The Ritchie Centre, Hudson Institute of Medical Research, 27-31 Wright St, Clayton, Victoria, 3168, Australia.
Department of Obstetrics and Gynaecology, Monash University, Clayton, 3168, Australia.
J Neuroinflammation. 2018 Feb 17;15(1):47. doi: 10.1186/s12974-018-1089-5.
It is well understood that hypoxic-ischemic (HI) brain injury during the highly vulnerable perinatal period can lead to cerebral palsy, the most prevalent cause of chronic disability in children. Recently, human clinical trials have reported safety and some efficacy following treatment of cerebral palsy using umbilical cord blood (UCB) cells. UCB is made up of many different cell types, including endothelial progenitor cells (EPCs), T regulatory cells (Tregs), and monocyte-derived suppressor cells (MDSCs). How each cell type contributes individually towards reducing neuroinflammation and/or repairing brain injury is not known. In this study, we examined whether human (h) UCB, or specific UCB cell types, could reduce peripheral and cerebral inflammation, and promote brain repair, when given early after perinatal HI brain injury.
HI brain injury was induced in postnatal day (PND) 7 rat pups and cells were administered intraperitoneally on PND 8. Behavioral testing was performed 7 days post injury, and then, brains and spleens were collected for analysis.
We found in vitro that all UCB cell types, except for EPCs, were immunomodulatory. Perinatal HI brain injury induced significant infiltration of CD4+ T cells into the injured cerebral hemisphere, and this was significantly reduced by all hUCB cell types tested. Compared to HI, UCB, Tregs, and EPCs were able to reduce motor deficits, reduce CD4+ T cell infiltration into the brain, and reduce microglial activation. In addition to the beneficial effects of UCB, EPCs also significantly reduced cortical cell death, returned CD4+ T cell infiltration to sham levels, and reduced the peripheral Th1-mediated pro-inflammatory shift.
This study highlights that cells found in UCB is able to mediate neuroinflammation and is an effective neuroprotective therapy. Our study also shows that particular cells found in UCB, namely EPCs, may have an added advantage over using UCB alone. This work has the potential to progress towards tailored UCB therapies for the treatment of perinatal brain injury.
众所周知,围生期极易发生的缺氧缺血性(HI)脑损伤可导致脑瘫,这是儿童最常见的慢性残疾原因。最近,人类临床试验报告了使用脐带血(UCB)细胞治疗脑瘫的安全性和一些疗效。UCB 由许多不同的细胞类型组成,包括内皮祖细胞(EPCs)、T 调节细胞(Tregs)和单核细胞衍生的抑制细胞(MDSCs)。每种细胞类型如何单独减少神经炎症和/或修复脑损伤尚不清楚。在这项研究中,我们研究了在围生期 HI 脑损伤后早期给予人(h)UCB 或特定 UCB 细胞类型是否可以减少外周和大脑炎症,并促进大脑修复。
在出生后第 7 天(PND)的大鼠幼崽中诱导 HI 脑损伤,并在 PND 8 时经腹腔给予细胞。在损伤后 7 天进行行为测试,然后收集大脑和脾脏进行分析。
我们在体外发现,除 EPCs 外,所有 UCB 细胞类型均具有免疫调节作用。围生期 HI 脑损伤诱导 CD4+T 细胞显著浸润损伤的大脑半球,所有测试的 hUCB 细胞类型均显著减少。与 HI 相比,UCB、Tregs 和 EPCs 能够减少运动缺陷,减少 CD4+T 细胞浸润大脑,并减少小胶质细胞激活。除了 UCB 的有益作用外,EPCs 还显著减少皮质细胞死亡,使 CD4+T 细胞浸润恢复到假手术水平,并减少外周 Th1 介导的促炎转移。
本研究强调,UCB 中发现的细胞能够介导神经炎症,是一种有效的神经保护治疗方法。我们的研究还表明,UCB 中发现的特定细胞,即 EPCs,可能比单独使用 UCB 具有更大的优势。这项工作有可能为治疗围生期脑损伤的定制 UCB 疗法提供进展。