Title
Cytokine production by infrapatellar fat pad can be stimulated by interleukin 1 <tex>$\beta$</tex> and inhibited by peroxisome proliferator activated receptor <tex>$\alpha$</tex> agonistCytokine production by infrapatellar fat pad can be stimulated by interleukin 1 <tex>$\beta$</tex> and inhibited by peroxisome proliferator activated receptor <tex>$\alpha$</tex> agonist
Author
Faculty/Department
Faculty of Medicine and Health Sciences
Research group
Antwerp Surgical Training, Anatomy and Research Centre (ASTARC)
Translational Pathophysiological Research (TPR)
Publication type
article
Publication
London :British Medical Association,
Subject
Human medicine
Source (journal)
Annals of the rheumatic diseases / European League Against Rheumatism [Kilchberg] - London, 1939, currens
Volume/pages
71(2012):6, p. 1012-1018
ISSN
0003-4967
1468-2060
ISI
000303756400039
Carrier
E
Target language
English (eng)
Full text (Publishers DOI)
Affiliation
University of Antwerp
Abstract
Background Infrapatellar fat pad (IPFP) might be involved in osteoarthritis (OA) by production of cytokines. It was hypothesised that production of cytokines is sensitive to environmental conditions. Objectives To evaluate cytokine production by IPFP in response to interleukin (IL)1b and investigate the ability to modulate this response with an agonist for peroxisome proliferator activated receptor alpha (PPAR alpha), which is also activated by lipid-lowering drugs such as fibrates. Methods Cytokine secretion of IPFP was analysed in the medium of explant cultures of 29 osteoarthritic patients. IPFP (five donors) and synovium (six donors) were cultured with IL-1b and PPAR alpha agonist Wy14643. Gene expression of IL-1b, monocyte chemoattractant protein (MCP1), (IL-6, tumour necrosis factor (TNF)alpha, leptin, vascular endothelial growth factor (VEGF), IL-10, prostaglandin-endoperoxide synthase (PTGS)2 and release of TNF alpha, MCP1 and prostaglandin E-2 were compared with unstimulated IPFP and synovium explants. Results IPFP released large amounts of inflammatory cytokines, adipokines and growth factors. IL-1b increased gene expression of PTGS2, TNF alpha, IL-1b, IL-6 and VEGF and increased TNF alpha release in IPFP. MCP1, leptin, IL-10 gene expression and MCP1, leptin and PGE(2) release did not increase significantly. Synovium responded to IL-1b similarly to IPFP, except for VEGF gene expression. Wy14643 decreased gene expression of PTGS2, IL-1b, TNF alpha, MCP1, VEGF and leptin in IPFP explants and IL-1b, TNF alpha, IL-6, IL-10 and VEGF in synovium that responded to IL-1b. Conclusion IPFP is an active tissue within the joint. IPFP cytokine production is increased by IL-1b and decreased by a PPAR alpha agonist. The effects were similar to effects seen in synovium. Fibrates may represent a potential disease-modifying drug for OA by modulating inflammatory properties of IPFP and synovium.
E-info
https://repository.uantwerpen.be/docman/iruaauth/223d92/1142146.pdf
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