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Springer Science and Business Media LLC

 

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Các bài báo tiêu biểu

Synovitis in osteoarthritis: current understanding with therapeutic implications
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Alexander Mathiessen, Philip G. Conaghan
Patient global assessment in measuring disease activity in rheumatoid arthritis: a review of the literature
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Elena Nikiphorou, Helga Radner, Katerina Chatzidionysiou, Carole Desthieux, Codruța Zăbălan, Yvonne van Eijk-Hustings, William G Dixon, Kimme L Hyrich, Johan Askling, Laure Gossec
Cell-cell interactions in synovitis Interactions between T lymphocytes and synovial cells
Tập 2 - Trang 1-5 - 2000
Iain B McInnes, Bernard P Leung, Foo Y Liew
Mechanisms whereby T lymphocytes contribute to synovial inflammation in rheumatoid arthritis are poorly understood. Here we review data that indicate an important role for cell contact between synovial T cells, adjacent macrophages and fibroblast-like synoviocytes (FLS). Thus, T cells activated by cytokines, endothelial transmigration, extracellular matrix or by auto-antigens can promote cytokine, particularly TNFα, metalloproteinase production by macrophages and FLS through cell-membrane interactions, mediated at least through β-integrins and membrane cytokines. Since soluble factors thus induced may in turn contribute directly to T cell activation, positive feedback loops are likely to be created. These novel pathways represent exciting potential therapeutic targets.
Fatigue in chronic inflammation - a link to pain pathways
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Karine Louati, Francis Bérenbaum
Molecular mechanisms underlying osteoarthritis development: Notch and NF-κB
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Taku Saito, Sakae Tanaka
Risk factors for ANA positivity in healthy persons
Tập 13 Số 2 - 2011
Quan Zhen Li, David R. Karp, Jia Quan, Valerie Klusas Branch, Jianuan Zhou, Yun Lian, Benjamin F. Chong, Edward K. Wakeland, Nancy J. Olsen
MicroRNAs in fibrosis: opportunities and challenges
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Steven O’Reilly
High mechanical strain of primary intervertebral disc cells promotes secretion of inflammatory factors associated with disc degeneration and pain
Tập 16 Số 1
Rahul Gawri, Derek H. Rosenzweig, Emerson Krock, Jean Ouellet, Laura S. Stone, Thomas M. Quinn, Lisbet Haglund
Abstract Introduction Excessive mechanical loading of intervertebral discs (IVDs) is thought to alter matrix properties and influence disc cell metabolism, contributing to degenerative disc disease and development of discogenic pain. However, little is known about how mechanical strain induces these changes. This study investigated the cellular and molecular changes as well as which inflammatory receptors and cytokines were upregulated in human intervertebral disc cells exposed to high mechanical strain (HMS) at low frequency. The impact of these metabolic changes on neuronal differentiation was also explored to determine a role in the development of disc degeneration and discogenic pain. Methods Isolated human annulus fibrosus (AF) and nucleus pulposus (NP) cells were exposed to HMS (20% cyclical stretch at 0.001 Hz) on high-extension silicone rubber dishes coupled to a mechanical stretching apparatus and compared to static control cultures. Gene expression of Toll-like receptors (TLRs), neuronal growth factor (NGF) and tumour necrosis factor α (TNFα) was assessed. Collected conditioned media were analysed for cytokine content and applied to rat pheocromocytoma PC12 cells for neuronal differentiation assessment. Results HMS caused upregulation of TLR2, TLR4, NGF and TNFα gene expression in IVD cells. Medium from HMS cultures contained elevated levels of growth-related oncogene, interleukin 6 (IL-6), IL-8, IL-15, monocyte chemoattractant protein 1 (MCP-1), MCP-3, monokine induced by γ interferon, transforming growth factor β1, TNFα and NGF. Exposure of PC12 cells to HMS-conditioned media resulted in both increased neurite sprouting and cell death. Conclusions HMS culture of IVD cells in vitro drives cytokine and inflammatory responses associated with degenerative disc disease and low-back pain. This study provides evidence for a direct link between cellular strain, secretory factors, neoinnervation and potential degeneration and discogenic pain in vivo.