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本文引用的文献

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Cholinergic Pathway Suppresses Pulmonary Innate Immunity Facilitating Pneumonia After Stroke.胆碱能通路抑制肺部固有免疫,促进中风后肺炎的发生。
Stroke. 2015 Nov;46(11):3232-40. doi: 10.1161/STROKEAHA.115.008989. Epub 2015 Oct 8.
2
Reflections on the Irreproducibility of Scientific Papers.关于科学论文不可重复性的思考
Circ Res. 2015 Sep 25;117(8):665-6. doi: 10.1161/CIRCRESAHA.115.307496.
3
Unmasking Silent Endothelial Activation in the Cardiovascular System Using Molecular Magnetic Resonance Imaging.使用分子磁共振成像揭示心血管系统中的沉默内皮激活
Theranostics. 2015 Aug 8;5(11):1187-202. doi: 10.7150/thno.11835. eCollection 2015.
4
Results of a preclinical randomized controlled multicenter trial (pRCT): Anti-CD49d treatment for acute brain ischemia.一项临床前随机对照多中心试验(pRCT)的结果:抗 CD49d 治疗急性脑缺血。
Sci Transl Med. 2015 Aug 5;7(299):299ra121. doi: 10.1126/scitranslmed.aaa9853.
5
Combination of the Immune Modulator Fingolimod With Alteplase in Acute Ischemic Stroke: A Pilot Trial.免疫调节剂芬戈莫德与阿替普酶联合用于急性缺血性卒中:一项试点试验。
Circulation. 2015 Sep 22;132(12):1104-1112. doi: 10.1161/CIRCULATIONAHA.115.016371. Epub 2015 Jul 22.
6
Letter by Gauberti and Vivien regarding article, "amplification of regulatory T cells using a CD28 superagonist reduces brain damage after ischemic stroke in mice".高贝蒂和维维恩就题为“使用CD28超级激动剂扩增调节性T细胞可减少小鼠缺血性中风后的脑损伤”的文章所写的信。
Stroke. 2015 Feb;46(2):e50-1. doi: 10.1161/STROKEAHA.114.008071. Epub 2015 Jan 13.
7
Molecular magnetic resonance imaging of brain-immune interactions.脑-免疫相互作用的分子磁共振成像
Front Cell Neurosci. 2014 Nov 27;8:389. doi: 10.3389/fncel.2014.00389. eCollection 2014.
8
Impact of an immune modulator fingolimod on acute ischemic stroke.免疫调节剂芬戈莫德对急性缺血性卒中的影响。
Proc Natl Acad Sci U S A. 2014 Dec 23;111(51):18315-20. doi: 10.1073/pnas.1416166111. Epub 2014 Dec 8.
9
Amplification of regulatory T cells using a CD28 superagonist reduces brain damage after ischemic stroke in mice.使用CD28超级激动剂扩增调节性T细胞可减少小鼠缺血性中风后的脑损伤。
Stroke. 2015 Jan;46(1):212-20. doi: 10.1161/STROKEAHA.114.007756. Epub 2014 Nov 6.
10
Post-ischemic inflammation regulates neural damage and protection.缺血后炎症调节神经损伤与保护。
Front Cell Neurosci. 2014 Oct 14;8:319. doi: 10.3389/fncel.2014.00319. eCollection 2014.

缺血性卒中的“炎症半暗带”:从临床数据到实验证据

The "inflammatory penumbra" in ischemic stroke: From clinical data to experimental evidence.

作者信息

Gauberti Maxime, De Lizarrondo Sara Martinez, Vivien Denis

机构信息

Institut National de la Santé et de la Recherche Médicale (INSERM), INSERM UMR-S U919, Serine Proteases and Pathophysiology of the Neurovascular Unit, GIP Cyceron, Caen, France. University of Caen Normandy, Caen, France.

出版信息

Eur Stroke J. 2016 Mar;1(1):20-27. doi: 10.1177/2396987316630249. Epub 2016 Mar 1.

DOI:10.1177/2396987316630249
PMID:31008264
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6301219/
Abstract

PURPOSE

The objective of the present review is to provide an overview of the available clinical and preclinical data supporting the existence of an "inflammatory penumbra" in ischemic stroke.

FINDINGS

Recent data from clinical trials suggest the existence of an inflammatory area at risk, surrounding the initial ischemic lesion and secondarily infiltrated by lymphocytes, that is ultimately recruited by the ischemic core: called the "inflammatory penumbra." Experimental results support this concept. Lymphocytes, especially T-cells, enter the brain in the perilesional area in a vascular-cell adhesion molecule-1 dependent manner and participate in delayed neuronal cell death.

METHODS

For writing this review, we used the more recent publications in the field, including the preclinical and clinical studies. We have also used our own experise in the field of in vivo imaging of inflammatory processes.

DISCUSSION

Consequently, the intensity of the inflammatory reaction and the size of the inflammatory penumbra may vary considerably in patients, as it is the case in experimental stroke models in mice. By analogy with the ischemic penumbra of the acute phase of stroke, this secondary inflammatory penumbra represents a therapeutic opportunity during the subacute phase of stroke. Large clinical trials that target lymphocyte trafficking are currently taking place. However, to improve the benefit of such therapeutic strategies, adequate patient selection may be mandatory.

CONCLUSION

In this context, innovative imaging methods including magnetic resonance imaging of adhesion molecules may contribute to noninvasively detect this inflammatory penumbra and thus to select patients eligible for such therapy.

摘要

目的

本综述的目的是概述支持缺血性卒中存在“炎症半暗带”的现有临床和临床前数据。

研究结果

临床试验的最新数据表明,存在一个处于风险中的炎症区域,该区域围绕着最初的缺血性病变,并继发淋巴细胞浸润,最终被缺血核心所募集,称为“炎症半暗带”。实验结果支持这一概念。淋巴细胞,尤其是T细胞,以血管细胞黏附分子-1依赖的方式进入病灶周围区域的大脑,并参与延迟性神经元细胞死亡。

方法

为撰写本综述,我们使用了该领域的最新出版物,包括临床前和临床研究。我们还运用了自己在炎症过程体内成像领域的专业知识。

讨论

因此,炎症反应的强度和炎症半暗带的大小在患者中可能有很大差异,正如在小鼠实验性卒中模型中一样。与卒中急性期的缺血半暗带类似,这个继发性炎症半暗带代表了卒中亚急性期的一个治疗机会。目前正在进行针对淋巴细胞运输的大型临床试验。然而,为了提高此类治疗策略的益处,可能必须进行适当的患者选择。

结论

在这种情况下,包括黏附分子磁共振成像在内的创新成像方法可能有助于无创检测这个炎症半暗带,从而选择适合此类治疗的患者。