Ferretti Mario, Gassner Robert, Wang Zheng, Perera Priyangi, Deschner James, Sowa Gwendolyn, Salter Robert B, Agarwal Sudha
Section of Oral Biology, Department of Orthopedics, Ohio State University, 305 West 12th Avenue, Columbus, OH 43210, USA.
J Immunol. 2006 Dec 15;177(12):8757-66. doi: 10.4049/jimmunol.177.12.8757.
Although biomechanical signals generated during joint mobilization are vital in maintaining integrity of inflamed cartilage, the molecular mechanisms of their actions are little understood. In an experimental model of arthritis, we demonstrate that biomechanical signals are potent anti-inflammatory signals that repress transcriptional activation of proinflammatory genes and augment expression of anti-inflammatory cytokine IL-10 to profoundly attenuate localized joint inflammation.
尽管关节松动过程中产生的生物力学信号对于维持炎症软骨的完整性至关重要,但其作用的分子机制却鲜为人知。在一个关节炎实验模型中,我们证明生物力学信号是强大的抗炎信号,可抑制促炎基因的转录激活,并增强抗炎细胞因子白细胞介素-10的表达,从而显著减轻局部关节炎症。