Long-Term Kinetics of Immunologic Components and Neurological Deficits in Rats Following Repetitive Mild Traumatic Brain Injury.
Long-Term Kinetics of Immunologic Components and Neurological Deficits in Rats Following Repetitive Mild Traumatic Brain Injury.
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重复性轻度创伤性脑损伤后大鼠免疫成分和神经缺陷的长期动力学
DOI：
10.12659/msm.901124
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发表时间：
2017-04-08
期刊：
影响因子：
--
通讯作者：
Lei P
中科院分区：
文献类型：
--
作者：
Bai R;Gao H;Han Z;Ge X;Huang S;Chen F;Lei P
尽管人们越来越认识到重复性轻度创伤性脑损伤（rmTBI），但对中枢和外周免疫系统中免疫成分参与的长期动力学的理解仍然不完整。本研究的目的是提供一个定量测定rmTBI大鼠的某些免疫系统参数。采用改良神经功能评分（mNSS）和Morris水迷宫（MWM）评定神经功能，流式细胞术（FCM）检测脑组织和外周血免疫组化成分，酶联免疫吸附法（ELISA）检测肿瘤坏死因子（TNF）-α、白细胞介素（IL）-6和IL-10的浓度。rmTBI大鼠神经功能严重受损。在大脑中，T细胞被上调，并在第1周达到峰值。CD 4 + T细胞的百分比从第1周到第4周下降，而CD 8 + T细胞在第1周显著下降，然后增加直到第4周。Treg细胞浸润比例在第1周减少，第2周达到高峰。CD 86 +/CD 11b + M1在第4周达到峰值，CD 206 +/CD 11b + M2在第1周升高。IL-6/IL-10表现出类似的模式，其升高与rmTBI后2周TNF-α的降低相对应。FCM显示rmTBI后外周免疫功能紊乱。mNSS和MWM在rmTBI大鼠中表现出神经元缺陷，并且中枢和外周免疫系统与rmTBI的病理生理过程有关。长期免疫应答可能在rmTBI损伤和修复中发挥双重作用。
Despite growing awareness of repetitive mild traumatic brain injury (rmTBI), understanding of the involvement of long-term kinetics of immunologic components in the central and peripheral immune system took part remains incomplete. The present study aimed to provide a quantitative assay for certain immune system parameters in rmTBI rats. Neurological functions were assessed by modified Neurological Severity Score (mNSS) and Morris Water Maze (MWM), immunologic components from brain and peripheral blood were analyzed by flow cytometry (FCM), and concentrations of inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-10 were measure by enzyme-linked immunosorbent assay (ELISA). Neurological functions of rmTBI rats were seriously impaired. In the brain, T cells were up-regulated and peaked at week 1. The percentage of CD4+ T cells decreased from week 1 to week 4, while CD8+ T cells notably decreased at week 1, then increased until week 4. The infiltration proportion of Treg cells was reduced at week 1 and peaked at week 2. CD86+/CD11b+ M1 peaked at week 4 and CD206+/CD11b+ M2 rose at week 1. IL-6/IL-10 showed a similar pattern, whose rise corresponded to the decrease in TNF-α at week 2 after rmTBI. FCM demonstrated peripheral immune dysfunction after rmTBI. mNSS and MWM demonstrated neuronal deficits in rmTBI rats, and central and peripheral immune systems were implicated in the pathophysiological processes of rmTBI. Long-term immune response may play dual roles in injury and repair of rmTBI.