Yilmaz Atilla, Fuchs Tanja, Dietel Barbara, Altendorf Regina, Cicha Iwona, Stumpf Christian, Schellinger Peter D, Blümcke Ingmar, Schwab Stefan, Daniel Werner G, Garlichs Christoph D, Kollmar Rainer
Clinic of Internal Medicine I, Department of Cardiology, University Hospital Jena, Jena, Germany.
Clin Sci (Lond). 2009 Oct 19;118(2):147-57. doi: 10.1042/CS20090154.
The role of DCs (dendritic cells) as potent mediators of inflammation has not been sufficiently investigated in stroke. Therefore, in the present study, circulating mDCPs (myeloid DC precursors), pDCPs (plasmacytoid DCPs) and tDCPs (total DCPs) were analysed by flow cytometry in (i) healthy controls (n=29), (ii) patients with ACI-S (asymptomatic cerebral infarction stenosis; n=46), (iii) patients with TIA (transient ischaemic attack; n=39), (iv) patients with AIS (acute ischaemic stroke; n=73), and (v) patients with AHS (acute haemorrhagic stroke; n=31). The NIHSS (National Institutes of Health Stroke Scale) and infarction size on a CT (computer tomography) scan were evaluated after stroke. In a patient subgroup, post-mortem immunohistochemical brain analyses were performed to detect mDCs (CD209), pDCs (CD123), T-cells (CD3) and HLA-DR. In AIS and AHS, the numbers of circulating mDCPs (P<0.005), pDCPs (P<0.005) and tDCPs (P<0.001) were significantly reduced. A significant inverse correlation was found between the NIHSS and circulating DCPs (P<0.02), as well as between hsCRP (high-sensitivity C-reactive protein) and circulating DCPs (P<0.001). Patients with large stroke sizes on a CT scan had significantly lower numbers of mDCPs (P=0.007), pDCPs (P=0.05) and tDCPs (P=0.01) than those with smaller stroke sizes. Follow-up analysis showed a significant recovery of circulating DCPs in the first few days after stroke. In the infarcted brain, a dense infiltration of mDCs co-localized with T-cells, single pDCs and high HLA-DR expression were observed. In conclusion, acute stroke leads to a decrease in circulating DCPs. Potentially, circulating DCPs are recruited from the blood into the infarcted brain and probably trigger cerebral immune reactions there.
树突状细胞（DCs）作为炎症的强效介质，在中风中的作用尚未得到充分研究。因此，在本研究中，通过流式细胞术分析了（i）健康对照者（n = 29）、（ii）无症状脑梗死狭窄患者（ACI-S；n = 46）、（iii）短暂性脑缺血发作患者（TIA；n = 39）、（iv）急性缺血性中风患者（AIS；n = 73）和（v）急性出血性中风患者（AHS；n = 31）的循环髓样DC前体（mDCPs）、浆细胞样DC前体（pDCPs）和总DC前体（tDCPs）。中风后评估美国国立卫生研究院卒中量表（NIHSS）和计算机断层扫描（CT）上的梗死面积。在一个患者亚组中，进行了死后免疫组化脑分析，以检测髓样DC（CD209）、浆细胞样DC（CD123）、T细胞（CD3）和HLA-DR。在AIS和AHS中，循环mDCPs（P < 0.005）、pDCPs（P < 0.005）和tDCPs（P < 0.001）的数量显著减少。发现NIHSS与循环DC前体之间存在显著负相关（P < 0.02），以及高敏C反应蛋白（hsCRP）与循环DC前体之间存在显著负相关（P < 0.001）。CT扫描显示中风面积大的患者的mDCPs（P = 0.007）、pDCPs（P = 0.05）和tDCPs（P = 0.01）数量明显低于中风面积小的患者。随访分析显示中风后最初几天循环DC前体有显著恢复。在梗死脑中，观察到髓样DC与T细胞共定位的密集浸润、单个浆细胞样DC和高HLA-DR表达。总之，急性中风导致循环DC前体减少。循环DC前体可能从血液中募集到梗死脑中，并可能在那里引发脑部免疫反应。
