ARD:抑制粒细胞-巨噬细胞集落刺激因子治疗类风湿关节炎和骨关节炎

2012-08-23 Beyond 生物谷

最新一项研究发现粒细胞巨噬细胞集落刺激因子GM-CSF在炎症部位的细胞之间的信号使者。 在该研究中,教授John Hamilton提出了一个问题:阻断GM-CSF能否是炎症性疾病一种新的治疗方法?在类风湿关节炎的实验模型,Hamilton博士和Andrew Cook教授曾表明用抗体阻断GM-CSF的功能能抑制疾病的发展,这一作用已在临床试验中显示出一定的效果。 他们发表在Annals of t

最新一项研究发现粒细胞巨噬细胞集落刺激因子GM-CSF在炎症部位的细胞之间的信号使者。

在该研究中,教授John Hamilton提出了一个问题:阻断GM-CSF能否是炎症性疾病一种新的治疗方法?在类风湿关节炎的实验模型,Hamilton博士和Andrew Cook教授曾表明用抗体阻断GM-CSF的功能能抑制疾病的发展,这一作用已在临床试验中显示出一定的效果。

他们发表在Annals of the Rheumatic Diseases杂志上的这项新研究已经表明,在这种模型中,GM-CSF的抑制也抑制疼痛,他们也在骨性关节炎实验模型中发现了类似的功效。

类风湿关节炎发病高峰在30多岁和40多岁,女性比男性更常见。Cook博士说:随着我们人口老龄化,骨性关节炎的发病呈上升趋势,这对我们的社会和医疗资源带来了巨大挑战。开发一种新的疗法以阻止这种疾病将会给医疗服务者和政府带来巨大好处。

编译自:New Attack On Pain Caused by Diseases Such as Rheumatoid Arthritis and Osteoarthritis

 

doi:10.1136/annrheumdis-2012-201703
PMC:
PMID:

Granulocyte-macrophage colony-stimulating factor is a key mediator in inflammatory and arthritic pain

A. D. Cook, J. Pobjoy, S. Sarros, S. Steidl, M. Durr, D. C. Lacey, J. A. Hamilton

Objectives Better therapies are needed for inflammatory pain. In arthritis the relationship between joint pain, inflammation and damage is unclear. Granulocyte-macrophage colony-stimulating factor (GM–CSF) is important for the progression of a number of inflammatory/autoimmune conditions including arthritis; clinical trials targeting its action in rheumatoid arthritis are underway. However, its contribution to inflammatory and arthritic pain is unknown. The aims of this study were to determine whether GM–CSF controls inflammatory and/or arthritic pain.

Methods A model of inflammatory pain (complete Freund's adjuvant footpad), as well as two inflammatory arthritis models, were induced in GM–CSF-/- mice and development of pain (assessment of weight distribution) and arthritic disease (histology) was assessed. Pain was further assessed in a GM–CSF-driven arthritis (methylated bovine serum albumin/GM–CSF) model and the cyclooxygenase-dependence determined using indomethacin.

Results GM–CSF was absolutely required for pain development in both the inflammatory pain and arthritis models, including for IL-1-dependent arthritic pain. Pain in a GM–CSF-driven arthritis model, but not the disease itself, was abolished by the cyclooxygenase inhibitor, indomethacin, indicating separate pathways downstream of GM–CSF for pain and arthritis control.

Conclusions GM–CSF is key to the development of inflammatory and arthritic pain, suggesting that pain alleviation could result from trials evaluating its role in inflammatory/autoimmune conditions.

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    2012-12-12 lisa438
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    2012-08-25 lmm397
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