoimmune Diseases.Frontiers in immunology · 2018Review
- Urokinase plasminogen activator and receptor promote collagen-induced arthritis through expression in hematopoietic cells.Blood advances · 2017Article
- Improved serological detection of rheumatoid arthritis: a highly antigenic mimotope of carbonic anhydrase III selected in a murine model by phage display.Arthritis research & therapy · 2015Article
- Protection against Chikungunya virus induced arthralgia following prophylactic treatment with adenovirus vectored interferon (mDEF201).Antiviral research · 2014Article
- Inhibition of P2X4 suppresses joint inflammation and damage in collagen-induced arthritis.Inflammation · 2014Article
- A multiplex immunoassay method for simultaneous quantification of iron, vitamin A and inflammation status markers.PloS one · 2014Article
- A trifluoromethyl analogue of celecoxib exerts beneficial effects in neuroinflammation.PloS one · 2013Article
- Molecular mechanism of the inhibition effect of Celecoxib on corneal collagen degradation in three dimensions.International journal of ophthalmology · 2012Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionCelecoxib, a highly specific cyclooxygenase-2 (COX-2) inhibitor has been reported to have COX-2-independent immunomodulatory effects. However, celecoxib itself has only mild suppressive effects on arthritis. Recently, we reported that a 4-trifluoromethyl analogue of celecoxib (TFM-C) with 205-fold lower COX-2-inhibitory activity inhibits secretion of IL-12 family cytokines through a COX-2-independent mechanism that involves Ca2+-mediated intracellular retention of the IL-12 polypeptide chains. In this study, we explored the capacity of TFM-C as a new therapeutic agent for arthritis.
methodsTo induce collagen-induced arthritis (CIA), DBA1/J mice were immunized with bovine type II collagen (CII) in Freund's adjuvant. Collagen antibody-induced arthritis (CAIA) was induced in C57BL/6 mice by injecting anti-CII antibodies. Mice received 10 μg/g of TFM-C or celecoxib every other day. The effects of TFM-C on clinical and histopathological severities were assessed. The serum levels of CII-specific antibodies were measured by ELISA. The effects of TFM-C on mast cell activation, cytokine producing capacity by macrophages, and neutrophil recruitment were also evaluated.
resultsTFM-C inhibited the severity of CIA and CAIA more strongly than celecoxib. TFM-C treatments had little effect on CII-specific antibody levels in serum. TFM-C suppressed the activation of mast cells in arthritic joints. TFM-C also suppressed the production of inflammatory cytokines by macrophages and leukocyte influx in thioglycollate-induced peritonitis.
conclusionThese results indicate that TFM-C may serve as an effective new disease-modifying drug for treatment of arthritis, such as rheumatoid arthritis.
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