Huang Jyun-Bin, Chen Nai-Ching, Chen Chien-Liang, Fu Mu-Hui, Pan Hsiu-Yung, Hsu Chung-Yao, Chen Shang-Der, Chuang Yao-Chung
Department of Emergency Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 83301, Taiwan.
College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan.
J Clin Med. 2020 Dec 26;10(1):61. doi: 10.3390/jcm10010061.
Stroke is a neurological emergency, where the mechanism of the blood supply to the brain is impaired, resulting in brain cell ischemia and death. Neuroinflammation is a key component in the ischemic cascade that results in cell damage and death after cerebral ischemia. The triggering receptor expressed on myeloid cells-1 (TREM-1) modulates neuroinflammation after acute ischemic stroke. In the present study, 60 patients with acute ischemic stroke, who had been subjected to neurological examinations and National Institutes of Health Stroke Scale (NIHSS) and brain magnetic resonance imaging studies, were enrolled in the emergency room of Kaohsiung Chang Gung Memorial Hospital. Twenty-four healthy volunteers were recruited as controls. The serum levels of soluble TREM-1 (sTREM-1), human S100 calcium-binding protein B (S100B), and proinflammatory cytokines and chemokines, including tumor necrosis α (TNF-α), interleukin 1β, interleukin 6 (IL-6), interleukin 8, and interferon-γ were measured immediately after acute ischemic stroke. The serum levels of sTREM-1, TNFα, IL-6, and S100B were correlated with the stroke volume and NIHSS, after acute ischemic stroke. Additionally, the serum levels of sTREM-1 were significantly positively correlated with S100B. The functional outcomes were evaluated 6 months after ischemic stroke by the Barthel index, which was correlated with the age and levels of sTREM-1 and S100B. We suggest that acute ischemic stroke induces neuroinflammation by the activation of the TREM-1 signaling pathway and the downstream inflammatory machinery that modulates the inflammatory response and ischemic neuronal cell death. From a translational perspective, our results may allow for the development of a new therapeutic strategy for acute ischemic stroke by targeting the TREM-1 signaling pathway.
中风是一种神经科急症，即脑部血液供应机制受损，导致脑细胞缺血和死亡。神经炎症是缺血级联反应的关键组成部分，可导致脑缺血后细胞损伤和死亡。髓样细胞表达的触发受体-1（TREM-1）可调节急性缺血性中风后的神经炎症。在本研究中，60例接受了神经学检查、美国国立卫生研究院卒中量表（NIHSS）评估及脑部磁共振成像检查的急性缺血性中风患者被纳入高雄长庚纪念医院急诊室。招募了24名健康志愿者作为对照。急性缺血性中风后立即检测可溶性TREM-1（sTREM-1）、人S100钙结合蛋白B（S100B）以及促炎细胞因子和趋化因子（包括肿瘤坏死因子α（TNF-α）、白细胞介素1β、白细胞介素6（IL-6）、白细胞介素8和干扰素-γ）的血清水平。急性缺血性中风后，sTREM-1、TNFα、IL-6和S100B的血清水平与中风体积和NIHSS相关。此外，sTREM-1的血清水平与S100B显著正相关。缺血性中风6个月后通过巴氏指数评估功能结局，该指数与年龄以及sTREM-1和S100B水平相关。我们认为急性缺血性中风通过激活TREM-1信号通路和调节炎症反应及缺血性神经元细胞死亡的下游炎症机制诱导神经炎症。从转化医学角度来看，我们的结果可能有助于通过靶向TREM-1信号通路开发急性缺血性中风的新治疗策略。
