Riegger T, Conrad S, Schluesener H J, Kaps H-P, Badke A, Baron C, Gerstein J, Dietz K, Abdizahdeh M, Schwab J M
Institute of Brain Research, Department of Anatomy, Medical School, University of Tuebingen, 72076 Tuebingen, Germany.
Neuroscience. 2009 Feb 6;158(3):1194-9. doi: 10.1016/j.neuroscience.2008.08.021. Epub 2008 Aug 22.
Experimental spinal cord injury (SCI) has been identified to trigger a systemic, neurogenic immune depression syndrome. Here, we have analyzed fluctuations of immune cell populations following human SCI by FACS analysis. In humans, a rapid and drastic decrease of CD14+ monocytes (<50% of control level), CD3+ T-lymphocytes (<20%, P<0.0001) and CD19+ B-lymphocytes (<30%, P=0.0009) and MHC class II (HLA-DR)+ cells (<30%, P<0.0001) is evident within 24 h after spinal cord injury reaching minimum levels within the first week. CD15+ granulocytes were the only leukocyte subpopulation not decreasing after SCI. A contributing, worsening effect of high dose methylprednisolone cannot be excluded with this pilot study. We demonstrate that spinal cord injury is associated with an early onset of immune suppression and secondary immune deficiency syndrome (SCI-IDS). Identification of patients suffering spinal cord injury as immune compromised is a clinically relevant, yet widely underappreciated finding.
实验性脊髓损伤（SCI）已被证实会引发一种全身性的神经源性免疫抑制综合征。在此，我们通过流式细胞术分析了人类脊髓损伤后免疫细胞群体的波动情况。在人类中，脊髓损伤后24小时内，CD14 +单核细胞（<对照水平的50%）、CD3 + T淋巴细胞（<20%，P<0.0001）、CD19 + B淋巴细胞（<30%，P = 0.0009）和MHC II类（HLA-DR）+细胞（<30%，P<0.0001）迅速且显著减少，在第一周内降至最低水平。CD15 +粒细胞是脊髓损伤后唯一未减少的白细胞亚群。这项初步研究不能排除高剂量甲基强的松龙的促成和恶化作用。我们证明脊髓损伤与免疫抑制和继发性免疫缺陷综合征（SCI-IDS）的早期发作有关。将脊髓损伤患者识别为免疫功能受损是一项具有临床相关性但尚未得到充分重视的发现。
