Celgene Cellular Therapeutics, Warren, NJ, USA.
Brain Behav Immun. 2013 Jan;27(1):185-92. doi: 10.1016/j.bbi.2012.10.015. Epub 2012 Oct 24.
Neuropathic pain is a debilitating condition of the somatosensory system caused by pathology of the nervous system. Current drugs treat symptoms but largely fail to target the underlying mechanisms responsible for the pathological changes seen in the central or peripheral nervous system. We investigated the therapeutic effects of PDA-001, a culture expanded placenta-derived adherent cell, in the rat neuritis model. Pain is induced in the model by applying carrageenan to the sciatic nerve trunk, causing perineural inflammation of the sciatic nerve. PDA-001, at doses ranging from 0.4×10(6) to 4×10(6) cells/animal, or vehicle control was intravenously administrated to assess the biological activity of the cells. A dose-dependent effect of PDA-001 on pain relief was demonstrated. PDA-001 at doses of 1×10(6) and 4×10(6), but not 0.4×10(6), reduced mechanical hyperalgesia within 24h following treatment and through day 8 after induction of neuritis. The mechanism underlying PDA-001-mediated reduction of neuroinflammatory pain was also explored. Ex vivo tissue analyses demonstrated that PDA-001 suppressed homing, maturation and differentiation of dendritic cells, thus inhibiting T-cell priming and activation in draining lymph nodes. PDA-001 also reduced interferon gamma and IL-17 in draining lymph nodes and in the ispilateral sciatic nerve, and increased the levels of IL-10 in draining lymph nodes and plasma, pointing to T-cell modulation as a possible mechanism mediating the observed anti-hyperalgesic effects. Furthermore, in the ipsilateral sciatic nerve, significantly less leukocyte infiltration was observed in PDA-001-treated animals. The results suggest that PDA-001may provide a novel therapeutic approach in the management of inflammatory neuropathic pain and similar conditions.
神经病理性疼痛是一种躯体感觉系统的衰弱性疾病,由神经系统的病变引起。目前的药物治疗症状,但在很大程度上未能针对中枢或周围神经系统中观察到的病理变化的根本机制。我们研究了 PDA-001,一种培养的胎盘衍生贴壁细胞,在大鼠神经炎模型中的治疗效果。通过在坐骨神经干上应用卡拉胶诱导模型中的疼痛,导致坐骨神经的神经周围炎症。PDA-001,剂量范围为 0.4×10(6)至 4×10(6)个细胞/动物,或载体对照,静脉内给药,以评估细胞的生物学活性。PDA-001 对疼痛缓解的剂量依赖性效应得到了证明。PDA-001 在剂量为 1×10(6)和 4×10(6),但不是 0.4×10(6),在治疗后 24 小时内和神经炎诱导后第 8 天内减轻机械性痛觉过敏。还探索了 PDA-001 介导的神经炎性疼痛减轻的机制。离体组织分析表明,PDA-001 抑制树突状细胞的归巢、成熟和分化,从而抑制引流淋巴结中的 T 细胞启动和激活。PDA-001 还减少了引流淋巴结和同侧坐骨神经中的干扰素 γ和 IL-17,并增加了引流淋巴结和血浆中的 IL-10 水平,表明 T 细胞调节可能是介导观察到的抗痛觉过敏效应的一种机制。此外,在同侧坐骨神经中,在 PDA-001 治疗的动物中观察到白细胞浸润明显减少。结果表明,PDA-001 可能为炎症性神经病理性疼痛和类似疾病的治疗提供一种新的方法。